IJNU Role of NGAL for the Early Detection of Acute Kidney Injury

filtration (1, 2, 4, 5). However, some urinary biomarkers such as casts, filtered high molecular weight proteins, fractional excretion of sodium and tubular proteins or enzymes are not enough sensitive and specific for the early diagnosis of AKI (3). Biomarkers for early AKI diagnosis represent a unique opportunity for an intervention to save the kidney from additional insults and avoid tissue damage. If we wait for the present paraclinical data which can certainly help, we will always be late. Therefore, we need a novel and more sensitive biomarker for the diagnosis of AKI in order to treat it as soon as possible (5). This biomarker must also be specific, practically easy to detect and measure, reproducible, feasible at bedside, correlative with severity, quantitatively describing the intensity of renal damage even when typical clinical signs are absent and is appropriate to indicate the initiation of the therapy (5). Fortunately, promising methods such as functional genomics and proteomics have discovered new candidates as biomarkers (3, 6), and among them neutrophil gelatinase-associated lipocalin (NGAL), which is a small molecular size (25 kDa) protein and resistance to degradation (7), is a promising biomarker. It usually excreted in urine, accumulates in human kidney cortical tubules which significantly The incidence of acute kidney injury (AKI) is estimated to be from 5% of hospitalized patients to 30–50% of patients in intensive care units, and nowadays there is significant evidence of an increase in its incidence (1, 2). The incidence of both AKI (formerly, acute renal failure) and chronic kidney disease (CKD) has already developed epidemic proportions. In both conditions, early intervention can substantially improve the prognosis. However, the lack of early, predictive and non-invasive biomarkers may lead to delayed initiation of potentially useful therapies for these common clinical settings (3). The diagnosis of AKI is usually based on increases in serum creatinine levels; however, it is a poor indicator of acute deterioration of kidney function. In addition, serum creatinine concentration is greatly influenced by numerous non-renal factors (such as lean muscle mass, race, age, gender, hydration status, medications, muscle metabolism, and protein intake). Measurement of serum creatinine is not ideal marker of renal function in AKI, because these patients are not in steady state. Therefore, changes in serum creatinine may lag far behind renal injury. Thus, considerable rises in serum creatinine are often not apparent until 48–72 h after the initial insult to the kidney. In addition, no significant changes in serum creatinine concentrations may be seen until about 50% of renal function has already been lost. It means that the significant renal disease can exist with minimal or no changes in serum creatinine because of renal reserve, enhanced tubular secretion of creatinine, and compensated lower rates of glomerular *Correspondence: Zohreh Rostami, MD Nephrology and Urology Research Center, Baqiyatallah University of Medical Sciences,Molla Sadra St. Vanak Sq. Tehran, I.R. Iran Email: [email protected] Received: 25 Mar 2010 Accepted: 2 Apr 2010 Editorial