• DOI:10.2174/138920021907180709121120
• Corpus ID: 51627849

Drug-Induced Nephrotoxicity and Drug Metabolism in Renal Failure.

@article{Huang2018DrugInducedNA,
  title={Drug-Induced Nephrotoxicity and Drug Metabolism in Renal Failure.},
  author={Jiaguo Huang},
  journal={Current drug metabolism},
  year={2018},
  volume={19 7},
  pages={
          558
        }
}

• Jiaguo Huang
• Published 31 May 2018
• Medicine, Biology, Chemistry
• Current drug metabolism

Chronic kidney disease (CKD) leading to kidney failure is becoming a global public health problem. Acute kidney injury (AKI) is also a major kidney disease characterized by a rapid decline of renal function. Drug-induced nephrotoxicity is a contributing factor to AKI in 19-25% of critically ill patients. Drugs exert their toxic effects to cause nephrotoxicity by one or more common pathogenic mechanisms. The progressive loss of kidney function associated with CKD not only leads to impaired renal excretion of numerous drugs and their metabolites in the kidneys, but also alters the non-renal disposition of moieties that are extensively metabolized by the liver. Various alterations in activity of metabolic enzyme system have been reported in CKD models, for example, reductions in expression and activity of hepatic cytochrome P450 (CYP) enzymes including CYP3A1, CYP3A2, CYP2C11, and other enzymes such as N-acetyltransferases. What’s more, other mechanisms such as the dysregulation of drug transporter systems are involved in decreasing the clearance of drugs in renal failure. With the development of renal failure, the renal secretion of organic ions mediated by organic anion transporters (OATs) and organic cation transporters (OCTs) is decreased. Some organic anionic uremic toxins may directly inhibit the renal excretion of various drugs and endogenous organic acids by competitively inhibiting OATs.