dc.description.abstract |
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. |
en_US |