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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Acute kidney injury &#40;AKI&#41; is a common problem in Intensive Care Units &#40;ICU&#41; with a high level of associated mortality&#46; Several studies had already demonstrated that even small increases in serum creatinine were associated with a poorer prognosis&#44;<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">1</span></a> considering acute kidney disease as an independent risk factor of mortality&#46; Therefore&#44; the early identification of patients at risk&#44; the application of preventive strategies and carrying out early diagnosis and treatment are fundamental for reducing its incidence&#46; In this chapter we will revise the situations most commonly related to AKI in critical patients&#44; discussing the most appropriate prevention measures&#46; If&#44; in spite of this&#44; AKI becomes unavoidable&#44; efforts should be made to reduce its duration and to achieve the most complete recovery possible of kidney function &#40;secondary prevention&#41;&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Primary prevention</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Patients at risk</span><p id="par0010" class="elsevierStylePara elsevierViewall">In patients with intrahospital AKI&#44; the cause is usually multifactorial&#44; with kidney hypoperfusion being the most common &#40;fundamentally related to hypovolemia&#44; heart failure and arterial hypotension&#41;&#44; followed by the administration of nephrotoxic drugs and thirdly&#44; contrast associated acute kidney injury &#40;CA-AKI&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">2</span></a> Critical patients&#44; given their differential characteristics&#44; more often experience AKI associated with sepsis and hypovolemia&#44; with nephrotoxic drugs occupying third position&#46;<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">3</span></a> Numerous risk factors have been identified in the literature connected with the development of AKI &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#44; having an age of over 75 years&#44; Diabetes Mellitus &#40;DM&#41; and the presence of chronic kidney disease &#40;CKD&#41; being the most notable&#46; The most significant clinical factors include sepsis&#44; hypovolemia&#44; arterial hypotension&#44; congestive heart failure&#44; time of clamping in patients who undergo heart surgery&#44; complex and prolonged surgery&#44; a high severity index score at hospital admission and recent administration of nephrotoxic medication&#46;<a class="elsevierStyleCrossRef" href="#bib0380"><span class="elsevierStyleSup">4</span></a> With all of this&#44; different scales have been proposed to stratify patients at risk&#44; although currently these types of tools have yet to be developed&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">AKI prevention measures in critical patients</span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Management of acute illness</span><p id="par0015" class="elsevierStylePara elsevierViewall">With regard to the actual pathologies of the critical patient&#44; sepsis stands out as the main cause of acute kidney dysfunction&#44; with an incidence of 15&#8211;20&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">3</span></a> Regarding the non-septic AKI&#44; it has a higher mortality rate&#44; a longer stay in the ICU&#44; but a better rate of renal recovery&#44; with similar continuous renal replacement therapy &#40;CRRT&#41; needs&#46;<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">5</span></a> In this clinical context&#44; hypovolemia and hypotension tend to trigger AKI&#44; and although cases have been reported with normal hemodynamic parameters&#44;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">6</span></a> early resuscitation with fluids<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">7</span></a> and vasoactive drugs are the basis for its prevention and treatment&#44; taking into account that water overload can lead to tissue edema&#44; intraabdominal hypertension&#44; multiorgan dysfunction and greater mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">8</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Acute heart failure &#40;HF&#41; is also associated with a higher risk of AKI and a worse prognosis&#46; Type 1 Cardio-renal syndrome &#40;CRS&#41; appears in 27&#8211;40&#37; of all acute descompensated heart failure&#44; having a complex physiopathology&#46;<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">9</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Traditionally&#44; secondary renal hypoperfusion has been attributed to a low cardiac output&#44; however&#44; the results of the ESCAPE trial<a class="elsevierStyleCrossRef" href="#bib0410"><span class="elsevierStyleSup">10</span></a> did not find a correlation between AKI and the cardiac index or values of systemic vascular resistance&#46; To achieve its prevention it is necessary to treat and avoid situations that might decompensate the HF such as anemia&#44; hydro-electrolytic disorders&#44; arrythmia and medication&#46; To prevent AKI&#44; the administration of inotropic intravenous agents such as dobutamine would be indicated in situations of low cardiac output&#46; Loop diuretics would be the pharmacological treatment of choice for the control of water overload&#46; Other treatments&#44; such as vasopressin antagonists&#44; natriuretic peptide and levosimendan have been evaluated for the treatment of acute descompensated HF&#46; Unfortunately&#44; none of these agents have been shown to significantly improve long-term outcomes of this patient population&#44; including renal function&#46;<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">9</span></a> Identifying risk factors&#44; improving cardiac function and preventing acute decompensation are the key elements for its prevention&#46; Therefore&#44; traditionally recommended measures include&#58; modifying cardiovascular risk factors&#59; avoiding nephrotoxic agents that could provoke salt retention&#59; and the appropriate pharmacological treatment of heart failure&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Measures to improve renal perfusion</span><p id="par0030" class="elsevierStylePara elsevierViewall">Under normal conditions the kidneys receive 25&#37; of total blood flow to ensure a good oxygen delivery and consumption but they are extremely sensitive to decreases in blood flow with a rapid deterioration of renal function&#46; In the same way to ensure an adequate glomerular filtration rate &#40;GFR&#41; it is important to maintain an adequate mean arterial pressure &#40;MAP&#41;&#59; in most cases values of 65&#8211;70<span class="elsevierStyleHsp" style=""></span>mmHg are a reasonable threshold&#44; but in patients with chronic hypertension&#44; diabetes or initially impaired renal function&#44; higher MAP values should be considered&#46;<a class="elsevierStyleCrossRef" href="#bib0415"><span class="elsevierStyleSup">11</span></a> Therefore&#44; to avoid hemodynamic instability and hypoperfusion it is critical to prevent AKI&#46; When these circumstances exist&#44; volume expansion is the first therapeutic measure to optimize preload and thus to improve cardiac output&#46; Moreover&#44; fluid overload may have adverse outcomes&#44; including increased mortality and a reduced recovery of renal function&#46; Therefore&#44; it is recommended to estimate a patient&#39;s volume status and the use of dynamic and ultrasound measures which are reliable for predicting volume response&#46; Regardless of the amount of fluid administered&#44; the type of fluid may also have an impact on the development of AKI and current recommendations suggest the use of isotonic crystalloids&#46; The use of large amounts of 0&#46;9&#37; NaCl is significantly associated with hyperchloremic metabolic acidosis&#44; nevertheless&#44; the role of the chloride in the critical ill patients remains controversial&#46; It has been shown that hyperchloremia is associated with AKI<a class="elsevierStyleCrossRef" href="#bib0420"><span class="elsevierStyleSup">12</span></a> and that restriction of chloride-rich fluid is associated with a significant decrease in the incidence of AKI and the need of renal replacement therapy &#40;RRT&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">13</span></a> However&#44; a recent randomized controlled trial found no difference in the use of balanced crystalloid solutions vs saline solution in the development of AKI&#46;<a class="elsevierStyleCrossRef" href="#bib0430"><span class="elsevierStyleSup">14</span></a> The use of hydroxyethyl starches &#40;HES&#41; has been associated with adverse effects on kidney function&#46; These products have probably a direct nephrotoxic effect that appears to be dose and time dependent&#46; A recent meta-analysis showed a signi&#64257;cant increased risk of RRT and mortality in critically ill HES treated individuals<a class="elsevierStyleCrossRef" href="#bib0435"><span class="elsevierStyleSup">15</span></a> and a Cochrane review<a class="elsevierStyleCrossRef" href="#bib0440"><span class="elsevierStyleSup">16</span></a> showed that all HES products increase the risk of AKI and the need for RRT so that the authors recommended to avoid its use&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">When the worsening of renal function is due to a drop in renal perfusion caused by low cardiac output the short-term administration of selected inotropic agents&#44; especially dobutamine is indicated&#46; In the case of sepsis&#44; the use of inotropic agents is recommended only when there are signs of hypoperfusion&#44; despite achieving adequate intravascular volume and adequate MAP&#59; or when myocardial dysfunction is present&#46;<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">17</span></a> Levosimendan&#44; a positive inotropic agent with vasodilator effect&#44; may have a beneficial impact on renal function probably related to an increase in renal perfusion pressure and a decreased need for RRT&#46;<a class="elsevierStyleCrossRef" href="#bib0450"><span class="elsevierStyleSup">18</span></a> However&#44; according to the results of a recent clinical trial&#44; in adult patients with septic shock&#44; the addition of levosimendan to standard care is not associated with less severe organ dysfunction&#44; including renal failure&#44; or lower mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0455"><span class="elsevierStyleSup">19</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">In patients who remain hypotensive and oliguric after adequate fluid resuscitation and with a normal or increased cardiac output&#44; the use of the vasopressor agent is recommended to restore the blood pressure and protect renal function&#46; In septic shock&#44; MAP of at least 65<span class="elsevierStyleHsp" style=""></span>mmHg<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">17</span></a> is recommended&#46; Although a recent trial found no significant differences in mortality when two MAP targets &#40;65&#8211;70<span class="elsevierStyleHsp" style=""></span>mmHg vs&#46; 80&#8211;85<span class="elsevierStyleHsp" style=""></span>mmHg&#41; were compared&#44; in patients with chronic hypertension the need of RRT was lower in the higher MAP target group&#46;<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">20</span></a> In septic shock&#44; norepinephrine is the vasopressor of first choice&#44; epinephrine or vasopressin &#40;not available in Europe&#41; being the reasonable second-line vasopressor&#46;<a class="elsevierStyleCrossRefs" href="#bib0445"><span class="elsevierStyleSup">17&#44;20</span></a> Renal dose dopamine is ineffective for improving kidney function in AKI and its use is not recommended for renal protection&#46;<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">21</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Fenoldopam&#44; a selective dopamine D1 receptor agonist&#44; is able to increase renal blood flow &#40;RBF&#41; inducing dose-dependent renal vasodilation in patients with AKI or at a high risk of AKI&#44; although not available in Spain&#46; In a recent meta-analysis it has been suggested that its administration may reduce post-operative AKI&#44;<a class="elsevierStyleCrossRef" href="#bib0470"><span class="elsevierStyleSup">22</span></a> slow progression to dialysis-dependent AKI and improve survival&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Diuretics</span><p id="par0050" class="elsevierStylePara elsevierViewall">Diuretics are widely used in critical patients when diuresis decreases&#44; in an attempt to prevent the development of AKI&#44; however&#44; the diuretic response to furosemide is only one marker of the grade of residual renal function and less severe kidney failure&#46;<a class="elsevierStyleCrossRef" href="#bib0475"><span class="elsevierStyleSup">23</span></a> Loop diuretics have the property of reducing renal oxygen consumption as they reduce the active transport of sodium&#44; reducing the energetic requirements of tubular cells and theoretically protecting them from ischemia&#44; but they can have deleterious effects as they increase urine output fostering a depletion in volume&#44; electrolyte imbalances&#44; nephrotoxicity and ototoxicity&#44; thus perpetuating AKI&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">The use of mannitol&#44; although able to protect the kidney&#44; decreasing tissue edema&#44; increasing tubular flow and decreasing intra-tubular obstruction&#44; is also not justified as a preventive measure&#46; Its use has been trialed in kidney transplant surgery<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">24</span></a> and in rhabdomyolysis<a class="elsevierStyleCrossRef" href="#bib0485"><span class="elsevierStyleSup">25</span></a> without providing conclusive results&#46; Therefore&#44; in light of the available evidence&#44; it is recommended not to use diuretics for preventing AKI&#44; except in the management of water overload&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a> Diuretics should be administered over a short period and should never lead to a delay in starting continuous renal replacement therapy &#40;CRRT&#41;&#46;</p></span></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Specific measures</span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Nephrotoxicity by drugs</span><p id="par0060" class="elsevierStylePara elsevierViewall">Nephrotoxic medication is the third cause of AKI in the ICU&#44;<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">3</span></a> due to the high number of prescribed drugs&#44; the potential for adverse drug reactions and the actual nephrotoxicity of the drug&#46; There are increases in risk due to the interrelation of these drugs with factors of susceptibility and exposure &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>&#41; and because of its inadequate prescription&#46;<a class="elsevierStyleCrossRefs" href="#bib0495"><span class="elsevierStyleSup">27&#44;28</span></a> Prognosis and evolution to CKD is usually the same as in all the causes of AKI&#46;<a class="elsevierStyleCrossRef" href="#bib0500"><span class="elsevierStyleSup">28</span></a></p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0065" class="elsevierStylePara elsevierViewall">The following are dependent modifiable risk factors&#58; Duration of treatment&#44; daily&#47;total accumulated dose and pharmacodynamic and pharmakinetic interactions&#46; The associations of drugs also constitute a frequent risk&#44;<a class="elsevierStyleCrossRef" href="#bib0505"><span class="elsevierStyleSup">29</span></a> such as triple therapy drugs&#58; non-steroid antiinflammatory drugs &#40;NSAIDs&#41;<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>angiotensin-converting-enzyme &#40;ACE&#41; inhibitors&#8211;angiotensin receptor blockers &#40;ARBs&#41;<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>Diuretics&#46; The toxicity mechanisms are complex&#44; in many cases affecting more than one aspect of kidney function&#46;<a class="elsevierStyleCrossRef" href="#bib0510"><span class="elsevierStyleSup">30</span></a> They can be classified according to their kidney injury mechanism&#44; as well as to their histopathological findings &#40;<a class="elsevierStyleCrossRef" href="#tbl0015">Table 3</a>&#41;&#44; many of them interacting on different levels&#46;</p><elsevierMultimedia ident="tbl0015"></elsevierMultimedia><p id="par0070" class="elsevierStylePara elsevierViewall">Prevention is the best method for avoiding AKI&#44; with the early identification of the patients at risk and controlling the potentially modifiable risk factors&#44; including the non-prescription or interruption of nephrotoxic drugs whenever possible&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Aminoglycoside antimicrobial agents are highly potent&#44; bactericidal antibiotics&#44; its toxicity is multifactorial and strengthened by the susceptibility to and exposure to other factors&#46; The mechanisms involved in nephrotoxicity are<a class="elsevierStyleCrossRefs" href="#bib0515"><span class="elsevierStyleSup">31&#44;32</span></a>&#58; 1&#41; proximal