Estadísticas

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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Renal Biopsy &#40;green masson tricromium stain&#41; 400&#215; &#8211; marked glomerular capillary stasis &#8211; glomerular thrombus&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Thrombotic microangiopathy &#40;TMA&#41; is a pathologic process characterized by inflammation and thickening of wall vessels&#44; endothelial edema&#44; basement membrane detachment&#44; intimal fibrosis and platelet thrombi formation with occlusion of vascular lumen&#46; It affects mainly kidney and central nervous system microvasculature<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a>&#59; depending on the lesion distribution&#44; two different syndromes are described&#58; Thrombotic Thrombocytopenic purpura &#40;TTP&#41; and hemolytic uremic syndrome &#40;HUS&#41;&#46; Both are characterized by microangiopathic hemolytic anemia and thrombocytopenia&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;3</span></a> Neurological disorders are dominant in TTP whereas renal failure is dominant in HUS&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">HUS is denominated <span class="elsevierStyleItalic">typical</span> &#40;90&#37; of the cases&#41; when caused by enteric shiga toxin-producing microorganisms&#44; as <span class="elsevierStyleItalic">Escherichia coli</span> serotype O157&#58;H7&#46; The other rare cases are classified as <span class="elsevierStyleItalic">atypical</span> &#40;<span class="elsevierStyleItalic">aHUS</span>&#41;&#44; due to alternate complement pathway deregulation&#44; or <span class="elsevierStyleItalic">secondary</span> to conditions such as pregnancy&#44; autoimmune disease&#44; invasive pneumococcal infections&#44; HIV and H1N1 infections&#44; cancer&#44; malignant hypertension&#44; and certain drugs&#46;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;2</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Most aHUS cases have a strong genetic component involving mutations and polymorphisms in the complement proteins genes&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> It is more common in children and young adults and the prognosis is poor with high morbidity and mortality in acute phase and 50&#37; of progression to chronic kidney disease&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The authors describe the case of a 35-year-old man who presented at the emergency department with fever&#44; abdominal pain&#44; nausea&#44; bilious vomiting and decrease urine output for two weeks&#46; He denied diarrhea and revealed history of intravenous drug abuse&#44; under methadone program&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">At admission he was pale&#44; with icteric sclera&#44; hypertensive &#40;197&#47;108<span class="elsevierStyleHsp" style=""></span>mmHg&#41; and tachypneic&#46; Biochemistry revealed&#58; normocytic normochromic anemia &#40;Hb 6<span class="elsevierStyleHsp" style=""></span>g&#47;dL&#41;&#59; platelet count 132<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span><span class="elsevierStyleHsp" style=""></span>L<span class="elsevierStyleSup">&#8722;1</span>&#44; acute kidney injury &#40;Urea 81<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#59; Creatinine 1487<span class="elsevierStyleHsp" style=""></span>&#956;mol&#47;L&#41;&#59; high Lactate dehydrogenase &#40;LDH 23<span class="elsevierStyleHsp" style=""></span>&#956;kat&#47;L&#41; and proteinuria &#40;100<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#41;&#46; In the following hours the patient developed agitation&#44; hallucinations and respiratory failure due to aspiration of gastric content&#44; for what he was intubated and mechanically ventilated&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">At the Intensive Care Unit he presented thrombocytopenia &#40;platelets 98<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>&#41;&#44; severe kidney impairment with anuria and started hemodialysis&#46; The anemia study revealed hemolysis&#58; schistocytes in peripheral blood smear&#44; haptoglobin &#60;7<span class="elsevierStyleHsp" style=""></span>mg&#47;dL and raised LDH &#40;26&#46;7<span class="elsevierStyleHsp" style=""></span>&#956;Kat&#47;L&#41;&#44; and the patient underwent regular blood transfusion&#44; during the first week&#46; TMA diagnosis was admitted and daily plasmaferesis was initiated&#44; with exchange of 1&#46;5 plasma volume per session&#46; He completed a total of eleven sessions&#44; with renal function recovery&#44; allowing the spacing of dialysis sessions&#44; as well as normalization of platelets count and LDH levels&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">Complementary laboratory study excluded malignant hypertension&#44; autoimmunity diseases&#44; HIV and H1N1 infection&#46; Shiga toxin was negative&#44; C3 factor decreased&#44; with no other changes in complement factors or respective antibodies&#46; The activity of ADAMTS13 was normal without anti-ADAMTS13 antibodies &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46; The total body CT-scan excluded neoplasia&#46; Kidney biopsy showed histopathological features of thrombotic microangiopathy &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41; and the genetic screening revealed a mutation in factor H&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">During the hospitalization the patient presented high blood pressure&#44; requiring labetalol perfusion followed by various antihypertensive agents&#46; On the seventh day&#44; he was successfully extubated&#46; As infectious complications&#44; he had <span class="elsevierStyleItalic">Staphylococcus epidermidis</span> bacteremia and <span class="elsevierStyleItalic">Stenotrophomonas maltophilia</span> on sputum smear&#44; both resolved with the appropriate antibiotherapy&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">At the time of discharge&#44; the platelet count was 275<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>&#47;L&#44; LDH 