Glomerular filtration rate NSAIDs

Kidney Function. Prostanoids influence a variety of kidney functions including renal blood flow, secretion of renin, glomerular filtration rate, and salt and water excretion. They do not have a critical role in modulating normal kidney function but play an important role when the kidney is under stress. Eor example, PGE2 and -I2 are renal vasodilators (70,71) and both are released as a result of various vasoconstrictor stimuli. They thus counterbalance the vasoconstrictor effects of the stimulus and prevent renal ischemia. The renal side effects of NSAIDS are primarily observed when normal kidney function is compromised. 

Gastrointestinal ulceration may occur less frequently than with some other NSAIDs. A preparation combining diclofenac and misoprostol decreases upper gastrointestinal ulceration but may result in diarrhea. Another combination of diclofenac and omeprazole was also effective with respect to the prevention of recurrent bleeding, but renal adverse effects were common in high-risk patients. Diclofenac, 150 mg/d, appears to impair renal blood flow and glomerular filtration rate. Elevation of serum aminotransferases occurs more commonly with this drug than with other NSAIDs. 

Irrespective of the pharmacokinetics of NSAIDs in patients with liver disease, the risks of adverse effects will outweigh the benefits of treatment in many patients. Side effects of note are gastrointestinal bleeding, reduction in glomerular filtration rate (GFR), inhibition... 

Abbreviations NSAID = nonsteroidal anti-inflammatory drugs, PG = prostaglandin, RBF = renal blood flow, GFR = glomerular filtration rate,HTN = hypertension, DM = diabetes mellitus, = potassium, RAA = renin-angiotensin- aldosterone, CHF = congestive heart failure, AGE = angiotensin-converting enzyme, SLF = systemic lupus erythematosis. 

In 11 patients with rheumatoid arthritis taking ciclosporin, naproxen and sulindac increased serum creatinine levels by 24% and reduced renal function (glomerular filtration rate reduced from 98 niL/minute at baseline to 67 mL/minute while taking an NSAID and ciclosporin). All patients had a clinical improvement in their rheumatoid arthritis. 

A patient with a kidney transplant had a rise in serum creatinine levels when sulindac was used. Ciclosporin blood levels fell and rose again when the sulindac was stopped. Another report states that the ciclosporin levels of a woman with a kidney transplant were more than doubled within 3 days of her starting to take sulindac 150 mg twice daily. In 11 patients with rheumatoid arthritis taking ciclosporin, both sulindac and naproxen increased serum creatinine levels by 24% and reduced renal function (glomerular filtration rate reduced from 98 mL/minute at baseline to 67 mL/minute while taking an NSAID and ciclosporin). All patients had a clinical improvement in their rheumatoid arthritis. "... 

Renal papillary necrosis and other renal injury with long-term use. Most of the unwanted renal side effects of the class of NSAIDs are related to the inhibi-ton of prostanoid synthesis. The COX-2 enzyme has been implicated as a mediator of renal blood flow, renin release and sodium excretion. As a result, COX-2 inhibitors may lead to an alteration of renal homeostasis resulting in decreases in glomerular filtration rate, renal blood flow, sodium and water retention, and hyperkalemia [1]. 

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