Related Experiment Videos
Sulindac is not renal sparing in man
Clinical Pharmacology and Therapeutics
|September 1, 1985
Summary
This study shows that both sulindac and indomethacin, nonsteroidal anti-inflammatory drugs, reduce kidney prostaglandin synthesis and affect sodium balance. They also inhibit the body's response to furosemide, indicating similar renal effects.
Area of Science:
- Nephrology
- Pharmacology
Background:
- Nonsteroidal anti-inflammatory drugs (NSAIDs) can affect kidney function.
- Cyclooxygenase (COX) inhibitors, like sulindac and indomethacin, are commonly used NSAIDs.
Purpose of the Study:
- To investigate the renal-sparing effects of sulindac compared to indomethacin.
- To assess the impact of these NSAIDs on renal prostaglandin synthesis and sodium balance.
Main Methods:
- A randomized controlled trial involving 15 women.
- Assessment of renal function via prostaglandin E2 excretion, sodium balance, plasma renin activity (PRA), and furosemide response.
- Evaluation of systemic effects through platelet aggregation, thromboxane B2 formation, and PGF2 alpha metabolite excretion.
Main Results:
- Both sulindac and indomethacin reduced urinary prostaglandin E2 excretion and led to positive sodium balance.
- Both drugs inhibited the increase in PRA and urinary PGE2 excretion in response to furosemide.
- Sulindac decreased furosemide-induced natriuresis, while indomethacin reduced the rise in inulin clearance.
Conclusions:
- Sulindac and indomethacin exhibit similar effects on the kidney, including reduced renal prostaglandin synthesis and altered sodium handling.
- Both NSAIDs interfere with the renal response to furosemide.
- Indomethacin demonstrated a stronger effect on platelet aggregation and thromboxane synthesis compared to sulindac.