Drug-induced nephropathy: an update

Expert Opin Drug Saf. 2005 Jul;4(4):689-706. doi: 10.1517/14740338.4.4.689.

Abstract

Medications cause renal disease by promoting various types of injury in the kidney. Several drugs reduce renal perfusion and cause prerenal azotemia. Vascular disease can develop following exposure to various medications through direct and indirect effects. A number of glomerular lesions have been described with therapeutic agents and illicit drugs. Acute interstitial nephritis occurs from a drug-induced allergic reaction, which promotes interstitial inflammation and tubular damage. Acute tubular necrosis is a dose-dependent process that occurs from direct drug toxicity on tubular epithelia. Other less common patterns of drug-induced tubular injury include osmotic nephropathy, crystal nephropathy and acute nephrocalcinosis. Finally, postrenal azotemia from structural or functional obstruction of the urinary tract also complicates therapy with a number of medications.

Publication types

  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Dose-Response Relationship, Drug
  • Drug-Related Side Effects and Adverse Reactions*
  • Humans
  • Kidney Diseases / chemically induced*
  • Syndrome
  • Vasoconstriction / drug effects
  • Vasodilation / drug effects

Substances

  • Anti-Inflammatory Agents, Non-Steroidal