tubular renal toxicity&#44; causing apoptosis and necrosis&#59; 2&#41; mesangial contraction with decreased glomerular filtration rate&#44; and 3&#41; reduction of renal blood flow secondary to increased vascular resistance&#46; Risk factors associated with the treatment include the length of it&#44; trough levels and dosing interval&#46; The pharmacokinetic and pharmacodynamic properties of aminoglycosides favor high dosing strategies with extended intervals between doses&#44; so in patients with normal kidney function in a steady state&#44; aminoglycosides should be administered as a single dose daily rather than multiple-dose daily treatment regimens&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Therapeutic efficacy is determined by peak blood level divided by minimum inhibitory concentration &#40;MIC&#41; of the infecting organism &#40;Cmax&#47;MIC&#41;&#46; The Cmax should be at least 10-fold greater than the MIC of the infecting microorganism&#44; and the sample must be taken within 30<span class="elsevierStyleHsp" style=""></span>min of administration&#46; Nephrotoxicity is associated with high levels of residual concentration &#40;trough level&#41;&#44; more than 20<span class="elsevierStyleHsp" style=""></span>h after being administered&#44; hence&#44; the importance of the determination of peak&#47;trough concentration for titration and dosing interval&#46; It is recommended monitoring aminoglycoside drug levels when treatment with single-daily dosing is used for more than 48<span class="elsevierStyleHsp" style=""></span>h or if multiple daily dosing is used for more than 24<span class="elsevierStyleHsp" style=""></span>h&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Therefore&#44; preventive strategies are extended-interval dosing&#44; limiting duration of therapy&#44; monitoring serum drug levels and renal function&#44; and manintaining trough levels&#44; measured between 18 and 24<span class="elsevierStyleHsp" style=""></span>h post-dose&#44; at 1<span class="elsevierStyleHsp" style=""></span>&#956;g&#47;ml or less&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">Amphotericin B deoxycholate is also an important nephrotoxic agent&#44; with an AKI incidence which can reach 80&#37;&#46; The nephrotoxicity mechanism is multifactorial and is associated with total accumulated dose&#46; Prevention is based on adequate hydroelectrolytic replacement and the administration of lipid-based formulations<a class="elsevierStyleCrossRefs" href="#bib0525"><span class="elsevierStyleSup">33&#44;34</span></a>&#58; liposomal form of Amphotericin B and Amphotericin B Lipid Complex&#46; Lipid-based formulations are less nephrotoxic as observed in several clinical studies and meta-analysis&#44; and some clinical studies suggest that liposomal form of Amphotericin B is less nephrotoxic than the other lipid-based formulations&#46;<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">34</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">With the increase of infections produced by beta-lactam-resistant Gram-positive bacteria&#44; other potential nephrotoxic antibiotics such as Vancomycin are being used increasingly in the ICU&#46; Its effectiveness is determined by the relationship AUC&#47;MIC<span class="elsevierStyleHsp" style=""></span>&#8805;<span class="elsevierStyleHsp" style=""></span>400&#44; being trough levels 15&#8211;20<span class="elsevierStyleHsp" style=""></span>mg&#47;L the clinical substitute for that relationship with MIC<span class="elsevierStyleHsp" style=""></span>&#8804;<span class="elsevierStyleHsp" style=""></span>1<span class="elsevierStyleHsp" style=""></span>mg&#47;L multi-resistant bacteria&#44; in case of MIC<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>1<span class="elsevierStyleHsp" style=""></span>mg&#47;L an alternative agent should be considered&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">35</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">Vancomycin-induced nephrotoxicity is based on their oxidative effects on cells of the proximal renal tubule&#44; which produces tubular renal ischemia&#46; It is related to trough levels &#8805;15<span class="elsevierStyleHsp" style=""></span>mg&#47;L&#44; duration of therapy&#44; renal dysfunction and previous use of other nephrotoxic drugs&#46; Hence the importance of strict monitoring of levels and dose adjustment&#44; with the possibility of administering a continuous intravenous infusion<a class="elsevierStyleCrossRefs" href="#bib0535"><span class="elsevierStyleSup">35&#44;36</span></a> as a protective factor of nephrotoxicity&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">Colistin &#40;Colistemetato Sodium&#41; is another nephrotoxic drug whose use has increased in ICU due to the increase in multidrug-resistant Gram negative bacteria&#46; Nephrotoxicity occurs due to the alteration of the tubular cell permeability and cell lysis&#46; Oxidative and inflammatory pathways are also implicated&#46; Risk factors are the cumulative dose administered&#44; treatment time&#44; concomitant use of other nephrotoxic and renal dysfunction with CrCl &#60;60<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#46; Dose is&#44; according to current recommendations&#44; carried out according to its Pk&#47;Pd properties&#44; with ascorbic acid being a possible independent protective factor administered at a twice-daily dose of 3 &#40;2&#8211;4&#41;<span class="elsevierStyleHsp" style=""></span>g&#46;<a class="elsevierStyleCrossRefs" href="#bib0545"><span class="elsevierStyleSup">37&#44;38</span></a></p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">AKI due to intra-tubular deposits</span><p id="par0110" class="elsevierStylePara elsevierViewall">Rhabdomyolysis is characterized by the destruction of skeletal muscle with the subsequent release of intracellular and enzymatic content into the bloodstream&#44; leading to systemic complications&#44; with the most common being AKI&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">39</span></a> It has an incidence of between 10 and 55&#37; and is associated with a poor prognosis when it is part of multiorgan dysfunction syndrome&#46; Apart from genetic predisposition&#44;<a class="elsevierStyleCrossRef" href="#bib0560"><span class="elsevierStyleSup">40</span></a> risk groups have been identified such as the morbid obese&#44; patients with chronic hypolipemiant drug consumption&#44; patients in a postoperative stage in some kinds of surgery&#44; etc&#46; Postoperative rhabdomyolysis has increased in recent years&#44; with risk factors related to surgical time&#44; immobility&#44; anesthetic drugs and comorbidities such as obesity and diabetes&#46;<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">41</span></a> There are many AKI mechanisms including&#58; hypovolemia&#44; myoglobinuria and metabolic acidosis&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">The treatment of the underlying etiology is the first measure to be taken and intensive fluid replacement is the cornerstone of the treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0570"><span class="elsevierStyleSup">42</span></a> Electrolytic corrections are fundamental&#44; with hyperkalemia being the only one requiring rapid correction due to the risk of cardiac arrythmia&#46; The use of bicarbonate is based on the concept that an acid setting promotes myoglobin toxicity&#59; therefore&#44; alkaline urine &#40;a pH greater than 6&#46;5&#41;&#44; could prevent AKI&#46; There is no consensus about the use of mannitol given that its secondary effects include volume depletion and potential prerenal azotemia&#46; However&#44; the theoretical benefits include an improvement in diuresis&#44; an increase in renal perfusion&#44; myoglobin excretion&#44; and a direct antioxidant effect on the renal parenchyma&#46;<a class="elsevierStyleCrossRef" href="#bib0485"><span class="elsevierStyleSup">25</span></a> The CRRT filters the myoglobin in the blood and normalizes creatinine and electrolyte levels&#44; although the mortality rate is unchanged&#46; Therefore&#44; it should only be used when the hydroelectrolytic alterations are life threatening&#46;<a class="elsevierStyleCrossRef" href="#bib0575"><span class="elsevierStyleSup">43</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">Other forms of AKI associated with intra-tubular deposits that we can observe in critical patients include tumor lysis syndrome and intravenous treatment with Acyclovir&#44; sulfonamides&#44; methotrexate&#44; indinavir and cysplatin&#46; Most of these patients are predisposed to having the following risk factors&#58; volume depletion and the presence of CKD&#44; with volume replacement being the most efficient preventive measure&#46; In the case of the administration of cysplatin&#44; at least 3<span class="elsevierStyleHsp" style=""></span>l of saline solution should be replaced 8<span class="elsevierStyleHsp" style=""></span>h before and after its administration together with a chelating agent such as aminophostine&#46; In order to prevent methotrexate precipitation it is recommended to administer saline solution with urinary alkalinization &#40;pH<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>6&#46;5&#41;&#44; and in the case of tumoral lysis syndrome&#44; prevention is carried out by expanding the volume to maintain an adequate urinary flow associated with the use of uricolytic agents like rasburicase&#46;<a class="elsevierStyleCrossRef" href="#bib0485"><span class="elsevierStyleSup">25</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Contrast-associated acute kidney injury</span><p id="par0125" class="elsevierStylePara elsevierViewall">Due to the increase in the use of contrast agents in the diagnosis and in interventionist processes&#44; CA-AKI has become the third most common cause of hospital-acquired kidney failure&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">2</span></a> The broadest definition used is an increase in serum creatinine &#8805;0&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dl or &#8805;25&#37; of the baseline level&#44; 48&#8211;72<span class="elsevierStyleHsp" style=""></span>h after exploration with contrast&#44; in the absence of any alternative etiology&#46; In the latest study carried out on critical patients&#44; an incidence level of 16&#46;3&#37; has been found&#46;<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">44</span></a> This incidence level is higher than that detected in Spanish ICUs&#44; according to the results of the NEFROCON study&#44;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">45</span></a> where an overall incidence of 12&#46;1&#37; was detected&#46; We also found significant differences among coronary patients&#44; with an incidence of 8&#46;2&#37;&#44; and the rest of critical patients&#44; with a higher incidence&#44; of 15&#46;3&#37;&#46;</p><p id="par0130" class="elsevierStylePara elsevierViewall">In spite of the clinical importance of this entity&#44; its pathogenesis is still unclear&#44; and it seems to be multifactorial&#44; including rheological alterations&#44; renal hemodynamic changes&#44; regional hypoxia&#44; auto&#47;paracrine factors &#40;adenosine&#44; endothelin&#44; reactive oxygen species&#41; even direct cytotoxic effects&#46;<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">46</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall">Of the patients who developed CA-AKI&#44; the most frequently identified risk factors were DM and CKD &#40;GFR lower than 60<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#47;1&#46;73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>&#41;&#46; Other reported risk factors were HF&#44; dehydration&#44; hyponatremia&#44; previous use of diuretics&#44; nephrotoxic drugs&#44; hypoalbuminemia&#44; advanced age&#44; female sex&#44; anemia&#44; administration of intra-arterial contrast and constrast dose&#46;<a class="elsevierStyleCrossRef" href="#bib0595"><span class="elsevierStyleSup">47</span></a> There is also an association between CA-AKI and indicators of hemodynamic instability&#44; such as periprocedural hypotension and the use of intra-aortic balloon counterpulsation &#40;IABC&#41;&#46; The effect of the risk factors is additive&#44; and the probability of CA-AKI increases considerably as the number of these increase&#46;<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">48</span></a> In critical patients&#44;<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">44</span></a> the variables associated with the development of CA-AKI were a higher level of serum creatinine&#44; arterial hypotension&#44; the administration of diuretics and vasoactive drugs&#46; These data have also been confirmed in the study carried out on critical Spanish patients&#44;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">45</span></a> where in addition&#44; level of severity&#44; estimated by APACHE II&#44; and anemia grade are factors related to CA-AKI&#46;</p><p id="par0140" class="elsevierStylePara elsevierViewall">Contrast media can be classified as hypo&#44; iso or hyperosmolar&#44; according to their osmolarity&#46; Several studies<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">49</span></a> suggest that in patients with a deterioration in kidney function&#44; hypo-osmolar &#40;500&#8211;1000<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#41; and iso-osmolar contrast &#40;290&#8211;300<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#41; are less nephrotoxic than hyperosmolar contrast media &#40;1000&#8211;2000<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#41;&#46; Based on current evidence&#44; their use is recommended in high risk patients&#59; both iso and hypo-osmolar contrast&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a> Contrast volume is also an independent predictor of CA-AKI<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">48</span></a>&#59; as a general rule it should not be more than two times the baseline GFR in milliliters&#46;<a class="elsevierStyleCrossRef" href="#bib0610"><span class="elsevierStyleSup">50</span></a></p><p id="par0145" class="elsevierStylePara elsevierViewall">To prevent CA-AKI different kinds of preventive therapies have been trialed&#46; The most adequate approach seems to be to identify patients at risk&#44; administer appropriate peri-procedural hydration and to minimize the quantity of contrast administered<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">51</span></a> &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0150" class="elsevierStylePara elsevierViewall">The objective of hydration is to maintain enough intravascular volume in order to be able to increase renal perfusion&#44; dilute the high concentrations of substances in the renal tubules&#44; prevent prolonged contact&#44; establish adequate diuresis prior to the administration of contrast and to prevent hypotension&#46;<a class="elsevierStyleCrossRef" href="#bib0620"><span class="elsevierStyleSup">52</span></a> Volume expansion should be intravenous&#44; and one of the most recommended hydration regimes is the administration of 1<span class="elsevierStyleHsp" style=""></span>ml&#47;kg&#47;h of 0&#46;9&#37; Saline 12<span class="elsevierStyleHsp" style=""></span>h before and after the procedure in patients with normal left ventricular ejection fraction &#40;LVEF&#41;&#46; For patients with low LVEF &#40;moderate or severe&#41; recommended hydration includes volume replacement according to urinary output to maintain an euvolemic state for 12<span class="elsevierStyleHsp" style=""></span>h pre and post-procedure&#46;</p><p id="par0155" class="elsevierStylePara elsevierViewall">Urinary alkalinization with sodium bicarbonate reduces renal damage by contrast by decreasing the quantity of free radicals dependent on pH&#44; although there are many studies that have assessed its preventive capacity with contradictory results&#46;<a class="elsevierStyleCrossRef" href="#bib0625"><span class="elsevierStyleSup">53</span></a> In 2009 probably the most complete systematic review of controlled randomized clinical trials was published&#44; analyzing 23 published and unpublished studies with significant heterogenicity between them&#44; concluding that the effectiveness of treatment with bicarbonate sodium in high risk patients is unclear&#44;<a class="elsevierStyleCrossRef" href="#bib0630"><span class="elsevierStyleSup">54</span></a> so that currently it is only used in emergency situations&#44; in which there is not enough time to begin adequate therapy with saline solution&#46;</p><p id="par0160" class="elsevierStylePara elsevierViewall">N-acetylcysteine &#40;NAC&#41; is a powerful antioxidant&#44; evaluated in many studies and meta-analyses&#44; that have been unable to demonstrate its preventive efficacy&#46; Not even the largest randomized multicenter study&#44;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">55</span></a> carried out in 2009&#44; could demonstrate the beneficial effect of N-acetylcysteine for reducing the incidence of CA-AKI&#46; This study included 2308 patients with at least one risk factor for its development &#40;&#62;70 years&#44; CKD&#44; DM&#44; CHF&#44; LVEF &#8804;45&#37; or shock&#41;&#46; The