Kidney Tubular Cell Protection; Recent Findings

Acute renal failure (ARF) or acute kidney injury (AKI) may develop due to numerous factors including obstruction of the urinary tract, toxic substances to kidney and low blood volume[1-3] . Acute renal failure may lead to numerous complications including metabolic acidosis, uremia and changes in body fluid balance. The diagnosis of acute kidney injury is based mainly on the laboratory findings, such as blood creatinine and urea nitrogen. Management includes treatment of the underlying disorder and supportive care[4-8]. Recently, attentions are mostly on protection or prevention as well as accelerating the regeneration of tubular cells against injurious insults to the kidney. To study acute kidney injury, various models have been defined for each specific condition. Gentamicin (GM) which is an aminoglycoside antibiotic and is derived from gram-positive bacteria, has a potential for the treatment of aerobic gramnegative infections. Gentamicin is extensively used for induction of ARF in preclinical studies and evaluation of renal protective agents. Gentamicin is usually accumulated in kidney proximal tubular cells which may trigger renal injury, leading to brush border network damage[9,11]. The kidney toxicity is usually caused by increased free radical production, suppression of antioxidant defense mechanisms as well as acute renal tubular cells necrosis[9-12], which lead to kidney dysfunction and diminished glomerular filtration rate (GFR).