Lithium-Induced Diabetes Insipidus in a Surgical Patient: Report of a Case and Review of the Literature
| Title: | Lithium-Induced Diabetes Insipidus in a Surgical Patient: Report of a Case and Review of the Literature |
|---|---|
| Authors: | Gray, DMD, Edward J.; Dierks, MD, Eric J. |
| Publisher: | Journal of Oral and Maxillofacial Surgery |
| Date Published: | July 01, 1996 |
| Reference Number: | 19 |
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)
People with any form of diabetes insipidus (DI) can't concentrate urine because either they don't secrete enough of the antidiuretic hormone, vasopressin (VP), or their kidneys don't respond to the VP that is secreted. In lithium-induced NDI, the kidneys do not respond to VP; therefore the kidneys don't reabsorb water or concentrate urine. This results in the common DI symptoms of chronic, excessive thirst and urination. More specifically, VP activates the enzyme adenylyl cyclase, located in the cells of the kidney collecting ducts. This catalyzes a metabolic process that produces cyclic adenosine monophosphate (cAMP), an important metabolic regulator that allows specific kidney cell membranes to become more water permeable. This in turn results in the reabsorption of free water and concentration of urine. Lithium is thought to interrupt this sequence by impairing adenylyl cyclase.
Gray and Dierks report of a 53-year-old white man referred to them because of a large lesion inside his cheek. The patient was currently taking a variety of medicines, including lithium, for a mental disorder. The patient underwent surgery for the tumorous growths inside his cheeks, and while in intensive care after surgery, he began drinking large volumes of water and had to urinate frequently. On questioning, the patient revealed a 30-year history of chronic, excessive thirst and urination. He was diagnosed with lithium-induced NDI.
The proposed treatments for lithium-induced NDI include reducing or discontinuing lithium use, and administering amiloride or thiazide diuretics to help reduce NDI's symptoms. Other possible lithium substitutes currently being researched are the nonsteroidal anti-inflammatory drugs indomethacin, desmopressin, lysine vasopressin, and carbamazepine. Amiloride seems to be the drug of choice for lithium-induced NDI. It alleviates the need for frequent urination without the need for potassium supplementation. It also increases urine concentration. Amiloride works by preventing lithium from entering the cells of the kidney walls. The authors close by warning that combining lithium with a diuretic may predispose a patient to lithium toxicity.