patients were randomized to receive oral NAC&#58; 1200<span class="elsevierStyleHsp" style=""></span>mg twice a day&#44; with two doses before the procedure and two doses after&#44; or a placebo&#46; In both groups similar rates of increase in plasma creatinine were found after 48&#8211;96<span class="elsevierStyleHsp" style=""></span>h&#46; Hoffman et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0640"><span class="elsevierStyleSup">56</span></a> assessed the efficacy of NAC in 50 healthy volunteers with normal kidney function&#44; finding a small but significant decrease in creatinine and urea in those patients who received it&#44; as well as an increase in glomerular filtrate without any changes in the levels of cystatin C&#46; This is due to its capacity to interfere with the metabolism of the creatinine&#44; bringing into question its efficacy for preventing CA-AKI&#46;</p><p id="par0165" class="elsevierStylePara elsevierViewall">It has also not been possible to demonstrate the protective effect of dopamine&#44; fenoldopam or theophylline<a class="elsevierStyleCrossRefs" href="#bib0645"><span class="elsevierStyleSup">57&#44;58</span></a> on kidney function and so its use is not currently recommended&#46;</p><p id="par0170" class="elsevierStylePara elsevierViewall">Owing to the capacity of dialysis to eliminate iodinated contrast from the blood flow&#44; several studies have been carried out to assess its role as a potential preventive measure&#46; Nevertheless&#44; it has not been possible to demonstrate a fall in the incidence of CA-AKI&#46; What is more&#44; in a meta-analysis carried out on several studies in which periprocedural extracorporeal techniques are performed it was not possible to demonstrate a beneficial effect either&#46;<a class="elsevierStyleCrossRef" href="#bib0655"><span class="elsevierStyleSup">59</span></a></p><p id="par0175" class="elsevierStylePara elsevierViewall">Recently&#44; there is controversy about the toxicity of modern low- or iso-osmolality iodinated contrast material as well as the role of nephroprotection&#46;<a class="elsevierStyleCrossRefs" href="#bib0660"><span class="elsevierStyleSup">60&#44;61</span></a> The methodology of the studies conducted are being questioned&#44; claiming that the studies included in the meta-analysis are heterogeneous and nonrandomized&#44; assuming a significant bias&#46; Most studies lacked a control group&#44; and in some including it&#44; the incidence is similar in both groups&#46; In addition to methodological issues&#44; many authors suggest that the incidence of AKI in ICU is multifactorial&#44; and the patient subjected to radiological contrast is also exposed to many other risk factors&#44; being the CA-AKI indistinguishable from acute kidney injury that occurs for other reasons&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Perioperative AKI</span><p id="par0180" class="elsevierStylePara elsevierViewall">The risk for its development is the interaction between renal susceptibility and the type and intensity of exposure to renal injury&#46; The knowledge of these risk factors could help in its prevention&#44; especially in the hospital setting&#44; with the most important risks being advanced age and CKD&#46;<a class="elsevierStyleCrossRefs" href="#bib0370"><span class="elsevierStyleSup">2&#44;4</span></a> The patients who meet the creatinine and diuresis criteria have worse results than the nonoliguric patients&#46; Along similar lines&#44; the FINNAKI study has noted that severe episodes of oliguria are independently associated with the development of AKI&#46;<a class="elsevierStyleCrossRef" href="#bib0670"><span class="elsevierStyleSup">62</span></a> However&#44; it should be taken into account that perioperative oliguria is&#44; commonly&#44; secondary to salt and water retention in response to tissue damage&#44; pain and moderate degrees of hypovolemia and hypotension&#46; Nearly 40&#37; of AKI in hospitalized patients occurs in the perioperative period&#44; and is mainly related to the specific surgical procedure&#46;<a class="elsevierStyleCrossRef" href="#bib0675"><span class="elsevierStyleSup">63</span></a> Heart surgery has the highest risk at RR&#58; 1&#46;22 &#40;95&#37; CI&#58; 1&#46;17&#8211;1&#46;27&#41;&#44; with major vascular surgery being another high risk surgical subgroup&#46; These results reinforce the importance of stratification of perioperative risk and the implementation of preventive strategies&#46; In addition&#44; several predictive risk models of AKI have been developed principally in the field of heart surgery&#46;</p><p id="par0185" class="elsevierStylePara elsevierViewall">The main causes of AKI include ischemia&#44; hypoxia&#44; inflammation and nephrotoxicity&#46; Other mechanisms are direct vascular injury or tubular obstruction&#46; Therefore&#44; it is not surprising that the simple restoration of circulating blood volume does not improve the results&#46; Recently&#44; the role of intraoperative hypotension has been related&#44;<a class="elsevierStyleCrossRef" href="#bib0680"><span class="elsevierStyleSup">64</span></a> finding an increase in risk when mean blood pressure was &#60;60<span class="elsevierStyleHsp" style=""></span>mmHg during &#62;20<span class="elsevierStyleHsp" style=""></span>min and &#60;55<span class="elsevierStyleHsp" style=""></span>mmHg during &#62;10<span class="elsevierStyleHsp" style=""></span>min&#46; The perioperative administration of levosimendan to patients who have undergone heart surgery reduces the incidence of AKI&#44; CRRT&#44; mortality&#44; mechanical ventilation time and stay in the ICU&#46; Remote ischemic preconditioning &#40;RIPC&#41; has proven cardiac and kidney protection with a possible reduction in mortality when it is used with halogenated anesthetics&#46; However&#44; two recent studies<a class="elsevierStyleCrossRefs" href="#bib0685"><span class="elsevierStyleSup">65&#44;66</span></a> suggest there is no difference between RIPC and standard treatment&#44; probably due to the use of propofol as a hypnotic drug&#46; Phenoldopam has not demonstrated its utility either&#44; being associated with a higher rate of hypotension&#46; Among the patients undergoing non heart-related major surgery&#44; neither aspirin nor clonidine reduced the perioperative risk of AKI&#46; In fact&#44; aspirin increases the risk of a severe hemorrhage and clonidine does the same to hypotension&#46;<a class="elsevierStyleCrossRef" href="#bib0695"><span class="elsevierStyleSup">67</span></a></p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">AKI in liver failure</span><p id="par0190" class="elsevierStylePara elsevierViewall">AKI is associated with a poor prognosis in cirrhotic patients&#46; The most common causes leading to it are listed in <a class="elsevierStyleCrossRef" href="#tbl0020">Table 4</a>&#46;<a class="elsevierStyleCrossRef" href="#bib0700"><span class="elsevierStyleSup">68</span></a> Splanchnic vasodilatation that is triggered by portal hypertension&#44; seems to induce hemodynamic changes and a deterioration in kidney function due to an increase in the production and activity of vasodilators such as nitric oxide&#44; a derivate of the endothelium&#44; due to bacterial translocation&#46;<a class="elsevierStyleCrossRef" href="#bib0700"><span class="elsevierStyleSup">68</span></a> The following preventive measures should be taken&#58; nephrotoxic drugs and NSAIDs should be avoided&#59; early antiviral treatment should be carried out in patients with Hepatitis C virus who fulfill the therapeutic criteria and are in a stable condition&#59; in hypovolemia or sepsis diuretics should be withdrawn&#59; and in the case of hemorrhagic shock&#44; hemoderivates should be administered&#44; variceal ligation should be performed together with preventive treatment of bleeding using propranolol&#46; Water overload should be prevented as this can aggravate hyponatremia and ascites&#46; It should be evacuated with albumin replacement &#40;8<span class="elsevierStyleHsp" style=""></span>g albumin per liter of ascites evacuated&#41;&#46; The appearance of Hepatorenal syndrome &#40;HRS&#41; after spontaneous bacterial peritonitis &#40;SBP&#41; can be efficiently prevented through the administration of albumin &#40;1&#46;5<span class="elsevierStyleHsp" style=""></span>g&#47;kg i&#46;v&#46; at the time of diagnosis and 1<span class="elsevierStyleHsp" style=""></span>g&#47;kg i&#46;v&#46; 48<span class="elsevierStyleHsp" style=""></span>h later&#41;<a class="elsevierStyleCrossRef" href="#bib0700"><span class="elsevierStyleSup">68</span></a> associated with the administration of norfloxacin &#40;400<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41;&#46; The albumin mechanism is unknown but has beneficial effects for heart function as well as antioxidant properties&#46;<a class="elsevierStyleCrossRef" href="#bib0705"><span class="elsevierStyleSup">69</span></a></p><elsevierMultimedia ident="tbl0020"></elsevierMultimedia></span></span></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Secondary prevention</span><p id="par0195" class="elsevierStylePara elsevierViewall">The early detection of the disease is the most important secondary prevention&#44; allowing us to detect the disease at its earliest stage to be able to apply all the measures aimed at preventing its progression&#46;</p><p id="par0200" class="elsevierStylePara elsevierViewall">The monitoring of diuresis and creatinine is recommended for the identification of the initial stages of AKI&#44; in accordance with the RIFLE&#44; AKIN or AKI-KDIGO scales&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a> In this way&#44; the presence of at least one of the following conditions is required&#58; an increase in creatinine of 0&#46;3<span class="elsevierStyleHsp" style=""></span>mg&#47;dl above the baseline value in less than 48<span class="elsevierStyleHsp" style=""></span>h&#59; an increase in creatinine 1&#46;5 times above the baseline value in less than 7 days&#59; or diuresis of under 0&#46;5<span class="elsevierStyleHsp" style=""></span>ml&#47;kg&#47;h for 6<span class="elsevierStyleHsp" style=""></span>h &#40;urine volume 0&#46;5<span class="elsevierStyleHsp" style=""></span>ml&#47;kg&#47;h for 6<span class="elsevierStyleHsp" style=""></span>h&#41;&#46;</p><p id="par0205" class="elsevierStylePara elsevierViewall">The frequency of this monitoring cannot be established generally for all patients&#46; In heart patients undergoing percutaneous coronary interventionist bladder catheterization is not usually used&#44; given that there is a general recommendation not to subject patients to unnecessary invasive procedures to prevent nosocomial infection&#46; This same rule could be applied to non heart-related patients in which bladder catheterization is not considered necessary&#46; Even so&#44; the registration and measurement of spontaneous diuresis can always be used&#46; The same occurs with readings of serum creatinine that could be less frequent in stable patients&#46; In any case&#44; the frequency used should allow for the detection of significant changes in the tendencies&#46;</p><p id="par0210" class="elsevierStylePara elsevierViewall">Once an AKI diagnosis has been established&#44; the patient should be reassessed from an angle more focused on renal function<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">51</span></a>&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#46;</span><p id="par0215" class="elsevierStylePara elsevierViewall">History&#58; antecedents&#44; nephrotoxic agents&#44; renal insults&#44; etc&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#46;</span><p id="par0220" class="elsevierStylePara elsevierViewall">Renal evaluation&#58;<ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">a&#46;</span><p id="par0225" class="elsevierStylePara elsevierViewall">Urine analysis &#40;ions and sediment&#41;&#46;</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">b&#46;</span><p id="par0230" class="elsevierStylePara elsevierViewall">Ultrasound in those cases in which the cause of AKI has not been identified&#44;<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">51</span></a> will make it possible to rule out obstructive problems&#44; collections&#44; evaluation of renal flow and the ruling out of alterations suggestive of chronicity&#46;</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">c&#46;</span><p id="par0235" class="elsevierStylePara elsevierViewall">Estimation of creatinine clearance by measuring urinary creatinine over a time interval &#40;2&#44; 6&#44; 12 or 24<span class="elsevierStyleHsp" style=""></span>h&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0710"><span class="elsevierStyleSup">70</span></a> It will allow for the adequate adjustment of drugs and the assessment of evolution&#46;</p></li></ul></p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">3&#46;</span><p id="par0240" class="elsevierStylePara elsevierViewall">Hemodynamic evaluation&#58; preload&#44; cardiac output&#44; blood pressure&#44; estimation of peripheral resistance&#44; tissue perfusion&#44; lactate and hemoglobin&#46;</p></li></ul></p><p id="par0245" class="elsevierStylePara elsevierViewall">In <a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a> there is a summary of recommended measures to be taken in the case of AKI&#46; Clinical evaluation from a renal standpoint&#44; will allow us to take the right measures in each case&#44; that will generally be&#58;<ul class="elsevierStyleList" id="lis0015"><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">-</span><p id="par0250" class="elsevierStylePara elsevierViewall">Volume expansion to optimize systolic volume and blood pressure &#40;BP&#41; in the case of shock&#46; Bolus of 250&#8211;500<span class="elsevierStyleHsp" style=""></span>ml can be administered until normalization of the preload&#46; It should always be ensured that the patient has a low preload and that there is a favorable response to the volume administration&#46;</p></li><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">-</span><p id="par0255" class="elsevierStylePara elsevierViewall">Early onset of amines<a class="elsevierStyleCrossRef" href="#bib0715"><span class="elsevierStyleSup">71</span></a> may help to improve blood pressure in combination with volume expansion&#46; Although it is controversial&#44; early use of amines can reduce fluid overload and positive balance that may have a deleterious effect&#46; The amine of choice is Norepinephrine&#46;<a class="elsevierStyleCrossRefs" href="#bib0445"><span class="elsevierStyleSup">17&#44;22</span></a></p></li><li class="elsevierStyleListItem" id="lsti0045"><span class="elsevierStyleLabel">-</span><p id="par0260" class="elsevierStylePara elsevierViewall">Daily monitoring of the water balance and measured rapid creatinine clearance &#40;2 or 4<span class="elsevierStyleHsp" style=""></span>h&#41;&#44; as well as general monitoring of every critical patient&#46;</p></li><li class="elsevierStyleListItem" id="lsti0050"><span class="elsevierStyleLabel">-</span><p id="par0265" class="elsevierStylePara elsevierViewall">Daily monitoring of AKI-related complications such as hyperpotasemia&#44; hypocalcemia and hyperphosphatemia&#46; Hyperpotasemia could be managed using medical measures in most cases&#46; Hypocalcemia should be treated with supplements&#46; Hyperphosphatemia in patients without symptoms can be treated using phosphoric chelates&#46;</p></li><li class="elsevierStyleListItem" id="lsti0055"><span class="elsevierStyleLabel">-</span><p id="par0270" class="elsevierStylePara elsevierViewall">Consistently high uremia values can produce changes in platelet aggregation and increase the bledding complications&#44; that can partially improve with the administration of desmopresin&#46;<a class="elsevierStyleCrossRef" href="#bib0720"><span class="elsevierStyleSup">72</span></a></p></li><li class="elsevierStyleListItem" id="lsti0060"><span class="elsevierStyleLabel">-</span><p id="par0275" class="elsevierStylePara elsevierViewall">In nearly 25&#37; of cases of sepsis-induced AKI the nephrotoxic drugs can contribute to renal deterioration<a class="elsevierStyleCrossRef" href="#bib0495"><span class="elsevierStyleSup">27</span></a> and must be discontinued&#44; if not done previously&#46; Only those considered as essential should be continued when they cannot be replaced by another equivalent and with a prior dose adjustment according to the patient&#39;s renal function&#46;</p></li><li class="elsevierStyleListItem" id="lsti0065"><span class="elsevierStyleLabel">-</span><p id="par0280" class="elsevierStylePara elsevierViewall">Adjustment of the drugs according to renal function because of levels or estimated levels of renal function using the creatinine clearance measurement in urine over short periods of time&#46;</p></li><li class="elsevierStyleListItem" id="lsti0070"><span class="elsevierStyleLabel">-</span><p id="par0285" class="elsevierStylePara elsevierViewall">Avoiding the use of furosemide as it can worsen the evolution of AKI&#44; hinder the daily assessment of renal function and delay the start of dialytic techniques&#46; When its use is considered necessary to increase diuresis because of volume overload&#44; and it is considered that it could add a prerenal component&#44; increases in the serum urea value can be used to guide the treatment and interrupt it if necessary&#46;</p></li><li class="elsevierStyleListItem" id="lsti0075"><span class="elsevierStyleLabel">-</span><p id="par0290" class="elsevierStylePara elsevierViewall">Avoiding the use of low-dose dopamine&#59; it does not improve the evolution of AKI&#44;<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">21</span></a> and it can worsen renal blood flow and produce a higher frequency of supraventricular tachiarrythmias&#46;</p></li><li class="elsevierStyleListItem" id="lsti0080"><span class="elsevierStyleLabel">-</span><p id="par0295" class="elsevierStylePara elsevierViewall">Providing adequate nutrition&#59; the basic requirements are usually similar to those of a critical patient according to his or her catabolic state&#46; The protein needs are usually 1&#8211;1&#46;5<span class="elsevierStyleHsp" style=""></span>g&#47;kg&#47;day&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a> Classic conceptions of hypoproteic diets should be avoided to prevent increases in urea and to delay the start of dialysis&#46;</p></li></ul></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0300" class="elsevierStylePara elsevierViewall">The majority of the episodes of AKI in patients admitted to the ICU are secondary to another disease that causes renal affectation&#46; The treatment of the cause of admission or the complication that has contributed to the development of AKI is crucial for preventing its progression&#46; In the case of sepsis it is of vital importance to control the focus of the disease using an early start of antibiotics and&#47;or surgical treatment when appropriate&#46;</p></span><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Funding source</span><p id="par0305" class="elsevierStylePara elsevierViewall">None&#46;</p></span><span id="sec0080" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Conflict of interests</span><p id="par0310" class="elsevierStylePara elsevierViewall">The authors declare no conflict of interest&#46;</p></span></span>"
