Biomarkers of nephrotoxic acute kidney injury

Abstract

Acute kidney injury (AKI) is a common condition with significant associated morbidity and mortality. Epidemiologic data suggest that a significant proportion of AKI cases is at least partially attributable to nephrotoxin exposure. This is not surprising given intrinsic renal susceptibility to toxicant-induced injury, a consequence of the unique physiologic and biochemical properties of the normally functioning kidney. A number of pathophysiologic mechanisms have been identified that mediate toxic effects on the kidney, resulting in a variety of clinical syndromes ranging from subtle changes in tubular function to fulminant renal failure. Unfortunately, standard metrics used to diagnose and monitor kidney injury, such as blood urea nitrogen and serum creatinine, are insensitive and nonspecific, resulting in delayed diagnosis and intervention. Considerable effort has been made to identify biomarkers that will allow the earlier diagnosis of AKI. Further characterization of these candidate biomarkers will clarify their utility in the setting of acute nephrotoxicity, define new diagnostic and prognostic paradigms for kidney injury, facilitate clinical trials, and lead to novel effective therapies.

Figure 1. Common Nephrotoxicants : Site and Mechanism of Injury

ACE-I: angiotensin-converting enzyme inhibitors; ARB: angiotensin II receptor blockers; NSAID: nonsteroidal anti-inflammatory drugs