Biomarkers for acute kidney injury: is NGAL ready for clinical use?

Abstract

The RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria were introduced in 2004, defining the clinical stage of acute kidney injury (AKI) and outcome measures based on serum creatinine, glomerular filtration rate, and urine output. However, a growing body of evidence suggests that these markers are insufficient in drawing an accurate illustration of kidney injury. Indeed, mortality and morbidity remain high in AKI, suggesting that accuracy and speed of patient evaluation are lacking. A great deal of evidence indicates that neutrophil gelatinase-associated lipocalin (NGAL) is a sensitive and specific early marker of various etiological classes of AKI and would be highly valuable in conjunction with existing markers of AKI for better classifying renal injury as well as dysfunction (kidney attack). Improvements in diagnosis, risk identification, stratification, prognosis, and therapeutic monitoring will benefit clinical decision-making in the individualized bundling of therapies and ongoing patient management. In particular, kidney protection and AKI prevention may become feasible if an earlier and more accurate diagnosis is made for AKI. Here, we discuss the opportunity to consider whether NGAL is ready for routine clinical use in a number of etiologies of AKI.

The ischemic/nephrotoxic acute kidney injury and the use of renal biomarkers in clinical practice

“…NGAL (Neutrophil Gelatinase-Associated Lipocalin) is a reliable diagnostic and prognostic biomarker for AKI, as its serum and urinary levels rise much earlier (2 h after the injury [62][63][64][65][66][67][68][69]) and exhibit better sensitivity than SCr [54,62,[70][71][72][73][74][75][76] in patients with ischemic AKI, as well as in AKI due to nephrotoxic drugs, such as tacrolimus, cisplatin, cyclosporine A and radiographic contrast media [68,69,[77][78][79][80][81][82][83][84][85].…”

Angiotensinogen as a biomarker of acute kidney injury

“…The current diagnostic criteria of AKI are based on oliguria and acute rise in serum creatinine. It usually takes 2–3 days to increase significantly because of the rate-limiting step of creatinine production and release by skeletal muscle [ 8 , 9 ]. Therefore, interventions administered at the time of diagnosis of AKI using elevated serum creatinine may not be effective, as judged by several clinical trials of promising therapies for AKI in humans [ 10–12 ].…”

The potential use of biomarkers in predicting contrast-induced acute kidney injury

“…32 Thus, NGAL has the potential to act as a powerful and independent predictor of AKI. [78][79][80][81] Many clinical studies and reviews are reported in the literature concerning the potential role of NGAL as a reliable diagnostic and prognostic biomarker of AKI, since its serum and urinary levels increase earlier and show a better sensitivity than serum creatinine. Some authors stated the plasma NGAL level to be less specific than its urinary concentration.…”