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Indomethacin-associated acute renal failure
The American Journal of Medicine
|July 1, 1980
Summary
Indomethacin can cause acute kidney injury, characterized by reduced urine output and high blood pressure. Symptoms resolved after discontinuing the drug, suggesting a drug-induced condition.
Area of Science:
- Nephrology
- Pharmacology
- Internal Medicine
Background:
- Nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin are commonly used for pain and inflammation.
- NSAIDs can affect renal function, particularly in susceptible individuals.
- Acute kidney injury (AKI) is a potential adverse effect of NSAID therapy.
Observation:
- A 61-year-old male patient developed oliguric acute renal failure during indomethacin treatment.
- The patient presented with significant proteinuria (5.1 g/24 hours) and hypertension.
- Renal function gradually improved after the discontinuation of indomethacin therapy.
Findings:
- The clinical presentation of oliguric acute renal failure, proteinuria, and hypertension in this patient suggests a direct link to indomethacin.
- Resolution of renal insufficiency, proteinuria, and hypertension upon drug withdrawal supports a diagnosis of drug-associated acute kidney injury.
- Indomethacin-induced nephrotoxicity can manifest as acute renal failure.
Implications:
- This case highlights the importance of considering drug-induced nephrotoxicity in patients presenting with acute kidney injury, especially those on NSAIDs.
- Clinicians should monitor renal function and urine protein levels in patients receiving indomethacin, particularly those with risk factors for kidney disease.
- Early recognition and discontinuation of the offending agent are crucial for favorable outcomes in drug-associated acute kidney injury.