Renal prostaglandins are
synthesized in certain disease states to maintain renal blood flow, glomerular
filtration rate, and salt, water, and potassium excretion. Chronic renal
failure, reduced cardiac output, therapy with diuretic drugs, and hypertension
depend on compensatory prostaglandin synthesis to maintain kidney function.
Acute papillary necrosis can occur with nonsteroidal anti-inflammatory drug
(NSAID) use but is often associated with gross hematuria and flank pain without
acute renal failure. Direct tubular injury is not an acute effect of NSAIDs.
Therapy with NSAIDs (eg, selective cyclooxygenase-2 inhibitors) blunts
prostaglandin synthesis and impairs renal physiologic responses, causing
acute renal failure, salt and water retention, and reduced potassium excretion.
This effect is reversible with discontinuation of the NSAIDs. Allergic interstitial
nephritis is unlikely to cause such rapid renal failure.
- Hemodynamic renal insufficiency from loss of compensatory prostaglandins
induced by cyclooxygenase-2 inhibition by celecoxib.
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Seminars in Medical Practice
Hospital Physician Board Review Manuals
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Updated 1/04/08 kkj