Braian M Beker, Carlos G Musso, Mateo G Corleto, Cecilia Fieiras
Journal: International urology and nephrology 2018;50(4):705-713
PMID: 29307055
Acute kidney injury (AKI) consists of a rapid renal function decline which usually increases serum urea and creatinine levels. Since kidney injury begins by inducing biological and molecular changes which evolve to cellular damage, biomarkers could be used as tools for monitoring early AKI appearance, and predicting its recovery. Among the main AKI biomarkers the neutrophil gelatinase-associated lipocalin, cystatin C, kidney injury molecule-1, monocyte chemotactic peptide-1, N-acetyl-β-D-glucosaminidase, interleukin-18, liver-type fatty acid-binding protein, netrin-1, cycle arrest markers, endogenous ouabain, selenium-binding protein 1, and BPIFA2 marker, have been described. Even though novel biomarkers seem to be more helpful to early detect AKI and/or predict the need for renal replacement, and mortality compared to serum creatinine, more comprehensive studies are still required to determine their clinical utility.
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