Abstract

ACUTE KIDNEY INJURY AND KIDNEY FAILURE: A REVIEW ON MECHANISMS OF NEPHROTOXICITY AND NEPHROTOXIC EXPERIMENTAL MODELS

Kavitha CH. N.*, Pratyusha R., Sai Nitish N. and Lakshmi Iswarya T.

ABSTRACT

Acute kidney injury (AKI) is a common condition with a high risk of death. Nephrotoxicity occurs when kidney-specific detoxification and excretion do not work properly due to the damage or destruction of kidney function by exogenous or endogenous toxicants. Exposure to drugs often results in toxicity in kidney which represents the major control system maintaining homeostasis of body and thus is especially susceptible to xenobiotics. Understanding the toxic mechanisms for nephrotoxicity provides useful information on the development of drugs with therapeutic benefits with reduced side effects. In this review, we discuss the mechanisms for drug-induced nephrotoxicity include changes in glomerular hemodynamic, tubular cell toxicity, inflammation, crystal nephropathy, rhabdomyolysis, and thrombotic microangiopathy. Due to the multiple causes of renal failure, many animal models have been developed to advance our understanding of human nephropathy. Among these experimental models, rodents have been extensively used to enable mechanistic understanding of kidney disease induction and progression, as well as to identify potential targets for therapy. In this review, we discuss AKI models induced by surgical operation and drugs or toxins. This review summarizes the current state of the field of nephrotoxicity and a variety of experimental induced nephrotoxic models which can be extensively used to explore nephroprotective effects of novel compounds. These animal models may serve as an early detection of drug-induced nephrotoxicity to investigate the different mechanisms involved in acute kidney injury and renal failure. It emphasizes integrating our understanding of nephrotoxicity with pathological-induced renal failure.

Keywords: Due to the multiple causes of renal failure, many animal models have been developed to advance our understanding of human nephropathy.