Some biomarkers of acute kidney injury are increased in pre-renal acute injury

• DOI: 10.1038/ki.2012.23
• Publication Date: 2012-03-14T13:48:22Z
• Authors: Maryam Nejat; John W. Pickering; Prasad Devarajan; Joseph V. Bonventre; Charles L. Edelstein; Robert J. Walker; Zoltán H. Endre
• Keywords: Adult; Male; Critical Illness; 610; acute renal failure; 03 medical and health sciences; 0302 clinical medicine; Lipocalin-2; 616; Humans; Hepatitis A Virus Cellular Receptor 1; Cystatin C; Least-Squares Analysis; Aged; Analysis of Variance; Chi-Square Distribution; creatinine; Interleukin-18; Acute Kidney Injury; Lipocalins; 3. Good health; acute kidney injury; Nephrology; Creatinine; Acute Disease; Disease Progression; Original Article; Female; Biomarkers; Acute-Phase Proteins

Pre-renal acute kidney injury (AKI) is assumed to represent a physiological response underperfusion. Its diagnosis retrospective after transient rise in plasma creatinine, usually associated with evidence of altered tubular transport, particularly that sodium. In order test whether pre-renal AKI reversible because less severe than sustained AKI, we measured urinary biomarkers (cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), γ-glutamyl transpeptidase, IL-18, and molecule-1 (KIM-1)) at 0, 12, 24 h following ICU admission. A total 529 patients were stratified into groups having no recovery by h, 48 or the composite greater dialysis. was identified 61 as within fractional sodium excretion <1%. Biomarker concentrations significantly progressively increased duration AKI. After restricting cohort this increase remained significant. The median concentration KIM-1, cystatin IL-18 compared no-AKI, while NGAL transpeptidase not least one biomarker all but three Thus, reason why some requires further study. results suggest represents milder form injury.