Biomarkers For Acute Kidney Injury

Abstract

A cute kidney injury (AKI) is the sudden loss of kidney function. It has been referred to as acute kidney failure in the past. The primary physiological function of the kidneys is to filter the blood and remove the waste, as well as excess salt and water. When AKI occurs, urea nitrogen and creatinine levels increase in the blood circulation, the daily urine output falls, and the fluid-electrolyte balance and the acid-base balance deteriorate. AKI is associated with prerenal, renal, and postrenal events (Table 1). Although AKI is often reversible, depending on the causes and severity, it may not be. The most common adverse events due to AKI are chronic renal failure, chronic kidney disease, and cardiovascular events. AKI is a major cause of morbidity and mortality in intensive care units. Therefore, early diagnosis of AKI is very important for the prognosis of patients as well as to reduce medical costs [1-6]. To diagnose AKI, the measurement of the daily quantity of urine output; routine urinalysis; blood tests examining urea and cre-atinine levels; imaging tests, such as ultrasound and computerized tomography; and/or a kidney biopsy may be performed. Regulation of blood pressure and circulation of the blood to the kidneys are primary treatments for patients with AKI. Short-term dialysis is used in some cases, but long-term dialysis or kidney transplantation may be required for patients with severe renal insufficiency [7, 8]. Several classification schemes have been proposed for patients with AKI according to the extent and duration of renal injury and to predict clinical outcomes (Table 2). The classification systems contain criteria for serum creatinine (SCr) and urine output. The KDIGO (Kidney Disease: Improving Global Outcomes) criteria for AKI diagnosis are: SCr level increase more than 0.3 mg/dL in 48 hours, or SCr level increase 1.5-fold over baseline within 7 days, or urine volume of less than 0.5 mL/kg/hour for 6 hours (also referred as Stage 1). In addition to the 3 stages of renal dysfunction, the RIFLE (Risk of renal dysfunction, Injury to the kidney, Failure of kidney function, Loss of kidney function and End-stage kidney disease) criteria, unlike KDIGO includes 2 additional clinical outcomes of loss, indicating the complete loss of kidney function and end-stage renal disease, requiring renal replacement therapy [7-11]. Objectives: Acute kidney injury (AKI) is associated with both a number of adverse outcomes and with morbidity and mortality. Therefore, early diagnosis of AKI is very important. Several novel AKI biomarkers have been found and studied. Markers include impaired filtration barriers, reduced tubular reabsorption, increased release of tubular proteins due to cell damage and/or activation of inflammatory cells, and the release of activation products in response to injury. Neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, interleukin-18, liver-type fatty acid-binding protein , cystatin C, tissue inhibitor of metalloproteinase-2, and insulin-like growth factor-binding protein 7 markers appear to be useful; however, the clinical uses of AKI biomarkers are not yet well defined and the number of clinical trials is limited. Additionally, analytical validation of tests for AKI markers is also required. Therefore, measurement of the daily quantity of urine and determination of blood urea and creatinine levels are most often used for both diagnosis and classification of AKI in clinical practice. Keywords: Acute kidney injury, cystatin c, insulin-like growth factor-binding protein 7, interleukin-18, kidney injury molecule 1, liver-type fatty acid-binding protein, neutrophil gelatinase-associated lipocalin, tissue inhibitor of metal-loproteinase-2 Abstract