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                3 => array:2 [
                  "identificador" => "sec0060"
                  "titulo" => "Perioperative AKI"
                ]
                4 => array:2 [
                  "identificador" => "sec0065"
                  "titulo" => "AKI in liver failure"
                ]
              ]
            ]
          ]
        ]
        6 => array:2 [
          "identificador" => "sec0070"
          "titulo" => "Secondary prevention"
        ]
        7 => array:2 [
          "identificador" => "sec0075"
          "titulo" => "Funding source"
        ]
        8 => array:2 [
          "identificador" => "sec0080"
          "titulo" => "Conflict of interests"
        ]
        9 => array:1 [
          "titulo" => "References"
        ]
      ]
    ]
    "pdfFichero" => "main.pdf"
    "tienePdf" => true
    "fechaRecibido" => "2016-09-15"
    "fechaAceptado" => "2016-12-01"
    "PalabrasClave" => array:2 [
      "en" => array:1 [
        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Keywords"
          "identificador" => "xpalclavsec817020"
          "palabras" => array:3 [
            0 => "Acute kidney injury"
            1 => "Primary prevention"
            2 => "Secondary prevention"
          ]
        ]
      ]
      "es" => array:1 [
        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Palabras clave"
          "identificador" => "xpalclavsec817019"
          "palabras" => array:3 [
            0 => "Lesi&#243;n renal aguda"
            1 => "Prevenci&#243;n primaria"
            2 => "Prevenci&#243;n secundaria"
          ]
        ]
      ]
    ]
    "tieneResumen" => true
    "resumen" => array:2 [
      "en" => array:2 [
        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Acute kidney injury &#40;AKI&#41; is a growing concern in Intensive Care Units&#46; The advanced age of our patients&#44; with the increase in associated morbidity and the complexity of the treatments provided favor the development of AKI&#46; Since no effective treatment for AKI is available&#44; all efforts are aimed at prevention and early detection of the disorder in order to establish secondary preventive measures to impede AKI progression&#46; In critical patients&#44; the most frequent causes are sepsis and situations that result in renal hypoperfusion&#59; preventive measures are therefore directed at securing hydration and correct hemodynamics through fluid perfusion and the use of inotropic or vasoactive drugs&#44; according to the underlying disease condition&#46; Apart from these circumstances&#44; a number of situations could lead to AKI&#44; related to the administration of nephrotoxic drugs&#44; intra-tubular deposits&#44; the administration of iodinated contrast media&#44; liver failure and major surgery &#40;mainly heart surgery&#41;&#46; In these cases&#44; in addition to hydration&#44; there are other specific preventive measures adapted to each condition&#46;</p></span>"
      ]
      "es" => array:2 [
        "titulo" => "Resumen"
        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La lesi&#243;n renal aguda &#40;LRA&#41; constituye un problema de importancia creciente en las unidades de cuidados intensivos&#46; La mayor edad de nuestros pacientes&#44; con el aumento de la morbilidad asociada&#44; y la complejidad de los tratamientos realizados favorecen su desarrollo&#46; Puesto que la LRA carece de tratamiento eficaz&#44; todos los esfuerzos se dirigen a la prevenci&#243;n y a su detecci&#243;n precoz con el fin de establecer medidas de prevenci&#243;n secundaria que impidan su progresi&#243;n&#46; En el paciente cr&#237;tico&#44; las causas m&#225;s frecuentemente implicadas son la sepsis y las situaciones que provocan hipoperfusi&#243;n renal&#44; por lo que las medidas preventivas ir&#225;n encaminadas a mantener un estado de hidrataci&#243;n y hemodin&#225;mico correcto mediante perfusi&#243;n de fluidos y el uso de f&#225;rmacos inotr&#243;picos o vasoactivos en funci&#243;n de la enfermedad subyacente&#46; Adem&#225;s de estas circunstancias&#44; existen distintas situaciones que pueden favorecer la LRA&#44; relacionadas con la administraci&#243;n de f&#225;rmacos nefrot&#243;xicos&#44; los dep&#243;sitos intratubulares&#44; la administraci&#243;n de contrastes iodados&#44; el fallo hep&#225;tico y la cirug&#237;a mayor&#44; fundamentalmente cirug&#237;a cardiaca&#46; En estos casos&#44; adem&#225;s de la hidrataci&#243;n&#44; se dispone de otros aspectos preventivos espec&#237;ficos de cada entidad&#46;</p></span>"
      ]
    ]
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        "tipo" => "MULTIMEDIAFIGURA"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Recommendations for CA-AKI prevention&#46; Modified from ref&#46; 51&#46; CA-AKI&#58; contrast associated acute kidney injury&#59; CKD&#58; chronic kidney disease&#59; GFR&#58; glomerular filtration rate&#59; DM&#58; diabetes mellitus&#59; HF&#58; heart failure&#59; NSAIDs&#58; non steroidal antiinflammatory drugs&#59; CRRT&#58; continuous renal replacement therapy&#59; AECI&#58; angiotensin converting enzyme inhibitors&#46;</p>"
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        "figura" => array:1 [
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Summary of recommendations to prevent progression to acute kidney injury&#46;</p>"
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          "leyenda" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Modified from Ref&#46; <a class="elsevierStyleCrossRef" href="#bib0380">4</a>&#46;</p>"
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            0 => array:2 [
              "tabla" => array:1 [
                0 => """
                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Risk factor&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Odds ratio &#40;95&#37; CI&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Disease severity&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">9&#46;08 &#40;4&#46;57&#8211;13&#46;60&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Age&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">4&#46;95 &#40;3&#46;79&#8211;6&#46;12&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Use of vasopressors&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">4&#46;52 &#40;2&#46;03&#8211;10&#46;05&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Sepsis&#47;SIRS&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">4&#46;15 &#40;2&#46;36&#8211;7&#46;32&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hypotension&#47;Shock&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">3&#46;33 &#40;1&#46;70&#8211;6&#46;52&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">High risk&#47;urgent surgery&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">2&#46;34 &#40;1&#46;23&#8211;4&#46;49&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Heart failure&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">2&#46;05 &#40;1&#46;77&#8211;2&#46;38&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Diabetes&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">1&#46;58 &#40;1&#46;36&#8211;1&#46;84&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Use of nephrotoxic medication&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">1&#46;53 &#40;1&#46;09&#8211;2&#46;14&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hypertension&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">1&#46;43 &#40;1&#46;08&#8211;1&#46;89&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Baseline creatinine&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">0&#46;14 &#40;0&#46;01&#8211;0&#46;27&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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        "descripcion" => array:1 [
          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Risk factors for the development of AKI&#46;</p>"
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      ]
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        "etiqueta" => "Table 2"
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          "leyenda" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">BDI&#58; body mass index&#59; CKD&#58; chronic kidney disease&#46;</p>"
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                0 => """
                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Susceptibility&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Age<br>Black race<br>Female sex<br>Diabetes mellitus<br>Obesity &#40;BMI<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>40&#41;<br>Arterial hypertension<br>CKD<br>Deshydration<br>Neoplasias<br>Hypoalbuminemia<br>Anemia<br>Chronic diseases&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Exposure&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Nephrotoxic drugs<br>Contrast media<br>Trauma&#44; burns<br>Sepsis<br>High risk surgery<br>Hypotension<br>Fluid overload&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Nephrotoxic drugs&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Treatment time<br>Total&#47;daily accumulated dose<br>High concentrations<br>Drug interactions&#58;<br><span class="elsevierStyleHsp" style=""></span>Pharmacokinetic<br><span class="elsevierStyleHsp" style=""></span>Pharmacodynamic&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
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        "descripcion" => array:1 [
          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Nephrotoxic drugs&#44; factors of susceptibility and exposure&#46;</p>"
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      4 => array:8 [
        "identificador" => "tbl0015"
        "etiqueta" => "Table 3"
        "tipo" => "MULTIMEDIATABLA"
        "mostrarFloat" => true
        "mostrarDisplay" => false
        "detalles" => array:1 [
          0 => array:3 [
            "identificador" => "at3"
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          "leyenda" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">NSAID&#58; non-steroid anti-inflammatory drugs&#59; AECI&#58; angiotensin-converting enzyme inhibitors&#59; ARB&#58; angiotensin receptor blockers&#59; ATN&#58; acute tubular necrosis&#46;</p>"
          "tablatextoimagen" => array:1 [
            0 => array:2 [
              "tabla" => array:1 [
                0 => """
                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Adverse mechanism&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Drugs&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Intraglomerular hemodynamics&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">NSAID<br>Cyclooxygenase inhibitors<br>AECI and ARB<br>Calcineurin inhibitors&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">ATN&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Aminoglycosides&#44; Anphotericin B<br>Contrast media<br>Antiretroviral drugs<br>Cysplatin&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Allergic interstitial nephritis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Antibiotics&#58; penicillin&#44; cephalosporins&#44; macrolids&#44; cyprofloxacine&#44; vancomicyn&#44; rifampicin&#44; tetracycline drugs<br>NSAID<br>Omeprazol<br>Phenytoin and valproic acid<br>Cimetidine<br>Diuretics&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Glomerulonephritis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">NSAID<br>Ampicillin&#44; riphampicin<br>Lithium&#44; penicillamine<br>Hydralazine&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Postrenal Obstruction&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Acyclovir<br>Methotrexate<br>Sulphadiazine<br>Foscarnet&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Osmotic nephrosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Immunoglobulins<br>Hydroxyethyl starch<br>Mannitol<br>Contrast media&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
              ]
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                0 => "xTab1378432.png"
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        "descripcion" => array:1 [
          "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Mechanism of kidney injury from nephrotoxic drugs&#46;</p>"
        ]
      ]
      5 => array:8 [
        "identificador" => "tbl0020"
        "etiqueta" => "Table 4"
        "tipo" => "MULTIMEDIATABLA"
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          "leyenda" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">HRS&#58; hepatorenal syndrome&#59; ATN&#58; acute tubular necrosis&#59; UGIH&#58; upper gastrointestinal hemorrhage&#59; NSAID&#58; non steroidal antiinflammatory drugs&#59; AMG&#58; aminoglycosides&#46;</p><p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Modified from Ref&#46; <a class="elsevierStyleCrossRef" href="#bib0690">66</a>&#46;</p>"
          "tablatextoimagen" => array:1 [
            0 => array:2 [
              "tabla" => array:1 [
                0 => """
                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Type of AKI&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Diagnosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hepatorenal s&#237;ndrome&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Diagnosis of HRS&#58; serum creatinine &#62;1&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; that does not decrease after the administration of albumin &#40;1<span class="elsevierStyleHsp" style=""></span>g&#47;kg weight&#41; at least two days after the suspension of diuretics&#44; in the absence of nephrotoxic drugs&#44; shock or findings suggestive of ATN&#46;<br>HRS type 1&#58; increase to double the amount of serum creatinine to more than 2&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dl in less than 2 weeks&#46;<br>HRS type 2&#58; a less progressive evolution than type 1&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">AKI induced by hypovolemia&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Generally due to a hemorrhage &#40;UGIH&#41; or fluid loss &#40;diuretics overdose&#44; diarrhea due to an excessive administration of lactulose&#44; acute gastroenteritis&#41;&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Acute tubular necrosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Suspected if proteinuria &#40;&#62;500<span class="elsevierStyleHsp" style=""></span>mg proteins&#47;day&#41; and&#47;or hematuria &#40;&#62;50 red blood cells per field&#41;&#46;<br>Differential diagnosis with HRS is difficult&#46; Suspicion of ATN if the tubular renal epithelial cells are in urinary sediment&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">AKI due to nephrotoxic drugs&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Recent or current treatment with NSAID or AMG&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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Special article
Prevention of acute kidney injury in Intensive Care Units
Prevención de la lesión renal aguda en las unidades de cuidados intensivos
S. Mas-Fonta,
Corresponding author
masf.sonia@gmail.com

Corresponding author.
