MECHANISM OF DRUG INDUCED RENAL FAILURE: A REVIEW

Acute renal failure (ARF) is characterized by a rapid, potentially reversible decline in renal function, including a rapid fall in glomerular filtration rate (GFR) and retention of nitrogenous waste products over a period of hours or days. The mortality rate of patients with ARF has remained 25–70% despite the use of various pharmacologic agents. Due to the multiple causes of renal failure, many animal models have been developed to advance our understanding of human nephropathy. Among the experimental models, rodents have been extensively used to enable a mechanistic understanding of kidney disease induction and progression, as well as to identify potential targets for therapy. Numerous experimental models have confirmed the nephrotoxicity induced by gentamicin, cisplatin, acetaminophen, glycerol, CCl₄, adenine, potassium dichromate, and others. Nephrotoxicity induced in these experimental models showed pathophysiological, ultrastructural and functional renal impairments in the form of tubular desquamation and necrosis and elevated blood urea and serum creatinine. The aim of this study was to know the mechanism of actions of different nephrotoxic agents for inducing renal failure in an animal model. That will help in the prevention and treatment of drug-induced nephrotoxicity.