Nephrogenic Diabetes Insipidus and Renal Tubular Acidosis Secondary to Foscarnet Therapy
| Title: | Nephrogenic Diabetes Insipidus and Renal Tubular Acidosis Secondary to Foscarnet Therapy |
|---|---|
| Authors: | Navarro, MD, Juan F.; Quereda, Carlos; Quereda, Carmen; Gallego, MD, Nieves; Antela, M.D., Antonio; Mora, M.D., Carmen; Ortuno, M.D., Joaquin |
| Publisher: | American Journal of Kidney Diseases |
| Date Published: | March 01, 1996 |
| Reference Number: | 29 |
Foscarnet is used as therapy of cytomegalovirus (CMV) infection in immunosuppressed subjects. We present a patient with human immunodeficiency virus infection under treatment with foscarnet for CMV retinitis who complained of thirst and polyuria. Laboratory data showed hypernatremia with increased plasma osmolality and metabolic hyperchloremic acidosis. A water deprivation test demonstrated a nephrogenic diabetes insipidus. Other laboratory studies, including urine pH, anion gap, titratable acidity, and bicarbonate, showed a distal tubular acidifcation defect. All abnormalities were transient, with recovery a few days after foscarnet withdrawal. No cases of renal acidosis, and only one case of nephrogenic diabetes insipidus, has been previously reported as a complication of foscarnet treatment. Our patient developed both nephrogenic diabetes insipidus and renal tubular acidosis with a temporal pattern that demonstrated a link between foscarnet therapy and these abnormalities
This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
Navarro, et al., report of a 27-year-old AIDS patient on foscarnet therapy who complained of excessive thirst and urination, two characteristic symptoms of NDI. Laboratory tests revealed the patient was suffering from both NDI and renal tubular acidosis (RTA), a kidney defect involving over acidification of a segment of the small filtering tubes in the kidney. After they stopped giving the patient foscarnet, the patient's NDI and RTA cleared up. Further laboratory tests indicated there was no other plausible cause for the NDI and RTA than foscarnet.
It is unclear as to how foscarnet induced NDI or RTA, but this case suggests a strong link between foscarnet and these disorders.