Urine albumin as a biomarker in acute kidney injury.

Abstract

ACUTE KIDNEY INJURY (AKI) is a common clinical condition that is associated with significantly high rates of morbidity and mortality particularly in critically ill patients (1, 2, 10, 18). Despite fundamental advances in understanding the etiology and pathophysiology of AKI the current therapeutic approaches remain limited to supportive measures (e.g., dialysis). Treatment for AKI is confounded by several variables including patient demographics, severity of AKI, and AKI associated with complex medical and surgical interventions. Therefore, there is a growing need to provide timely and accurate diagnosis to allow for the implementation of potentially novel therapeutic interventions to overcome AKI. Studies in animal models of AKI have highlighted the therapeutic potential for a number of interventions. However, translation of these potential therapies to humans has yielded inconclusive and equivocal results (2, 5, 12). One of the proposed reasons for such failure is the lack of early markers for AKI and hence an unacceptable delay in initiating therapy. In current clinical practice, identification and severity of AKI is generally based on elevations in serum creatinine levels. Unfortunately, creatinine is an unreliable indicator of early AKI for multiple reasons. For example, a significant decrease (50%) in glomerular filtration rate (GFR) may be necessary to raise the serum creatinine above the normal laboratory range (2, 9, 11). In sepsis, production of creatinine from the muscle is reduced, and relying on changes in serum creatinine to diagnose AKI in such settings could delay diagnosis of AKI (3). Recent studies have conclusively shown that the morbidity and mortality associated with AKI are correlated with the severity of kidney injury. The data from these studies and animal models indicate that prevention or decrease in the extent of injury could significantly lower negative outcomes