Indomethacin Treatment in Amphotericin B Induced Nephrogenic Diabetes Insipidus
| Title: | Indomethacin Treatment in Amphotericin B Induced Nephrogenic Diabetes Insipidus |
|---|---|
| Authors: | Hohler, T.; Teuber, G.; Wanitschke, R.; zum Buschenfelde, K.-H. Meyer |
| Publisher: | Clinical Investigator |
| Date Published: | October 01, 1994 |
| Reference Number: | 89 |
Nephrogenic diabetes insipidus (NDI) is a serious side effect of various drugs. Elevated renal prostaglandin E2 levels have been found in patients with lithium-induced NDI and have been implicated in the pathogenesis. We report the case of a patient who developed NDI following treatment with amphotericin B. Prostaglandin levels were elevated. Indomethacin had an antidiuretic effect and normalized prostaglandin levels
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)
Nephrogenic diabetes insipidus occurs when the collecting duct in the kidney fails to respond to antidiuretic hormone (ADH). When this happens the kidneys get rid of water that they should have retained. Most people suffering from the congenital form of the disease have a mutant form of the V2 receptor gene which makes the renal tubule (in the kidneys) insensitive to vasopressin.
(Vasopressin is another word for the ADH. Vasopressin tells the kidneys to retain water. In doing this two things are accomplished: first, the blood gets the water it needs because the water that the kidneys retain goes into the blood; and second, the urine becomes more concentrated.) Drug-induced NDI (DNDI) is a serious side effect of various drugs that has been most frequently observed in patients treated with lithium, demeclocycline, and methoxyflurane. In addition, other drugs, including amphotericin B and bentamicin, have been reported to similarly impair the kidneys' urine-concentrating ability.
Our report involves a patient who developed DNDI following treatment with tobramicin and amphotericin B.
Case Report
A 49-year-old woman was transferred to our intensive care unit (ICU) because of septicemia (blood poisoning) and respiratory failure.
Three weeks prior to transfer she was diagnosed as having acute myelomoncytic leukemia and a pelvic tumor that caused uropathy (obstruction of the urinary tract) and pyelonephritis of the left kidney (inflammation of the kidney usually caused by bacterial infection). A nephrostomy catheter was inserted (a tube which brings urine to the abdominal wall bypassing the ureter) and she was treated with entamicin and cefotaxim.
Four days before being transferred to the ICU, she developed a fever and left-sided pulmonary infiltrates. She was treated with antibiotics and other drugs. A chemotherapy was begun. Despite these treatments, her fever rose to 40 degrees C. The drugs were adjusted. Two days later she developed respiratory failure which required artificial ventilation. She was then transferred to the ICU.