, J. Ros-Martinezb, C. Pérez-Calvoc, P. Villa-Díazd, S. Aldunate-Calvoe, E. Moreno-Claria, on belhaf of the Workgroup on Nephrology Intensive Care of the SEMICYUC
a Intensive Care Medicine, Hospital General Universitario de Castellón, Spain
b Intensive Care Medicine, Hospital Clínico Universitario Virgen de la Arrixaca, Murcia, Spain
c Intensive Care Medicine, Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain
d Intensive Care Medicine, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain
e Intensive Care Medicine, Complejo Hospitalario de Navarra, Pamplona, Spain
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Recommendations for CA-AKI prevention&#46; Modified from ref&#46; 51&#46; CA-AKI&#58; contrast associated acute kidney injury&#59; CKD&#58; chronic kidney disease&#59; GFR&#58; glomerular filtration rate&#59; DM&#58; diabetes mellitus&#59; HF&#58; heart failure&#59; NSAIDs&#58; non steroidal antiinflammatory drugs&#59; CRRT&#58; continuous renal replacement therapy&#59; AECI&#58; angiotensin converting enzyme inhibitors&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Acute kidney injury &#40;AKI&#41; is a common problem in Intensive Care Units &#40;ICU&#41; with a high level of associated mortality&#46; Several studies had already demonstrated that even small increases in serum creatinine were associated with a poorer prognosis&#44;<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">1</span></a> considering acute kidney disease as an independent risk factor of mortality&#46; Therefore&#44; the early identification of patients at risk&#44; the application of preventive strategies and carrying out early diagnosis and treatment are fundamental for reducing its incidence&#46; In this chapter we will revise the situations most commonly related to AKI in critical patients&#44; discussing the most appropriate prevention measures&#46; If&#44; in spite of this&#44; AKI becomes unavoidable&#44; efforts should be made to reduce its duration and to achieve the most complete recovery possible of kidney function &#40;secondary prevention&#41;&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Primary prevention</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Patients at risk</span><p id="par0010" class="elsevierStylePara elsevierViewall">In patients with intrahospital AKI&#44; the cause is usually multifactorial&#44; with kidney hypoperfusion being the most common &#40;fundamentally related to hypovolemia&#44; heart failure and arterial hypotension&#41;&#44; followed by the administration of nephrotoxic drugs and thirdly&#44; contrast associated acute kidney injury &#40;CA-AKI&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">2</span></a> Critical patients&#44; given their differential characteristics&#44; more often experience AKI associated with sepsis and hypovolemia&#44; with nephrotoxic drugs occupying third position&#46;<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">3</span></a> Numerous risk factors have been identified in the literature connected with the development of AKI &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#44; having an age of over 75 years&#44; Diabetes Mellitus &#40;DM&#41; and the presence of chronic kidney disease &#40;CKD&#41; being the most notable&#46; The most significant clinical factors include sepsis&#44; hypovolemia&#44; arterial hypotension&#44; congestive heart failure&#44; time of clamping in patients who undergo heart surgery&#44; complex and prolonged surgery&#44; a high severity index score at hospital admission and recent administration of nephrotoxic medication&#46;<a class="elsevierStyleCrossRef" href="#bib0380"><span class="elsevierStyleSup">4</span></a> With all of this&#44; different scales have been proposed to stratify patients at risk&#44; although currently these types of tools have yet to be developed&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">AKI prevention measures in critical patients</span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Management of acute illness</span><p id="par0015" class="elsevierStylePara elsevierViewall">With regard to the actual pathologies of the critical patient&#44; sepsis stands out as the main cause of acute kidney dysfunction&#44; with an incidence of 15&#8211;20&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">3</span></a> Regarding the non-septic AKI&#44; it has a higher mortality rate&#44; a longer stay in the ICU&#44; but a better rate of renal recovery&#44; with similar continuous renal replacement therapy &#40;CRRT&#41; needs&#46;<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">5</span></a> In this clinical context&#44; hypovolemia and hypotension tend to trigger AKI&#44; and although cases have been reported with normal hemodynamic parameters&#44;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">6</span></a> early resuscitation with fluids<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">7</span></a> and vasoactive drugs are the basis for its prevention and treatment&#44; taking into account that water overload can lead to tissue edema&#44; intraabdominal hypertension&#44; multiorgan dysfunction and greater mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">8</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Acute heart failure &#40;HF&#41; is also associated with a higher risk of AKI and a worse prognosis&#46; Type 1 Cardio-renal syndrome &#40;CRS&#41; appears in 27&#8211;40&#37; of all acute descompensated heart failure&#44; having a complex physiopathology&#46;<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">9</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Traditionally&#44; secondary renal hypoperfusion has been attributed to a low cardiac output&#44; however&#44; the results of the ESCAPE trial<a class="elsevierStyleCrossRef" href="#bib0410"><span class="elsevierStyleSup">10</span></a> did not find a correlation between AKI and the cardiac index or values of systemic vascular resistance&#46; To achieve its prevention it is necessary to treat and avoid situations that might decompensate the HF such as anemia&#44; hydro-electrolytic disorders&#44; arrythmia and medication&#46; To prevent AKI&#44; the administration of inotropic intravenous agents such as dobutamine would be indicated in situations of low cardiac output&#46; Loop diuretics would be the pharmacological treatment of choice for the control of water overload&#46; Other treatments&#44; such as vasopressin antagonists&#44; natriuretic peptide and levosimendan have been evaluated for the treatment of acute descompensated HF&#46; Unfortunately&#44; none of these agents have been shown to significantly improve long-term outcomes of this patient population&#44; including renal function&#46;<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">9</span></a> Identifying risk factors&#44; improving cardiac function and preventing acute decompensation are the key elements for its prevention&#46; Therefore&#44; traditionally recommended measures include&#58; modifying cardiovascular risk factors&#59; avoiding nephrotoxic agents that could provoke salt retention&#59; and the appropriate pharmacological treatment of heart failure&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Measures to improve renal perfusion</span><p id="par0030" class="elsevierStylePara elsevierViewall">Under normal conditions the kidneys receive 25&#37; of total blood flow to ensure a good oxygen delivery and consumption but they are extremely sensitive to decreases in blood flow with a rapid deterioration of renal function&#46; In the same way to ensure an adequate glomerular filtration rate &#40;GFR&#41; it is important to maintain an adequate mean arterial pressure &#40;MAP&#41;&#59; in most cases values of 65&#8211;70<span class="elsevierStyleHsp" style=""></span>mmHg are a reasonable threshold&#44; but in patients with chronic hypertension&#44; diabetes or initially impaired renal function&#44; higher MAP values should be considered&#46;<a class="elsevierStyleCrossRef" href="#bib0415"><span class="elsevierStyleSup">11</span></a> Therefore&#44; to avoid hemodynamic instability and hypoperfusion it is critical to prevent AKI&#46; When these circumstances exist&#44; volume expansion is the first therapeutic measure to optimize preload and thus to improve cardiac output&#46; Moreover&#44; fluid overload may have adverse outcomes&#44; including increased mortality and a reduced recovery of renal function&#46; Therefore&#44; it is recommended to estimate a patient&#39;s volume status and the use of dynamic and ultrasound measures which are reliable for predicting volume response&#46; Regardless of the amount of fluid administered&#44; the type of fluid may also have an impact on the development of AKI and current recommendations suggest the use of isotonic crystalloids&#46; The use of large amounts of 0&#46;9&#37; NaCl is significantly associated with hyperchloremic metabolic acidosis&#44; nevertheless&#44; the role of the chloride in the critical ill patients remains controversial&#46; It has been shown that hyperchloremia is associated with AKI<a class="elsevierStyleCrossRef" href="#bib0420"><span class="elsevierStyleSup">12</span></a> and that restriction of chloride-rich fluid is associated with a significant decrease in the incidence of AKI and the need of renal replacement therapy &#40;RRT&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">13</span></a> However&#44; a recent randomized controlled trial found no difference in the use of balanced crystalloid solutions vs saline solution in the development of AKI&#46;<a class="elsevierStyleCrossRef" href="#bib0430"><span class="elsevierStyleSup">14</span></a> The use of hydroxyethyl starches &#40;HES&#41; has been associated with adverse effects on kidney function&#46; These products have probably a direct nephrotoxic effect that appears to be dose and time dependent&#46; A recent meta-analysis showed a signi&#64257;cant increased risk of RRT and mortality in critically ill HES treated individuals<a class="elsevierStyleCrossRef" href="#bib0435"><span class="elsevierStyleSup">15</span></a> and a Cochrane review<a class="elsevierStyleCrossRef" href="#bib0440"><span class="elsevierStyleSup">16</span></a> showed that all HES products increase the risk of AKI and the need for RRT so that the authors recommended to avoid its use&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">When the worsening of renal function is due to a drop in renal perfusion caused by low cardiac output the short-term administration of selected inotropic agents&#44; especially dobutamine is indicated&#46; In the case of sepsis&#44; the use of inotropic agents is recommended only when there are signs of hypoperfusion&#44; despite achieving adequate intravascular volume and adequate MAP&#59; or when myocardial dysfunction is present&#46;<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">17</span></a> Levosimendan&#44; a positive inotropic agent with vasodilator effect&#44; may have a beneficial impact on renal function probably related to an increase in renal perfusion pressure and a decreased need for RRT&#46;<a class="elsevierStyleCrossRef" href="#bib0450"><span class="elsevierStyleSup">18</span></a> However&#44; according to the results of a recent clinical trial&#44; in adult patients with septic shock&#44; the addition of levosimendan to standard care is not associated with less severe organ dysfunction&#44; including renal failure&#44; or lower mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0455"><span class="elsevierStyleSup">19</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">In patients who remain hypotensive and oliguric after adequate fluid resuscitation and with a normal or increased cardiac output&#44; the use of the vasopressor agent is recommended to restore the blood pressure and protect renal function&#46; In septic shock&#44; MAP of at least 65<span class="elsevierStyleHsp" style=""></span>mmHg<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">17</span></a> is recommended&#46; Although a recent trial found no significant differences in mortality when two MAP targets &#40;65&#8211;70<span class="elsevierStyleHsp" style=""></span>mmHg vs&#46; 80&#8211;85<span class="elsevierStyleHsp" style=""></span>mmHg&#41; were compared&#44; in patients with chronic hypertension the need of RRT was lower in the higher MAP target group&#46;<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">20</span></a> In septic shock&#44; norepinephrine is the vasopressor of first choice&#44; epinephrine or vasopressin &#40;not available in Europe&#41; being the reasonable second-line vasopressor&#46;<a class="elsevierStyleCrossRefs" href="#bib0445"><span class="elsevierStyleSup">17&#44;20</span></a> Renal dose dopamine is ineffective for improving kidney function in AKI and its use is not recommended for renal protection&#46;<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">21</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Fenoldopam&#44; a selective dopamine D1 receptor agonist&#44; is able to increase renal blood flow &#40;RBF&#41; inducing dose-dependent renal vasodilation in patients with AKI or at a high risk of AKI&#44; although not available in Spain&#46; In a recent meta-analysis it has been suggested that its administration may reduce post-operative AKI&#44;<a class="elsevierStyleCrossRef" href="#bib0470"><span class="elsevierStyleSup">22</span></a> slow progression to dialysis-dependent AKI and improve survival&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Diuretics</span><p id="par0050" class="elsevierStylePara elsevierViewall">Diuretics are widely used in critical patients when diuresis decreases&#44; in an attempt to prevent the development of AKI&#44; however&#44; the diuretic response to furosemide is only one marker of the grade of residual renal function and less severe kidney failure&#46;<a class="elsevierStyleCrossRef" href="#bib0475"><span class="elsevierStyleSup">23</span></a> Loop diuretics have the property of reducing renal oxygen consumption as they reduce the active transport of sodium&#44; reducing the energetic requirements of tubular cells and theoretically protecting them from ischemia&#44; but they can have deleterious effects as they increase urine output fostering a depletion in volume&#44; electrolyte imbalances&#44; nephrotoxicity and ototoxicity&#44; thus perpetuating AKI&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">The use of mannitol&#44; although able to protect the kidney&#44; decreasing tissue edema&#44; increasing tubular flow and decreasing intra-tubular obstruction&#44; is also not justified as a preventive measure&#46; Its use has been trialed in kidney transplant surgery<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">24</span></a> and in rhabdomyolysis<a class="elsevierStyleCrossRef" href="#bib0485"><span class="elsevierStyleSup">25</span></a> without providing conclusive results&#46; Therefore&#44; in light of the available evidence&#44; it is recommended not to use diuretics for preventing AKI&#44; except in the management of water overload&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a> Diuretics should be administered over a short period and should never lead to a delay in starting continuous renal replacement therapy &#40;CRRT&#41;&#46;</p></span></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Specific measures</span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Nephrotoxicity by drugs</span><p id="par0060" class="elsevierStylePara elsevierViewall">Nephrotoxic medication is the third cause of AKI in the ICU&#44;<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">3</span></a> due to the high number of prescribed drugs&#44; the potential for adverse drug reactions and the actual nephrotoxicity of the drug&#46; There are increases in risk due to the interrelation of these drugs with factors of susceptibility and exposure &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>&#41; and because of its inadequate prescription&#46;<a class="elsevierStyleCrossRefs" href="#bib0495"><span class="elsevierStyleSup">27&#44;28</span></a> Prognosis and evolution to CKD is usually the same as in all the causes of AKI&#46;<a class="elsevierStyleCrossRef" href="#bib0500"><span class="elsevierStyleSup">28</span></a></p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0065" class="elsevierStylePara elsevierViewall">The following are dependent modifiable risk factors&#58; Duration of treatment&#44; daily&#47;total accumulated dose and pharmacodynamic and pharmakinetic interactions&#46; The associations of drugs also constitute a frequent risk&#44;<a class="elsevierStyleCrossRef" href="#bib0505"><span class="elsevierStyleSup">29</span></a> such as triple therapy drugs&#58; non-steroid antiinflammatory drugs &#40;NSAIDs&#41;<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>angiotensin-converting-enzyme &#40;ACE&#41; inhibitors&#8211;angiotensin receptor blockers &#40;ARBs&#41;<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>Diuretics&#46; The toxicity mechanisms are complex&#44; in many cases affecting more than one aspect of kidney function&#46;<a class="elsevierStyleCrossRef" href="#bib0510"><span class="elsevierStyleSup">30</span></a> They can be classified according to their kidney injury mechanism&#44; as well as to their histopathological findings &#40;<a class="elsevierStyleCrossRef" href="#tbl0015">Table 3</a>&#41;&#44; many of them interacting on different levels&#46;</p><elsevierMultimedia ident="tbl0015"></elsevierMultimedia><p id="par0070" class="elsevierStylePara elsevierViewall">Prevention is the best method for