Drug-induced nephropathy: an update

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.

Keywords::

• acute interstitial nephritis (AIN)
• acute renal failure (ARF)
• acute tubular necrosis (ATN)
• crystal nephropathy
• nonsteroidal anti-inflammatory drug (NSAID)
• nephrocalcinosis
• nephrolithiasis
• obstructive nephropathy
• osmotic nephropathy