Editorial
Another piece to add to the puzzle of procalcitonin in renal dysfunction
Otra pieza para el rompecabezas de la procalcitonina en la disfunción renal
E. Estenssoro
Intensive Care Unit, Hospital Interzonal de Agudos General San Martin de La Plata, La Plata, Buenos Aires, Argentina
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"apellidos" => "Restrepo" ] 12 => array:1 [ "colaborador" => "on behalf GETGAG study group" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2173572718301644" "doi" => "10.1016/j.medine.2017.12.011" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2173572718301644?idApp=WMIE" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0210569117303637?idApp=WMIE" "url" => "/02105691/0000004200000007/v1_201809220816/S0210569117303637/v1_201809220816/en/main.assets" ] ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial</span>" "titulo" => "Another piece to add to the puzzle of procalcitonin in renal dysfunction" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "397" "paginaFinal" => "398" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "E. Estenssoro" "autores" => array:1 [ 0 => array:3 [ "nombre" => "E." "apellidos" => "Estenssoro" "email" => array:1 [ 0 => "estenssoro.elisa@gmail.com" ] ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Intensive Care Unit, Hospital Interzonal de Agudos General San Martin de La Plata, La Plata, Buenos Aires, Argentina" "identificador" => "aff0005" ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Otra pieza para el rompecabezas de la procalcitonina en la disfunción renal" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Procalcitonin is a ubiquitous polypeptide which is rapidly released in the presence of bacterial toxins and proinflammatory mediators (IL-1B, TNF-α, and IL-6).<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> In recent years, many researchers have established its relevance for the diagnosis of moderate-to-severe bacterial infections, especially of the respiratory tract.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,3</span></a> In viral infections, however, procalcitonin elevation can be blocked by concomitantly released cytokines (e.g. interferon), and this interaction facilitates differential diagnosis between bacterial and viral infections.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> Furthermore, since PCT levels decrease with ongoing resolution of infection, repeated evaluation of this biomarker over time might indicate when to stop unnecessary antimicrobial treatment, thus preventing adverse effects on patients, and also decreasing antimicrobial pressure on the high-resistant microorganisms which grow in the complex ICU environment.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> A recent metaanalysis determined that procalcitonin guidance of antimicrobial treatment in suspected/confirmed sepsis was safe, and resulted in a significant decrease in antibiotic treatment duration, with no impact on mortality or on ICU length-of-stay.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">A particular clinical situation is pneumonia produced by influenza viruses requiring ICU admission. Up to one third of these severely affected patients might have concurrent lung bacterial infection, as described during the 2009 pandemia.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> Theoretically, PCT might aid to discard coinfection and discontinue redundant antimicrobials. Nevertheless, the concomitant development of acute renal dysfunction/failure occurs in 17% of patients with severe influenza<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> might produce increased procalcitonin levels due to decreased elimination, making interpretation difficult.</p><p id="par0015" class="elsevierStylePara elsevierViewall">In this issue of Medicina Intensiva,<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a> Rodriguez et al. analyze procalcitonin levels in 663 patients admitted to 148 ICUs in Spain with influenza infection and acute kidney failure (AKI), defined by an elevation in creatinine of 1.60–2.50<span class="elsevierStyleHsp" style=""></span>mg/dL (AKI I) and 2.51–3.99<span class="elsevierStyleHsp" style=""></span>mg/dL (AKI II). They excluded more severe forms of kidney failure. In this study, patients had bacterial lung infection on admission carefully discarded after an intensive screening protocol; therefore, any elevation in procalcitonin would be only ascribable to renal dysfunction. The researchers sought to characterize the relationship between procalcitonin and creatinine and procalcitonin and urea (creatinine clearance was not available). Had any of those relations been linear, creatinine elevations might predict the increases in procalcitonin levels exclusively due to renal dysfunction or failure; any further increase might be produced by bacterial coinfection, thus permitting rapid diagnosis and treatment.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Unfortunately, the correlations between procalcitonin and creatinine were weak, even adjusted for other relevant covariates which might act as surrogates of widespread inflammation, such as elevations of APACHE II or white blood cell count. Indeed the metabolism of procalcitonin is poorly understood; it is synthetized in the leukocytes, especially in mononuclear cells and in other tissues in response to microbial toxins and certain proinflammatory mediators (e.g., IL-1B, TNF-α, and IL-6),<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> but the mechanisms of elimination still remain to be elucidated. Conversely, other researchers reported a parallel increase of procalcitonin with renal deteriorating function; they also measured procalcitonin in mononuclear cells and detected an elevation in absence of infection which, they speculated, might serve as a marker of low-grade inflammation in advanced kidney disease.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Notwithstanding this, there are other possible explanations to the authors’ negative findings: only half of the patients of the entire cohort had procalcitonin measured; and the number of patients with renal dysfunction/failure included might have been insufficient to detect a significant association between renal dysfunction and procalcitonin, since only less than 10% of patients experienced AKI stages I-II.</p><p id="par0030" class="elsevierStylePara elsevierViewall">It is also likely that patients actually had bacterial coinfections which went undetected; sepsis and septic shock are frequently associated with negative cultures. And, last but not least, the real correlation might be between procalcitonin and glomerular filtration rate, which was not estimated by any method; it is known that serum creatinine might not reflect the true renal function in the critically ill.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">What is the main message of this study? It might well be that procalcitonin dynamics in renal compromise is complex and poorly understood, and that there might be other mechanisms of elimination, given that the authors found higher values of procalcitonin than those predicted by their equation when progressing from AKI I to AKI II. While renal dysfunction/failure is a state of increased inflammation, the study of Rodriguez et al. point to different mediators other than creatinine and urea to explain increased procalcitonin levels in their patients. And, more importantly, the authors give a word of caution to clinicians about interpreting high procalcitonin levels in the setting of renal dysfunction/failure: they should not give up searching for its most common cause, which is bacterial infection.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0040" class="elsevierStylePara elsevierViewall">None declared.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Funding" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0055" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Overview of procalcitonin assays and procalcitonin-guided protocols for the management of patients with infections and sepsis" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "P. 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| año/Mes | Html | Total | |
|---|---|---|---|
| 2024 Noviembre | 9 | 11 | 20 |
| 2024 Octubre | 71 | 45 | 116 |
| 2024 Septiembre | 63 | 30 | 93 |
| 2024 Agosto | 73 | 35 | 108 |
| 2024 Julio | 60 | 31 | 91 |
| 2024 Junio | 75 | 42 | 117 |
| 2024 Mayo | 68 | 29 | 97 |
| 2024 Abril | 78 | 70 | 148 |
| 2024 Marzo | 83 | 45 | 128 |
| 2024 Febrero | 83 | 39 | 122 |
| 2024 Enero | 81 | 33 | 114 |
| 2023 Diciembre | 67 | 36 | 103 |
| 2023 Noviembre | 61 | 31 | 92 |
| 2023 Octubre | 70 | 33 | 103 |
| 2023 Septiembre | 82 | 36 | 118 |
| 2023 Agosto | 52 | 20 | 72 |
| 2023 Julio | 83 | 27 | 110 |
| 2023 Junio | 72 | 21 | 93 |
| 2023 Mayo | 81 | 33 | 114 |
| 2023 Abril | 75 | 24 | 99 |
| 2023 Marzo | 117 | 36 | 153 |
| 2023 Febrero | 107 | 36 | 143 |
| 2023 Enero | 82 | 31 | 113 |
| 2022 Diciembre | 105 | 66 | 171 |
| 2022 Noviembre | 104 | 42 | 146 |
| 2022 Octubre | 84 | 49 | 133 |
| 2022 Septiembre | 66 | 37 | 103 |
| 2022 Agosto | 52 | 44 | 96 |
| 2022 Julio | 37 | 39 | 76 |
| 2022 Junio | 44 | 22 | 66 |
| 2022 Mayo | 41 | 45 | 86 |
| 2022 Abril | 39 | 44 | 83 |
| 2022 Marzo | 54 | 57 | 111 |
| 2022 Febrero | 41 | 35 | 76 |
| 2022 Enero | 32 | 34 | 66 |
| 2021 Diciembre | 50 | 43 | 93 |
| 2021 Noviembre | 40 | 49 | 89 |
| 2021 Octubre | 54 | 62 | 116 |
| 2021 Septiembre | 37 | 37 | 74 |
| 2021 Agosto | 37 | 44 | 81 |
| 2021 Julio | 29 | 33 | 62 |
| 2021 Junio | 43 | 26 | 69 |
| 2021 Mayo | 55 | 77 | 132 |
| 2021 Abril | 114 | 99 | 213 |
| 2021 Marzo | 103 | 37 | 140 |
| 2021 Febrero | 77 | 30 | 107 |
| 2021 Enero | 75 | 36 | 111 |
| 2020 Diciembre | 58 | 22 | 80 |
| 2020 Noviembre | 44 | 22 | 66 |
| 2020 Octubre | 39 | 32 | 71 |
| 2020 Septiembre | 63 | 26 | 89 |
| 2020 Agosto | 31 | 19 | 50 |
| 2020 Julio | 47 | 22 | 69 |
| 2020 Junio | 29 | 29 | 58 |
| 2020 Mayo | 21 | 13 | 34 |
| 2020 Abril | 70 | 26 | 96 |
| 2020 Marzo | 15 | 10 | 25 |
| 2020 Febrero | 50 | 43 | 93 |
| 2020 Enero | 43 | 41 | 84 |
| 2019 Diciembre | 29 | 22 | 51 |
| 2019 Noviembre | 31 | 19 | 50 |
| 2019 Octubre | 22 | 22 | 44 |
| 2019 Septiembre | 34 | 27 | 61 |
| 2019 Agosto | 42 | 20 | 62 |
| 2019 Julio | 38 | 26 | 64 |
| 2019 Junio | 35 | 35 | 70 |
| 2019 Mayo | 50 | 33 | 83 |
| 2019 Abril | 35 | 23 | 58 |
| 2019 Marzo | 47 | 31 | 78 |
| 2019 Febrero | 35 | 41 | 76 |
| 2019 Enero | 37 | 24 | 61 |
| 2018 Diciembre | 1 | 2 | 3 |
| 2018 Noviembre | 3 | 10 | 13 |
| 2018 Octubre | 43 | 28 | 71 |
| 2018 Septiembre | 17 | 11 | 28 |
| 2018 Mayo | 0 | 1 | 1 |
| 2018 Abril | 0 | 3 | 3 |
| 2018 Marzo | 5 | 0 | 5 |
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