avoiding AKI&#44; with the early identification of the patients at risk and controlling the potentially modifiable risk factors&#44; including the non-prescription or interruption of nephrotoxic drugs whenever possible&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Aminoglycoside antimicrobial agents are highly potent&#44; bactericidal antibiotics&#44; its toxicity is multifactorial and strengthened by the susceptibility to and exposure to other factors&#46; The mechanisms involved in nephrotoxicity are<a class="elsevierStyleCrossRefs" href="#bib0515"><span class="elsevierStyleSup">31&#44;32</span></a>&#58; 1&#41; proximal tubular renal toxicity&#44; causing apoptosis and necrosis&#59; 2&#41; mesangial contraction with decreased glomerular filtration rate&#44; and 3&#41; reduction of renal blood flow secondary to increased vascular resistance&#46; Risk factors associated with the treatment include the length of it&#44; trough levels and dosing interval&#46; The pharmacokinetic and pharmacodynamic properties of aminoglycosides favor high dosing strategies with extended intervals between doses&#44; so in patients with normal kidney function in a steady state&#44; aminoglycosides should be administered as a single dose daily rather than multiple-dose daily treatment regimens&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Therapeutic efficacy is determined by peak blood level divided by minimum inhibitory concentration &#40;MIC&#41; of the infecting organism &#40;Cmax&#47;MIC&#41;&#46; The Cmax should be at least 10-fold greater than the MIC of the infecting microorganism&#44; and the sample must be taken within 30<span class="elsevierStyleHsp" style=""></span>min of administration&#46; Nephrotoxicity is associated with high levels of residual concentration &#40;trough level&#41;&#44; more than 20<span class="elsevierStyleHsp" style=""></span>h after being administered&#44; hence&#44; the importance of the determination of peak&#47;trough concentration for titration and dosing interval&#46; It is recommended monitoring aminoglycoside drug levels when treatment with single-daily dosing is used for more than 48<span class="elsevierStyleHsp" style=""></span>h or if multiple daily dosing is used for more than 24<span class="elsevierStyleHsp" style=""></span>h&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Therefore&#44; preventive strategies are extended-interval dosing&#44; limiting duration of therapy&#44; monitoring serum drug levels and renal function&#44; and manintaining trough levels&#44; measured between 18 and 24<span class="elsevierStyleHsp" style=""></span>h post-dose&#44; at 1<span class="elsevierStyleHsp" style=""></span>&#956;g&#47;ml or less&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">Amphotericin B deoxycholate is also an important nephrotoxic agent&#44; with an AKI incidence which can reach 80&#37;&#46; The nephrotoxicity mechanism is multifactorial and is associated with total accumulated dose&#46; Prevention is based on adequate hydroelectrolytic replacement and the administration of lipid-based formulations<a class="elsevierStyleCrossRefs" href="#bib0525"><span class="elsevierStyleSup">33&#44;34</span></a>&#58; liposomal form of Amphotericin B and Amphotericin B Lipid Complex&#46; Lipid-based formulations are less nephrotoxic as observed in several clinical studies and meta-analysis&#44; and some clinical studies suggest that liposomal form of Amphotericin B is less nephrotoxic than the other lipid-based formulations&#46;<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">34</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">With the increase of infections produced by beta-lactam-resistant Gram-positive bacteria&#44; other potential nephrotoxic antibiotics such as Vancomycin are being used increasingly in the ICU&#46; Its effectiveness is determined by the relationship AUC&#47;MIC<span class="elsevierStyleHsp" style=""></span>&#8805;<span class="elsevierStyleHsp" style=""></span>400&#44; being trough levels 15&#8211;20<span class="elsevierStyleHsp" style=""></span>mg&#47;L the clinical substitute for that relationship with MIC<span class="elsevierStyleHsp" style=""></span>&#8804;<span class="elsevierStyleHsp" style=""></span>1<span class="elsevierStyleHsp" style=""></span>mg&#47;L multi-resistant bacteria&#44; in case of MIC<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>1<span class="elsevierStyleHsp" style=""></span>mg&#47;L an alternative agent should be considered&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">35</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">Vancomycin-induced nephrotoxicity is based on their oxidative effects on cells of the proximal renal tubule&#44; which produces tubular renal ischemia&#46; It is related to trough levels &#8805;15<span class="elsevierStyleHsp" style=""></span>mg&#47;L&#44; duration of therapy&#44; renal dysfunction and previous use of other nephrotoxic drugs&#46; Hence the importance of strict monitoring of levels and dose adjustment&#44; with the possibility of administering a continuous intravenous infusion<a class="elsevierStyleCrossRefs" href="#bib0535"><span class="elsevierStyleSup">35&#44;36</span></a> as a protective factor of nephrotoxicity&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">Colistin &#40;Colistemetato Sodium&#41; is another nephrotoxic drug whose use has increased in ICU due to the increase in multidrug-resistant Gram negative bacteria&#46; Nephrotoxicity occurs due to the alteration of the tubular cell permeability and cell lysis&#46; Oxidative and inflammatory pathways are also implicated&#46; Risk factors are the cumulative dose administered&#44; treatment time&#44; concomitant use of other nephrotoxic and renal dysfunction with CrCl &#60;60<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#46; Dose is&#44; according to current recommendations&#44; carried out according to its Pk&#47;Pd properties&#44; with ascorbic acid being a possible independent protective factor administered at a twice-daily dose of 3 &#40;2&#8211;4&#41;<span class="elsevierStyleHsp" style=""></span>g&#46;<a class="elsevierStyleCrossRefs" href="#bib0545"><span class="elsevierStyleSup">37&#44;38</span></a></p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">AKI due to intra-tubular deposits</span><p id="par0110" class="elsevierStylePara elsevierViewall">Rhabdomyolysis is characterized by the destruction of skeletal muscle with the subsequent release of intracellular and enzymatic content into the bloodstream&#44; leading to systemic complications&#44; with the most common being AKI&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">39</span></a> It has an incidence of between 10 and 55&#37; and is associated with a poor prognosis when it is part of multiorgan dysfunction syndrome&#46; Apart from genetic predisposition&#44;<a class="elsevierStyleCrossRef" href="#bib0560"><span class="elsevierStyleSup">40</span></a> risk groups have been identified such as the morbid obese&#44; patients with chronic hypolipemiant drug consumption&#44; patients in a postoperative stage in some kinds of surgery&#44; etc&#46; Postoperative rhabdomyolysis has increased in recent years&#44; with risk factors related to surgical time&#44; immobility&#44; anesthetic drugs and comorbidities such as obesity and diabetes&#46;<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">41</span></a> There are many AKI mechanisms including&#58; hypovolemia&#44; myoglobinuria and metabolic acidosis&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">The treatment of the underlying etiology is the first measure to be taken and intensive fluid replacement is the cornerstone of the treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0570"><span class="elsevierStyleSup">42</span></a> Electrolytic corrections are fundamental&#44; with hyperkalemia being the only one requiring rapid correction due to the risk of cardiac arrythmia&#46; The use of bicarbonate is based on the concept that an acid setting promotes myoglobin toxicity&#59; therefore&#44; alkaline urine &#40;a pH greater than 6&#46;5&#41;&#44; could prevent AKI&#46; There is no consensus about the use of mannitol given that its secondary effects include volume depletion and potential prerenal azotemia&#46; However&#44; the theoretical benefits include an improvement in diuresis&#44; an increase in renal perfusion&#44; myoglobin excretion&#44; and a direct antioxidant effect on the renal parenchyma&#46;<a class="elsevierStyleCrossRef" href="#bib0485"><span class="elsevierStyleSup">25</span></a> The CRRT filters the myoglobin in the blood and normalizes creatinine and electrolyte levels&#44; although the mortality rate is unchanged&#46; Therefore&#44; it should only be used when the hydroelectrolytic alterations are life threatening&#46;<a class="elsevierStyleCrossRef" href="#bib0575"><span class="elsevierStyleSup">43</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">Other forms of AKI associated with intra-tubular deposits that we can observe in critical patients include tumor lysis syndrome and intravenous treatment with Acyclovir&#44; sulfonamides&#44; methotrexate&#44; indinavir and cysplatin&#46; Most of these patients are predisposed to having the following risk factors&#58; volume depletion and the presence of CKD&#44; with volume replacement being the most efficient preventive measure&#46; In the case of the administration of cysplatin&#44; at least 3<span class="elsevierStyleHsp" style=""></span>l of saline solution should be replaced 8<span class="elsevierStyleHsp" style=""></span>h before and after its administration together with a chelating agent such as aminophostine&#46; In order to prevent methotrexate precipitation it is recommended to administer saline solution with urinary alkalinization &#40;pH<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>6&#46;5&#41;&#44; and in the case of tumoral lysis syndrome&#44; prevention is carried out by expanding the volume to maintain an adequate urinary flow associated with the use of uricolytic agents like rasburicase&#46;<a class="elsevierStyleCrossRef" href="#bib0485"><span class="elsevierStyleSup">25</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Contrast-associated acute kidney injury</span><p id="par0125" class="elsevierStylePara elsevierViewall">Due to the increase in the use of contrast agents in the diagnosis and in interventionist processes&#44; CA-AKI has become the third most common cause of hospital-acquired kidney failure&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">2</span></a> The broadest definition used is an increase in serum creatinine &#8805;0&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dl or &#8805;25&#37; of the baseline level&#44; 48&#8211;72<span class="elsevierStyleHsp" style=""></span>h after exploration with contrast&#44; in the absence of any alternative etiology&#46; In the latest study carried out on critical patients&#44; an incidence level of 16&#46;3&#37; has been found&#46;<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">44</span></a> This incidence level is higher than that detected in Spanish ICUs&#44; according to the results of the NEFROCON study&#44;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">45</span></a> where an overall incidence of 12&#46;1&#37; was detected&#46; We also found significant differences among coronary patients&#44; with an incidence of 8&#46;2&#37;&#44; and the rest of critical patients&#44; with a higher incidence&#44; of 15&#46;3&#37;&#46;</p><p id="par0130" class="elsevierStylePara elsevierViewall">In spite of the clinical importance of this entity&#44; its pathogenesis is still unclear&#44; and it seems to be multifactorial&#44; including rheological alterations&#44; renal hemodynamic changes&#44; regional hypoxia&#44; auto&#47;paracrine factors &#40;adenosine&#44; endothelin&#44; reactive oxygen species&#41; even direct cytotoxic effects&#46;<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">46</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall">Of the patients who developed CA-AKI&#44; the most frequently identified risk factors were DM and CKD &#40;GFR lower than 60<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#47;1&#46;73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>&#41;&#46; Other reported risk factors were HF&#44; dehydration&#44; hyponatremia&#44; previous use of diuretics&#44; nephrotoxic drugs&#44; hypoalbuminemia&#44; advanced age&#44; female sex&#44; anemia&#44; administration of intra-arterial contrast and constrast dose&#46;<a class="elsevierStyleCrossRef" href="#bib0595"><span class="elsevierStyleSup">47</span></a> There is also an association between CA-AKI and indicators of hemodynamic instability&#44; such as periprocedural hypotension and the use of intra-aortic balloon counterpulsation &#40;IABC&#41;&#46; The effect of the risk factors is additive&#44; and the probability of CA-AKI increases considerably as the number of these increase&#46;<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">48</span></a> In critical patients&#44;<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">44</span></a> the variables associated with the development of CA-AKI were a higher level of serum creatinine&#44; arterial hypotension&#44; the administration of diuretics and vasoactive drugs&#46; These data have also been confirmed in the study carried out on critical Spanish patients&#44;<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">45</span></a> where in addition&#44; level of severity&#44; estimated by APACHE II&#44; and anemia grade are factors related to CA-AKI&#46;</p><p id="par0140" class="elsevierStylePara elsevierViewall">Contrast media can be classified as hypo&#44; iso or hyperosmolar&#44; according to their osmolarity&#46; Several studies<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">49</span></a> suggest that in patients with a deterioration in kidney function&#44; hypo-osmolar &#40;500&#8211;1000<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#41; and iso-osmolar contrast &#40;290&#8211;300<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#41; are less nephrotoxic than hyperosmolar contrast media &#40;1000&#8211;2000<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#41;&#46; Based on current evidence&#44; their use is recommended in high risk patients&#59; both iso and hypo-osmolar contrast&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a> Contrast volume is also an independent predictor of CA-AKI<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">48</span></a>&#59; as a general rule it should not be more than two times the baseline GFR in milliliters&#46;<a class="elsevierStyleCrossRef" href="#bib0610"><span class="elsevierStyleSup">50</span></a></p><p id="par0145" class="elsevierStylePara elsevierViewall">To prevent CA-AKI different kinds of preventive therapies have been trialed&#46; The most adequate approach seems to be to identify patients at risk&#44; administer appropriate peri-procedural hydration and to minimize the quantity of contrast administered<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">51</span></a> &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0150" class="elsevierStylePara elsevierViewall">The objective of hydration is to maintain enough intravascular volume in order to be able to increase renal perfusion&#44; dilute the high concentrations of substances in the renal tubules&#44; prevent prolonged contact&#44; establish adequate diuresis prior to the administration of contrast and to prevent hypotension&#46;<a class="elsevierStyleCrossRef" href="#bib0620"><span class="elsevierStyleSup">52</span></a> Volume expansion should be intravenous&#44; and one of the most recommended hydration regimes is the administration of 1<span class="elsevierStyleHsp" style=""></span>ml&#47;kg&#47;h of 0&#46;9&#37; Saline 12<span class="elsevierStyleHsp" style=""></span>h before and after the procedure in patients with normal left ventricular ejection fraction &#40;LVEF&#41;&#46; For patients with low LVEF &#40;moderate or severe&#41; recommended hydration includes volume replacement according to urinary output to maintain an euvolemic state for 12<span class="elsevierStyleHsp" style=""></span>h pre and post-procedure&#46;</p><p id="par0155" class="elsevierStylePara elsevierViewall">Urinary alkalinization with sodium bicarbonate reduces renal damage by contrast by decreasing the quantity of free radicals dependent on pH&#44; although there are many studies that have assessed its preventive capacity with contradictory results&#46;<a class="elsevierStyleCrossRef" href="#bib0625"><span class="elsevierStyleSup">53</span></a> In 2009 probably the most complete systematic review of controlled randomized clinical trials was published&#44; analyzing 23 published and unpublished studies with significant heterogenicity between them&#44; concluding that the effectiveness of treatment with bicarbonate sodium in high risk patients is unclear&#44;<a class="elsevierStyleCrossRef" href="#bib0630"><span class="elsevierStyleSup">54</span></a> so that currently it is only used in emergency situations&#44; in which there is not enough time to begin adequate therapy with saline solution&#46;</p><p id="par0160" class="elsevierStylePara elsevierViewall">N-acetylcysteine &#40;NAC&#41; is a powerful antioxidant&#44; evaluated in many studies and meta-analyses&#44; that have been unable to demonstrate its preventive efficacy&#46; Not even the largest randomized multicenter study&#44;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">55</span></a> carried out in 2009&#44; could demonstrate the