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Acute renal failure induced by foscarnet: 4 cases
P Cacoub1, G Deray, A Baumelou
1Department of Nephrology, Hôpital Pitié-Salpétrière, Paris, France.
Clinical Nephrology
|June 1, 1988
Summary
Foscarnet (FC), an antiviral for cytomegalovirus (CMV), may cause acute kidney injury. Careful monitoring of renal function and hydration is recommended during FC treatment to prevent nephrotoxicity.
Area of Science:
- Nephrology
- Infectious Diseases
- Pharmacology
Background:
- Foscarnet (FC) is an antiviral agent used for severe cytomegalovirus (CMV) infections in immunocompromised patients.
- FC is often considered non-nephrotoxic, with renal function decline attributed to other factors.
- Reported adverse effects include anemia, elevated liver enzymes, and hypercalcemia.
Observation:
- Four cases of acute renal failure (ARF) exclusively attributed to FC are presented.
- Patients received FC for CMV chorioretinitis; ARF developed between days 6-15 of treatment.
- Three patients had no other nephrotoxic drugs; one received sulfadiazine concurrently.
Findings:
- ARF was likely due to acute toxic tubulopathy secondary to FC.
- Renal function improved after FC discontinuation in the fourth patient, despite continued sulfadiazine.
- Oligoanuria occurred in two patients, with one requiring hemodialysis.
Implications:
- Foscarnet may be nephrotoxic, causing acute tubulopathy.
- Close renal function monitoring is crucial for patients on FC.
- Prompt correction of dehydration may mitigate FC-induced nephrotoxicity.