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

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 24h following ICU admission. A total of 529 patients were stratified into groups having no AKI, AKI with recovery by 24h, recovery by 48h, or the composite of AKI greater than 48h or dialysis. Pre-renal AKI was identified in 61 patients as acute injury with recovery within 48h and a fractional sodium excretion