beneficial effect of N-acetylcysteine for reducing the incidence of CA-AKI&#46; This study included 2308 patients with at least one risk factor for its development &#40;&#62;70 years&#44; CKD&#44; DM&#44; CHF&#44; LVEF &#8804;45&#37; or shock&#41;&#46; The patients were randomized to receive oral NAC&#58; 1200<span class="elsevierStyleHsp" style=""></span>mg twice a day&#44; with two doses before the procedure and two doses after&#44; or a placebo&#46; In both groups similar rates of increase in plasma creatinine were found after 48&#8211;96<span class="elsevierStyleHsp" style=""></span>h&#46; Hoffman et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0640"><span class="elsevierStyleSup">56</span></a> assessed the efficacy of NAC in 50 healthy volunteers with normal kidney function&#44; finding a small but significant decrease in creatinine and urea in those patients who received it&#44; as well as an increase in glomerular filtrate without any changes in the levels of cystatin C&#46; This is due to its capacity to interfere with the metabolism of the creatinine&#44; bringing into question its efficacy for preventing CA-AKI&#46;</p><p id="par0165" class="elsevierStylePara elsevierViewall">It has also not been possible to demonstrate the protective effect of dopamine&#44; fenoldopam or theophylline<a class="elsevierStyleCrossRefs" href="#bib0645"><span class="elsevierStyleSup">57&#44;58</span></a> on kidney function and so its use is not currently recommended&#46;</p><p id="par0170" class="elsevierStylePara elsevierViewall">Owing to the capacity of dialysis to eliminate iodinated contrast from the blood flow&#44; several studies have been carried out to assess its role as a potential preventive measure&#46; Nevertheless&#44; it has not been possible to demonstrate a fall in the incidence of CA-AKI&#46; What is more&#44; in a meta-analysis carried out on several studies in which periprocedural extracorporeal techniques are performed it was not possible to demonstrate a beneficial effect either&#46;<a class="elsevierStyleCrossRef" href="#bib0655"><span class="elsevierStyleSup">59</span></a></p><p id="par0175" class="elsevierStylePara elsevierViewall">Recently&#44; there is controversy about the toxicity of modern low- or iso-osmolality iodinated contrast material as well as the role of nephroprotection&#46;<a class="elsevierStyleCrossRefs" href="#bib0660"><span class="elsevierStyleSup">60&#44;61</span></a> The methodology of the studies conducted are being questioned&#44; claiming that the studies included in the meta-analysis are heterogeneous and nonrandomized&#44; assuming a significant bias&#46; Most studies lacked a control group&#44; and in some including it&#44; the incidence is similar in both groups&#46; In addition to methodological issues&#44; many authors suggest that the incidence of AKI in ICU is multifactorial&#44; and the patient subjected to radiological contrast is also exposed to many other risk factors&#44; being the CA-AKI indistinguishable from acute kidney injury that occurs for other reasons&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Perioperative AKI</span><p id="par0180" class="elsevierStylePara elsevierViewall">The risk for its development is the interaction between renal susceptibility and the type and intensity of exposure to renal injury&#46; The knowledge of these risk factors could help in its prevention&#44; especially in the hospital setting&#44; with the most important risks being advanced age and CKD&#46;<a class="elsevierStyleCrossRefs" href="#bib0370"><span class="elsevierStyleSup">2&#44;4</span></a> The patients who meet the creatinine and diuresis criteria have worse results than the nonoliguric patients&#46; Along similar lines&#44; the FINNAKI study has noted that severe episodes of oliguria are independently associated with the development of AKI&#46;<a class="elsevierStyleCrossRef" href="#bib0670"><span class="elsevierStyleSup">62</span></a> However&#44; it should be taken into account that perioperative oliguria is&#44; commonly&#44; secondary to salt and water retention in response to tissue damage&#44; pain and moderate degrees of hypovolemia and hypotension&#46; Nearly 40&#37; of AKI in hospitalized patients occurs in the perioperative period&#44; and is mainly related to the specific surgical procedure&#46;<a class="elsevierStyleCrossRef" href="#bib0675"><span class="elsevierStyleSup">63</span></a> Heart surgery has the highest risk at RR&#58; 1&#46;22 &#40;95&#37; CI&#58; 1&#46;17&#8211;1&#46;27&#41;&#44; with major vascular surgery being another high risk surgical subgroup&#46; These results reinforce the importance of stratification of perioperative risk and the implementation of preventive strategies&#46; In addition&#44; several predictive risk models of AKI have been developed principally in the field of heart surgery&#46;</p><p id="par0185" class="elsevierStylePara elsevierViewall">The main causes of AKI include ischemia&#44; hypoxia&#44; inflammation and nephrotoxicity&#46; Other mechanisms are direct vascular injury or tubular obstruction&#46; Therefore&#44; it is not surprising that the simple restoration of circulating blood volume does not improve the results&#46; Recently&#44; the role of intraoperative hypotension has been related&#44;<a class="elsevierStyleCrossRef" href="#bib0680"><span class="elsevierStyleSup">64</span></a> finding an increase in risk when mean blood pressure was &#60;60<span class="elsevierStyleHsp" style=""></span>mmHg during &#62;20<span class="elsevierStyleHsp" style=""></span>min and &#60;55<span class="elsevierStyleHsp" style=""></span>mmHg during &#62;10<span class="elsevierStyleHsp" style=""></span>min&#46; The perioperative administration of levosimendan to patients who have undergone heart surgery reduces the incidence of AKI&#44; CRRT&#44; mortality&#44; mechanical ventilation time and stay in the ICU&#46; Remote ischemic preconditioning &#40;RIPC&#41; has proven cardiac and kidney protection with a possible reduction in mortality when it is used with halogenated anesthetics&#46; However&#44; two recent studies<a class="elsevierStyleCrossRefs" href="#bib0685"><span class="elsevierStyleSup">65&#44;66</span></a> suggest there is no difference between RIPC and standard treatment&#44; probably due to the use of propofol as a hypnotic drug&#46; Phenoldopam has not demonstrated its utility either&#44; being associated with a higher rate of hypotension&#46; Among the patients undergoing non heart-related major surgery&#44; neither aspirin nor clonidine reduced the perioperative risk of AKI&#46; In fact&#44; aspirin increases the risk of a severe hemorrhage and clonidine does the same to hypotension&#46;<a class="elsevierStyleCrossRef" href="#bib0695"><span class="elsevierStyleSup">67</span></a></p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">AKI in liver failure</span><p id="par0190" class="elsevierStylePara elsevierViewall">AKI is associated with a poor prognosis in cirrhotic patients&#46; The most common causes leading to it are listed in <a class="elsevierStyleCrossRef" href="#tbl0020">Table 4</a>&#46;<a class="elsevierStyleCrossRef" href="#bib0700"><span class="elsevierStyleSup">68</span></a> Splanchnic vasodilatation that is triggered by portal hypertension&#44; seems to induce hemodynamic changes and a deterioration in kidney function due to an increase in the production and activity of vasodilators such as nitric oxide&#44; a derivate of the endothelium&#44; due to bacterial translocation&#46;<a class="elsevierStyleCrossRef" href="#bib0700"><span class="elsevierStyleSup">68</span></a> The following preventive measures should be taken&#58; nephrotoxic drugs and NSAIDs should be avoided&#59; early antiviral treatment should be carried out in patients with Hepatitis C virus who fulfill the therapeutic criteria and are in a stable condition&#59; in hypovolemia or sepsis diuretics should be withdrawn&#59; and in the case of hemorrhagic shock&#44; hemoderivates should be administered&#44; variceal ligation should be performed together with preventive treatment of bleeding using propranolol&#46; Water overload should be prevented as this can aggravate hyponatremia and ascites&#46; It should be evacuated with albumin replacement &#40;8<span class="elsevierStyleHsp" style=""></span>g albumin per liter of ascites evacuated&#41;&#46; The appearance of Hepatorenal syndrome &#40;HRS&#41; after spontaneous bacterial peritonitis &#40;SBP&#41; can be efficiently prevented through the administration of albumin &#40;1&#46;5<span class="elsevierStyleHsp" style=""></span>g&#47;kg i&#46;v&#46; at the time of diagnosis and 1<span class="elsevierStyleHsp" style=""></span>g&#47;kg i&#46;v&#46; 48<span class="elsevierStyleHsp" style=""></span>h later&#41;<a class="elsevierStyleCrossRef" href="#bib0700"><span class="elsevierStyleSup">68</span></a> associated with the administration of norfloxacin &#40;400<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#41;&#46; The albumin mechanism is unknown but has beneficial effects for heart function as well as antioxidant properties&#46;<a class="elsevierStyleCrossRef" href="#bib0705"><span class="elsevierStyleSup">69</span></a></p><elsevierMultimedia ident="tbl0020"></elsevierMultimedia></span></span></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Secondary prevention</span><p id="par0195" class="elsevierStylePara elsevierViewall">The early detection of the disease is the most important secondary prevention&#44; allowing us to detect the disease at its earliest stage to be able to apply all the measures aimed at preventing its progression&#46;</p><p id="par0200" class="elsevierStylePara elsevierViewall">The monitoring of diuresis and creatinine is recommended for the identification of the initial stages of AKI&#44; in accordance with the RIFLE&#44; AKIN or AKI-KDIGO scales&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a> In this way&#44; the presence of at least one of the following conditions is required&#58; an increase in creatinine of 0&#46;3<span class="elsevierStyleHsp" style=""></span>mg&#47;dl above the baseline value in less than 48<span class="elsevierStyleHsp" style=""></span>h&#59; an increase in creatinine 1&#46;5 times above the baseline value in less than 7 days&#59; or diuresis of under 0&#46;5<span class="elsevierStyleHsp" style=""></span>ml&#47;kg&#47;h for 6<span class="elsevierStyleHsp" style=""></span>h &#40;urine volume 0&#46;5<span class="elsevierStyleHsp" style=""></span>ml&#47;kg&#47;h for 6<span class="elsevierStyleHsp" style=""></span>h&#41;&#46;</p><p id="par0205" class="elsevierStylePara elsevierViewall">The frequency of this monitoring cannot be established generally for all patients&#46; In heart patients undergoing percutaneous coronary interventionist bladder catheterization is not usually used&#44; given that there is a general recommendation not to subject patients to unnecessary invasive procedures to prevent nosocomial infection&#46; This same rule could be applied to non heart-related patients in which bladder catheterization is not considered necessary&#46; Even so&#44; the registration and measurement of spontaneous diuresis can always be used&#46; The same occurs with readings of serum creatinine that could be less frequent in stable patients&#46; In any case&#44; the frequency used should allow for the detection of significant changes in the tendencies&#46;</p><p id="par0210" class="elsevierStylePara elsevierViewall">Once an AKI diagnosis has been established&#44; the patient should be reassessed from an angle more focused on renal function<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">51</span></a>&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#46;</span><p id="par0215" class="elsevierStylePara elsevierViewall">History&#58; antecedents&#44; nephrotoxic agents&#44; renal insults&#44; etc&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#46;</span><p id="par0220" class="elsevierStylePara elsevierViewall">Renal evaluation&#58;<ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">a&#46;</span><p id="par0225" class="elsevierStylePara elsevierViewall">Urine analysis &#40;ions and sediment&#41;&#46;</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">b&#46;</span><p id="par0230" class="elsevierStylePara elsevierViewall">Ultrasound in those cases in which the cause of AKI has not been identified&#44;<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">51</span></a> will make it possible to rule out obstructive problems&#44; collections&#44; evaluation of renal flow and the ruling out of alterations suggestive of chronicity&#46;</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">c&#46;</span><p id="par0235" class="elsevierStylePara elsevierViewall">Estimation of creatinine clearance by measuring urinary creatinine over a time interval &#40;2&#44; 6&#44; 12 or 24<span class="elsevierStyleHsp" style=""></span>h&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0710"><span class="elsevierStyleSup">70</span></a> It will allow for the adequate adjustment of drugs and the assessment of evolution&#46;</p></li></ul></p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">3&#46;</span><p id="par0240" class="elsevierStylePara elsevierViewall">Hemodynamic evaluation&#58; preload&#44; cardiac output&#44; blood pressure&#44; estimation of peripheral resistance&#44; tissue perfusion&#44; lactate and hemoglobin&#46;</p></li></ul></p><p id="par0245" class="elsevierStylePara elsevierViewall">In <a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a> there is a summary of recommended measures to be taken in the case of AKI&#46; Clinical evaluation from a renal standpoint&#44; will allow us to take the right measures in each case&#44; that will generally be&#58;<ul class="elsevierStyleList" id="lis0015"><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">-</span><p id="par0250" class="elsevierStylePara elsevierViewall">Volume expansion to optimize systolic volume and blood pressure &#40;BP&#41; in the case of shock&#46; Bolus of 250&#8211;500<span class="elsevierStyleHsp" style=""></span>ml can be administered until normalization of the preload&#46; It should always be ensured that the patient has a low preload and that there is a favorable response to the volume administration&#46;</p></li><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">-</span><p id="par0255" class="elsevierStylePara elsevierViewall">Early onset of amines<a class="elsevierStyleCrossRef" href="#bib0715"><span class="elsevierStyleSup">71</span></a> may help to improve blood pressure in combination with volume expansion&#46; Although it is controversial&#44; early use of amines can reduce fluid overload and positive balance that may have a deleterious effect&#46; The amine of choice is Norepinephrine&#46;<a class="elsevierStyleCrossRefs" href="#bib0445"><span class="elsevierStyleSup">17&#44;22</span></a></p></li><li class="elsevierStyleListItem" id="lsti0045"><span class="elsevierStyleLabel">-</span><p id="par0260" class="elsevierStylePara elsevierViewall">Daily monitoring of the water balance and measured rapid creatinine clearance &#40;2 or 4<span class="elsevierStyleHsp" style=""></span>h&#41;&#44; as well as general monitoring of every critical patient&#46;</p></li><li class="elsevierStyleListItem" id="lsti0050"><span class="elsevierStyleLabel">-</span><p id="par0265" class="elsevierStylePara elsevierViewall">Daily monitoring of AKI-related complications such as hyperpotasemia&#44; hypocalcemia and hyperphosphatemia&#46; Hyperpotasemia could be managed using medical measures in most cases&#46; Hypocalcemia should be treated with supplements&#46; Hyperphosphatemia in patients without symptoms can be treated using phosphoric chelates&#46;</p></li><li class="elsevierStyleListItem" id="lsti0055"><span class="elsevierStyleLabel">-</span><p id="par0270" class="elsevierStylePara elsevierViewall">Consistently high uremia values can produce changes in platelet aggregation and increase the bledding complications&#44; that can partially improve with the administration of desmopresin&#46;<a class="elsevierStyleCrossRef" href="#bib0720"><span class="elsevierStyleSup">72</span></a></p></li><li class="elsevierStyleListItem" id="lsti0060"><span class="elsevierStyleLabel">-</span><p id="par0275" class="elsevierStylePara elsevierViewall">In nearly 25&#37; of cases of sepsis-induced AKI the nephrotoxic drugs can contribute to renal deterioration<a class="elsevierStyleCrossRef" href="#bib0495"><span class="elsevierStyleSup">27</span></a> and must be discontinued&#44; if not done previously&#46; Only those considered as essential should be continued when they cannot be replaced by another equivalent and with a prior dose adjustment according to the patient&#39;s renal function&#46;</p></li><li class="elsevierStyleListItem" id="lsti0065"><span class="elsevierStyleLabel">-</span><p id="par0280" class="elsevierStylePara elsevierViewall">Adjustment of the drugs according to renal function because of levels or estimated levels of renal function using the creatinine clearance measurement in urine over short periods of time&#46;</p></li><li class="elsevierStyleListItem" id="lsti0070"><span class="elsevierStyleLabel">-</span><p id="par0285" class="elsevierStylePara elsevierViewall">Avoiding the use of furosemide as it can worsen the evolution of AKI&#44; hinder the daily assessment of renal function and delay the start of dialytic techniques&#46; When its use is considered necessary to increase diuresis because of volume overload&#44; and it is considered that it could add a prerenal component&#44; increases in the serum urea value can be used to guide