Drug-induced renal failure: update on new medications and unique mechanisms of nephrotoxicity

Am J Med Sci. 2003 Jun;325(6):349-62. doi: 10.1097/00000441-200306000-00006.


Medications cause renal failure through a variety of mechanisms. Hemodynamic renal failure may result from drugs that reduce renal prostaglandins and hence renal blood flow and glomerular filtration rate. A relatively new group of drugs with this potential is the cyclooxygenase-2 selective inhibitors. Direct renal tubular toxicity has also been described with a number of new medications with unique effects on the epithelial cells of the kidney. These include the antiviral agents cidofovir, adefovir, and tenofovir as well as the bisphosphonate pamidronate. Additionally, crystal deposition in the kidney may promote the development of renal failure. Several different drugs have been described to induce crystal nephropathy, including the antiparasitic drug sulfadiazine, the antiviral agent acyclovir, and the protease inhibitor indinavir. Finally, an unusual form of renal failure characterized by swollen, vacuolated proximal tubular cells can develop from hyperosmolar substances. Agents recently described to induce an "osmotic nephrosis" include intravenous immunoglobulin and the plasma expander hydroxyethyl starch.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects
  • Anti-Inflammatory Agents, Non-Steroidal / toxicity
  • Antiviral Agents / adverse effects
  • Antiviral Agents / toxicity
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors / adverse effects
  • Cyclooxygenase Inhibitors / toxicity
  • Humans
  • Isoenzymes / antagonists & inhibitors
  • Isoenzymes / metabolism
  • Membrane Proteins
  • Prostaglandin-Endoperoxide Synthases / metabolism
  • Renal Insufficiency / chemically induced*
  • Renal Insufficiency / pathology


  • Anti-Inflammatory Agents, Non-Steroidal
  • Antiviral Agents
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • Isoenzymes
  • Membrane Proteins
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases