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NSAID nephropathy

  • NSAID or Non-steroidal anti-inflammatory drug, are drugs with analgesic, antipyretic and anti-inflammatory effects - they reduce pain, fever and inflammation. The term "non-steroidal" is used to distinguish these drugs from steroids which have similar effects.
  • Nephropathy or nephrosis refers to damage to or disease of the kidney.

Therefore NSAID Nephropathy is damage to the kidney as a result of taking NSAID drugs.



  • Acute renal failure secondary to renal hemodynamic changes
  • Interstitial nephritis with or without proteinuria/nephrotic syndrome
  • Hypertension


Epidemiology is the scientific study of factors affecting the health and illness of individuals and populations

  • Very low, 1% to 3% of patients exposed experience one of the previously mentioned
  • Delayed onset from initial use of NSAID
  • Described with use in all types of NSAIDs

The number of people taking NSAIDs is very high, offsetting low rate per user to high rate per population.


Pathophysiology is the study of the disturbance of normal mechanical, physical, and biochemical functions that a disease causes, or that which causes the disease

Inhibition of renal prostaglandin synthesis interferes with renal hemodynamics.

PGI2, PGE2 are responsible for:

  • vasodilation in the arterioles and glomeruli
  • decreased Na transport and natriuresis in the distal tubules
  • Interferes with ADH action in the distal tubules

TXA2 shown to vasoconstrict glomeruli

Clinical features: NSAID-Induced hemodynamic deterioration of Renal Function

  • Prostaglandin Inhibition leads to further renal vasoconstriction
  • Especially in the setting of already vasocontricted states such as CHF, nephrotic syndrome, cirrhosis, volume depletion, chronic kidney disease (CKD)
  • 30% of patient with CKD on NSAIDS develop this syndrome
  • Elderly also at increased risk mostly secondary to pharmacokinetics
  • Fully reversible if caught early
  • Rarely the sole cause of end-stage renal disease (ESRD)

Clinical Features: NSAID Associated Tubulointerstitial nephritis

  • Heavy Proteinuria/Nephrotic syndrome – 83%
  • Eosinophilia and Eosinophiluria uncommon – 19%
  • Focal tubulointerstitial infiltrates on biopsy
  • Some + immunofluorescence for IgG, IgA, IgM and C3 in interstitial membranes
  • Non-oliguric course typical
  • Variable delayed onset
  • May take weeks to many months to resolve, after stopping NSAID

Clinical Features: NSAID associated Hypertension

  • Usually only a modest increase in BP – an average increase of 6-8mmHg of MAP in patient on NSAIDs
  • NSAIDs mitigate effects of B-blockers and diuretics
  • CCB less susceptible to effects of NSAIDs
  • Elderly, Blacks, low renin hypertension most susceptible

Clinical Oddballs

  • Minimal change disease/Nephrotic syndrome
  • Hyperkalemia – NSAIDs anecdotally used to treat Bartter syndrome.


  • Withdraw NSAIDs
  • Avoid Nephrotoxic meds
  • +/- Steroids with NSAID associated tubulointerstitial nephritis

See also

  • Nephropathy

External links

  • NSAID nephropathy
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "NSAID_nephropathy". A list of authors is available in Wikipedia.
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