the treatment and interrupt it if necessary&#46;</p></li><li class="elsevierStyleListItem" id="lsti0075"><span class="elsevierStyleLabel">-</span><p id="par0290" class="elsevierStylePara elsevierViewall">Avoiding the use of low-dose dopamine&#59; it does not improve the evolution of AKI&#44;<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">21</span></a> and it can worsen renal blood flow and produce a higher frequency of supraventricular tachiarrythmias&#46;</p></li><li class="elsevierStyleListItem" id="lsti0080"><span class="elsevierStyleLabel">-</span><p id="par0295" class="elsevierStylePara elsevierViewall">Providing adequate nutrition&#59; the basic requirements are usually similar to those of a critical patient according to his or her catabolic state&#46; The protein needs are usually 1&#8211;1&#46;5<span class="elsevierStyleHsp" style=""></span>g&#47;kg&#47;day&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">26</span></a> Classic conceptions of hypoproteic diets should be avoided to prevent increases in urea and to delay the start of dialysis&#46;</p></li></ul></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0300" class="elsevierStylePara elsevierViewall">The majority of the episodes of AKI in patients admitted to the ICU are secondary to another disease that causes renal affectation&#46; The treatment of the cause of admission or the complication that has contributed to the development of AKI is crucial for preventing its progression&#46; In the case of sepsis it is of vital importance to control the focus of the disease using an early start of antibiotics and&#47;or surgical treatment when appropriate&#46;</p></span><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Funding source</span><p id="par0305" class="elsevierStylePara elsevierViewall">None&#46;</p></span><span id="sec0080" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Conflict of interests</span><p id="par0310" class="elsevierStylePara elsevierViewall">The authors declare no conflict of interest&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Acute kidney injury &#40;AKI&#41; is a growing concern in Intensive Care Units&#46; The advanced age of our patients&#44; with the increase in associated morbidity and the complexity of the treatments provided favor the development of AKI&#46; Since no effective treatment for AKI is available&#44; all efforts are aimed at prevention and early detection of the disorder in order to establish secondary preventive measures to impede AKI progression&#46; In critical patients&#44; the most frequent causes are sepsis and situations that result in renal hypoperfusion&#59; preventive measures are therefore directed at securing hydration and correct hemodynamics through fluid perfusion and the use of inotropic or vasoactive drugs&#44; according to the underlying disease condition&#46; Apart from these circumstances&#44; a number of situations could lead to AKI&#44; related to the administration of nephrotoxic drugs&#44; intra-tubular deposits&#44; the administration of iodinated contrast media&#44; liver failure and major surgery &#40;mainly heart surgery&#41;&#46; In these cases&#44; in addition to hydration&#44; there are other specific preventive measures adapted to each condition&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La lesi&#243;n renal aguda &#40;LRA&#41; constituye un problema de importancia creciente en las unidades de cuidados intensivos&#46; La mayor edad de nuestros pacientes&#44; con el aumento de la morbilidad asociada&#44; y la complejidad de los tratamientos realizados favorecen su desarrollo&#46; Puesto que la LRA carece de tratamiento eficaz&#44; todos los esfuerzos se dirigen a la prevenci&#243;n y a su detecci&#243;n precoz con el fin de establecer medidas de prevenci&#243;n secundaria que impidan su progresi&#243;n&#46; En el paciente cr&#237;tico&#44; las causas m&#225;s frecuentemente implicadas son la sepsis y las situaciones que provocan hipoperfusi&#243;n renal&#44; por lo que las medidas preventivas ir&#225;n encaminadas a mantener un estado de hidrataci&#243;n y hemodin&#225;mico correcto mediante perfusi&#243;n de fluidos y el uso de f&#225;rmacos inotr&#243;picos o vasoactivos en funci&#243;n de la enfermedad subyacente&#46; Adem&#225;s de estas circunstancias&#44; existen distintas situaciones que pueden favorecer la LRA&#44; relacionadas con la administraci&#243;n de f&#225;rmacos nefrot&#243;xicos&#44; los dep&#243;sitos intratubulares&#44; la administraci&#243;n de contrastes iodados&#44; el fallo hep&#225;tico y la cirug&#237;a mayor&#44; fundamentalmente cirug&#237;a cardiaca&#46; En estos casos&#44; adem&#225;s de la hidrataci&#243;n&#44; se dispone de otros aspectos preventivos espec&#237;ficos de cada entidad&#46;</p></span>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Recommendations for CA-AKI prevention&#46; Modified from ref&#46; 51&#46; CA-AKI&#58; contrast associated acute kidney injury&#59; CKD&#58; chronic kidney disease&#59; GFR&#58; glomerular filtration rate&#59; DM&#58; diabetes mellitus&#59; HF&#58; heart failure&#59; NSAIDs&#58; non steroidal antiinflammatory drugs&#59; CRRT&#58; continuous renal replacement therapy&#59; AECI&#58; angiotensin converting enzyme inhibitors&#46;</p>"
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                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Risk factor&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Odds ratio &#40;95&#37; CI&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Disease severity&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">9&#46;08 &#40;4&#46;57&#8211;13&#46;60&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Age&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">4&#46;95 &#40;3&#46;79&#8211;6&#46;12&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Use of vasopressors&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">4&#46;52 &#40;2&#46;03&#8211;10&#46;05&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Sepsis&#47;SIRS&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">4&#46;15 &#40;2&#46;36&#8211;7&#46;32&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hypotension&#47;Shock&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">3&#46;33 &#40;1&#46;70&#8211;6&#46;52&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">High risk&#47;urgent surgery&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">2&#46;34 &#40;1&#46;23&#8211;4&#46;49&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Heart failure&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">2&#46;05 &#40;1&#46;77&#8211;2&#46;38&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Diabetes&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">1&#46;58 &#40;1&#46;36&#8211;1&#46;84&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Use of nephrotoxic medication&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">1&#46;53 &#40;1&#46;09&#8211;2&#46;14&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hypertension&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">1&#46;43 &#40;1&#46;08&#8211;1&#46;89&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Baseline creatinine&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">0&#46;14 &#40;0&#46;01&#8211;0&#46;27&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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        "descripcion" => array:1 [
          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Risk factors for the development of AKI&#46;</p>"
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          "leyenda" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">BDI&#58; body mass index&#59; CKD&#58; chronic kidney disease&#46;</p>"
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              "tabla" => array:1 [
                0 => """
                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Susceptibility&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Age<br>Black race<br>Female sex<br>Diabetes mellitus<br>Obesity &#40;BMI<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>40&#41;<br>Arterial hypertension<br>CKD<br>Deshydration<br>Neoplasias<br>Hypoalbuminemia<br>Anemia<br>Chronic diseases&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Exposure&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Nephrotoxic drugs<br>Contrast media<br>Trauma&#44; burns<br>Sepsis<br>High risk surgery<br>Hypotension<br>Fluid overload&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Nephrotoxic drugs&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Treatment time<br>Total&#47;daily accumulated dose<br>High concentrations<br>Drug interactions&#58;<br><span class="elsevierStyleHsp" style=""></span>Pharmacokinetic<br><span class="elsevierStyleHsp" style=""></span>Pharmacodynamic&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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        "descripcion" => array:1 [
          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Nephrotoxic drugs&#44; factors of susceptibility and exposure&#46;</p>"
        ]
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        "identificador" => "tbl0015"
        "etiqueta" => "Table 3"
        "tipo" => "MULTIMEDIATABLA"
        "mostrarFloat" => true
        "mostrarDisplay" => false
        "detalles" => array:1 [
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            "identificador" => "at3"
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          "leyenda" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">NSAID&#58; non-steroid anti-inflammatory drugs&#59; AECI&#58; angiotensin-converting enzyme inhibitors&#59; ARB&#58; angiotensin receptor blockers&#59; ATN&#58; acute tubular necrosis&#46;</p>"
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              "tabla" => array:1 [
                0 => """
                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Adverse mechanism&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Drugs&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Intraglomerular hemodynamics&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">NSAID<br>Cyclooxygenase inhibitors<br>AECI and ARB<br>Calcineurin inhibitors&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">ATN&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Aminoglycosides&#44; Anphotericin B<br>Contrast media<br>Antiretroviral drugs<br>Cysplatin&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Allergic interstitial nephritis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Antibiotics&#58; penicillin&#44; cephalosporins&#44; macrolids&#44; cyprofloxacine&#44; vancomicyn&#44; rifampicin&#44; tetracycline drugs<br>NSAID<br>Omeprazol<br>Phenytoin and valproic acid<br>Cimetidine<br>Diuretics&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Glomerulonephritis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">NSAID<br>Ampicillin&#44; riphampicin<br>Lithium&#44; penicillamine<br>Hydralazine&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Postrenal Obstruction&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Acyclovir<br>Methotrexate<br>Sulphadiazine<br>Foscarnet&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Osmotic nephrosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Immunoglobulins<br>Hydroxyethyl starch<br>Mannitol<br>Contrast media&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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        "descripcion" => array:1 [
          "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Mechanism of kidney injury from nephrotoxic drugs&#46;</p>"
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        "etiqueta" => "Table 4"
        "tipo" => "MULTIMEDIATABLA"
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          "leyenda" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">HRS&#58; hepatorenal syndrome&#59; ATN&#58; acute tubular necrosis&#59; UGIH&#58; upper gastrointestinal hemorrhage&#59; NSAID&#58; non steroidal antiinflammatory drugs&#59; AMG&#58; aminoglycosides&#46;</p><p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Modified from Ref&#46; <a class="elsevierStyleCrossRef" href="#bib0690">66</a>&#46;</p>"
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            0 => array:2 [
              "tabla" => array:1 [
                0 => """
                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Type of AKI&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Diagnosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hepatorenal s&#237;ndrome&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Diagnosis of HRS&#58; serum creatinine &#62;1&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; that does not decrease after the administration of albumin &#40;1<span class="elsevierStyleHsp" style=""></span>g&#47;kg weight&#41; at least two days after the suspension of diuretics&#44; in the absence of nephrotoxic drugs&#44; shock or findings suggestive of ATN&#46;<br>HRS type 1&#58; increase to double the amount of serum creatinine to more than 2&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;dl in less than 2 weeks&#46;<br>HRS type 2&#58; a less progressive evolution than type 1&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">AKI induced by hypovolemia&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Generally due to a hemorrhage &#40;UGIH&#41; or fluid loss &#40;diuretics overdose&#44; diarrhea due to an excessive administration of lactulose&#44; acute gastroenteritis&#41;&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Acute tubular necrosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Suspected if proteinuria &#40;&#62;500<span class="elsevierStyleHsp" style=""></span>mg proteins&#47;day&#41; and&#47;or hematuria &#40;&#62;50 red blood cells per field&#41;&#46;<br>Differential diagnosis with HRS is difficult&#46; Suspicion of ATN if the tubular renal epithelial cells are in urinary sediment&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">AKI due to nephrotoxic drugs&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Recent or current treatment with NSAID or AMG&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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        "descripcion" => array:1 [
          "en" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Main type of AKI in cirrhotic patients&#46;</p>"
        ]
      ]
    ]
    "bibliografia" => array:2 [
      "titulo" => "References"
      "seccion" => array:1 [
        0 => array:2 [
          "identificador" => "bibs0005"
          "bibliografiaReferencia" => array:72 [
            0 => array:3 [
              "identificador" => "bib0365"
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              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Acute kidney injury&#44; mortality&#44; length of stay and costs in hospitalized patients"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
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                            0 => "G&#46;M&#46; Chertow"
                            1 => "E&#46; Burdick"
                            2 => "M&#46; Honour"
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                          ]
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                  ]
                  "host" => array:1 [
                    0 => array:2 [
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                      "autores" => array:1 [
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            2 => array:3 [
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                  "contribucion" => array:1 [
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                      "titulo" => "Epidemiology of acute kidney injury in critically ill patients&#58; the multinacional AKI-EPI study"
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                        0 => array:2 [
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                            0 => "E&#46; Hoste"
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                            2 => "R&#46; Bellomo"
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                  "host" => array:1 [
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            3 => array:3 [
              "identificador" => "bib0380"
              "etiqueta" => "4"
              "referencia" => array:1 [
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                  "contribucion" => array:1 [
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            4 => array:3 [
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                  "contribucion" => array:1 [
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                          "etal" => true
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            5 => array:3 [
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                  "contribucion" => array:1 [
                    0 => array:2 [
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                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
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                            0 => "H&#46; Gomez"
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                      "Revista" => array:6 [
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                        "fecha" => "2014"
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Idiomas
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¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

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