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Answer 1
  1. Hemodynamic renal insufficiency from loss of compensatory prostaglandins induced by cyclooxygenase-2 inhibition by celecoxib. 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.

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