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NSAID nephropathy

Drugs & Medication

NSAID nephropathy

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  • 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.

Contents

Symptoms

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

Epidemiology

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

  • Very low, 1% to 3% of patient 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

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

  • Prostoglandin Inhibtion leads to further renal vasoconstriction
    Especially in setting of already vasocontricted states such as CHF, nephrotic syndrome, cirrhosis, volume depletion, CRI
    30% of patient with CRI on NSAIDS develop this syndrome
    Elderly also at increased risk mostly secondary to pharmacokinetics
    Fully reversible if caught early
    Rarely the sole cause of ESRD

Clinical Features: NSAID Associated Tubulointerstial 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 pf 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 Barter’s

Treatment

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

See also

External links


Home | Up | NSAID nephropathy | Aspirin | Diclofenac | Ibuprofen | Indometacin | Ketoprofen | Naproxen | Piroxicam | Rofecoxib

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