4&#46;48<span class="elsevierStyleHsp" style=""></span>&#956;kat&#47;L&#44; Urea 27&#46;8<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#44; Creatinine 223&#46;6<span class="elsevierStyleHsp" style=""></span>&#956;mol&#47;L&#46; Due to the persistence of kidney dysfunction the patient was transferred to nephrology ward where he continued on hemodialysis and started treatment with eculizumab&#44; in the dosis of 900<span class="elsevierStyleHsp" style=""></span>mg weekly in the first month&#44; followed by 1200<span class="elsevierStyleHsp" style=""></span>mg every 2 weeks thereafter&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Hemolytic anemia&#44; thrombocytopenia and acute renal failure as initial presentation were suggestive of TMA most likely HUS due to the magnitude of renal impairment&#46; Subsequent finding of a regular ADAMTS13 activity excluded TTP&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> Absence of diarrhea on presentation&#44; negative Shiga toxin made less probable typical HUS diagnosis&#46; Moreover&#44; drugs and pathological conditions that cause secondary HUS were excluded&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">Atypical HUS associated with genetic or immune complement abnormalities was the most probable hypothesis&#46; Activation of the alternative complement pathway with low serum C3&#44; normal C4 and Factor B as well as absence of anti-factor H antibodies and normal levels of Factor H and I indicated a possible mutation in genes encoding C3&#44; factor H or factor I&#44;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> that was confirmed by the genetic screening&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">Mutation in factor H was first identified in 1973 and it courses with low or normal plasma levels of factor H&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> It is the most frequent genetic abnormality in aHUS patients &#40;20&#8211;30&#37;&#41; and is associated with 50&#8211;70&#37; risk of death or end stage renal disease in the first episode &#40;&#60;1 year&#41; with a 50&#37; risk of relapse and 75&#8211;90&#37; risk of recurrence after kidney transplantation&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Initial approach of aHUS requires red blood cells transfusion and hemodialysis&#44; which were promptly initiated in this case&#46; Platelet transfusion is contraindicated despite thrombocytopenia&#44; except in cases of active bleeding&#44; since it may exacerbate TMA&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> Plasma therapy is the classical first choice treatment for all cases of aHUS&#46;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;2&#44;6</span></a> Plasmapheresis is prefered to plasma infusion because it assures the delivery of functional complement regulatory proteins and the removal of dysfunctional factors&#44; with lower risk of volume overload&#46; Should be initiated as early as possible&#44; with exchange of 1&#46;5 plasma volume per session&#44; and continued until platelet count&#44; hemoglobin&#44; and LDH levels normalization&#46;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;5&#8211;7</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Plasmapheresis has been the cornerstone of aHUS treatment since 1980 and was the only therapy available until 2010&#46; A recent therapeutic alternative is eculizumab &#8211; a humanized monoclonal IgG antibody which binds to the C5 complement protein preventing the formation of C5b-9 &#40;membrane attack complex&#41; &#8211; already approved by the EMA and FDA&#46;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;2&#44;4&#44;6</span></a> Two prospective phase II trials have demonstrated its efficacy on improving the platelet count and renal function of aHUS patients&#44; including those with progressing TMA and those with long-standing&#44; substantial kidney damage&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a> A posterior analysis confirmed the persistence of the clinical benefits after two years of follow-up&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Eculizumab was also associated with significant improvements in health-related quality of life&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Barriers to eculizumab use include patient safety concerns&#44; as infection with encapsulated bacterial organisms and the elevated cost&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> On the other hand no cumulative toxicity or unexpected serious infections were observed&#44; and survival was 100&#37; on pivotal prospective studies&#44;<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">8&#8211;10</span></a> turning Eculizumab into a very promising option for aHUS patients treatment&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0080" class="elsevierStylePara elsevierViewall">None&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interest</span><p id="par0085" class="elsevierStylePara elsevierViewall">None&#46;</p></span></span>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Renal Biopsy &#40;green masson tricromium stain&#41; 400&#215; &#8211; marked glomerular capillary stasis &#8211; glomerular thrombus&#46;</p>"
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          "leyenda" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">HIV&#58; Human immunodeficiency virus&#59; PCR&#58; polymerase chain reaction&#59; CFH&#58; factor H&#59; CFI&#58; factor I&#59; CFB&#58; factor B&#59; ADAMTS13&#58; a desintegrin and metalloprotease with thrombospondin type1 domain 13&#59; ANA&#58; antinuclear antibody&#59; dsDNA&#58; double-stranded DNA&#59; Sm&#58; Smith&#59; SSA&#58; Sj&#246;gren syndrome A&#59; SSB&#58; Sj&#246;gren syndrome B&#59; RNP&#58; ribonucleic protein&#46;</p>"
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                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">73&#37; &#40;normal &#62;6&#37;&#41;&nbsp;\t\t\t\t\t\t\n
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