another kidney que - kallastro

[ArchivalUser]

A 61-year-old woman with hypertension, type 2 diabetes mellitus, ischemic cardiomyopathy, and chronic renal insufficiency reports pain in her right knee. Her blood pressure is 140/84 mm Hg, and her pulse is 70 bpm. Because of tenderness and effusion in the knee joint, the patient is prescribed celecoxib 200 mg once daily. After 14 days of therapy, she reports dyspnea, increased swelling in the lower extremities, and fatigue. Blood pressure is now 188/100 mm Hg, blood urea nitrogen (BUN) is 67 mg/dL (baseline, 41 mg/dL), and serum creatinine level is 3.9 mg/dL (baseline, 1.9 mg/dL). Which of the following is the most likely mechanism by which celecoxib caused acute renal failure?

1..Acute papillary necrosis with renal obstruction


2..Acute tubular necrosis from drug-induced nephrotoxicity


3..Drug reaction causing allergic interstitial nephritis


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

[ArchivalUser]

1?

[ArchivalUser]

4,,

[ArchivalUser]

only in 14 days?.....keep it in mind analgesics causes papillary necrosis changes to take place around 3 yrs with dose of 1 gm/day ....

[ArchivalUser]

ok,then either 2 or 3??

[ArchivalUser]

yes answer is 4..........

4....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.