title: Some biomarkers of acute kidney injury are increased in pre-renal acute injury.
abstract: Pre-renal acute kidney injury (AKI) is assumed to represent a physiological response to underperfusion. Its diagnosis is retrospective after a transient rise in plasma creatinine, usually associated with evidence of altered tubular transport, particularly that of sodium. In order to test whether pre-renal AKI is reversible because injury is less severe than that of sustained AKI, we measured urinary biomarkers of injury (cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), γ-glutamyl transpeptidase, IL-18, and kidney injury molecule-1 (KIM-1)) at 0, 12, and 24 h following ICU admission. A total of 529 patients were stratified into groups having no AKI, AKI with recovery by 24 h, recovery by 48 h, or the composite of AKI greater than 48 h or dialysis. Pre-renal AKI was identified in 61 patients as acute injury with recovery within 48 h and a fractional sodium excretion <1%. Biomarker concentrations significantly and progressively increased with the duration of AKI. After restricting the AKI recovery within the 48 h cohort to pre-renal AKI, this increase remained significant. The median concentration of KIM-1, cystatin C, and IL-18 were significantly greater in pre-renal AKI compared with no-AKI, while NGAL and γ-glutamyl transpeptidase concentrations were not significant. The median concentration of at least one biomarker was increased in all but three patients with pre-renal AKI. Thus, the reason why some but not all biomarkers were increased requires further study. The results suggest that pre-renal AKI represents a milder form of injury.
authors.affiliation: Christchurch Kidney Research Group, Department of Medicine, University of Otago, Christchurch, New Zealand.
authors.forename: Maryam
authors.initials: M
authors.lastname: Nejat
authors.forename: John W
authors.initials: JW
authors.lastname: Pickering
authors.forename: Prasad
authors.initials: P
authors.lastname: Devarajan
authors.forename: Joseph V
authors.initials: JV
authors.lastname: Bonventre
authors.forename: Charles L
authors.initials: CL
authors.lastname: Edelstein
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Walker
authors.forename: Zoltán H
authors.initials: ZH
authors.lastname: Endre
mesh_terms: D000208:Acute Disease; D058186:Acute Kidney Injury / Q000097:blood / Q000175:diagnosis* / Q000401:mortality / Q000628:therapy / Q000652:urine; D000209:Acute-Phase Proteins / Q000652:urine; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood / Q000652:urine; D016009:Chi-Square Distribution; D003404:Creatinine / Q000097:blood; D016638:Critical Illness; D055316:Cystatin C / Q000652:urine; D018450:Disease Progression; D005260:Female; D000072596:Hepatitis A Virus Cellular Receptor 1; D006801:Humans; D020382:Interleukin-18 / Q000652:urine; D016018:Least-Squares Analysis; D000071068:Lipocalin-2; D054834:Lipocalins / Q000652:urine; D008297:Male; D008562:Membrane Glycoproteins / Q000652:urine; D008875:Middle Aged; D009520:New Zealand; D011237:Predictive Value of Tests; D011379:Prognosis; D011446:Prospective Studies; D011518:Proto-Oncogene Proteins / Q000652:urine; D011991:Receptors, Virus; D017582:Renal Replacement Therapy; D013997:Time Factors; D015854:Up-Regulation; D005723:gamma-Glutamyltransferase / Q000652:urine
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; C525030:CST3 protein, human; D055316:Cystatin C; C491143:HAVCR1 protein, human; D000072596:Hepatitis A Virus Cellular Receptor 1; D020382:Interleukin-18; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D008562:Membrane Glycoproteins; D011518:Proto-Oncogene Proteins; D011991:Receptors, Virus; D003404:Creatinine; D005723:gamma-Glutamyltransferase