Nephrogenic Diabetes Insipidus Presenting After Head Trauma
| Title: | Nephrogenic Diabetes Insipidus Presenting After Head Trauma |
|---|---|
| Authors: | Trivedi, Hariprasad S.; Nolph, MD, Karl D. |
| Publisher: | American Journal of Nephrology |
| Date Published: | 1994 |
| Reference Number: | 114 |
Water diuresis after head trauma is most often due to central diabetes insipidus (DI). We report a patient with a history of a bipolar disorder and past lithium use who was noted to have polyuria and hypernatremia after head trauma. Inappropriate high sodium and volume replacement resulted in an increase in the polyuria. A lack of response to antidiuretic hormone/antidiuretic-hormone-like preparations led to the diagnosis of nephrogenic DI. The case illustrates the importance of calculating electrolyte-free osmolar clearance in the correction of hypernatremia. Persistence of the DI and mild renal impairment probably due to past lithium use are discussed.
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)
After seeing a hospital kidney specialist, the patient's saline solution was reduced in both the amount of fluid and concentration of sodium, and he was given aqueous arginine vasopressin (AVP) in order to reduce his urine rate and sodium count. However, the patient showed no response to the AVP, so it was concluded that the patient did not have CDI. It was discovered that the patient had been taking lithium to treat a psychological problem for over ten years. Acquired nephrogenic diabetes (NDI) can result from lithium use. The fact that the patient did not respond to the antidiuretic hormone, AVP indicated the possibility of NDI, for in NDI the antidiuretic hormone supply is sufficient, but the patient's vasopressin-2 receptor genes, which are supposed to take the instructions of the hormone, are faulty. Careful monitoring of the patient's urine chemistry and flow and blood chemistry indicated that the patient did indeed have acquired NDI.
The authors noted that though the patient had been off lithium for years, his acquired NDI persisted. Studies show that the persistence is not unusual. Studies have also shown that lithium can cause chronic kidney damage.
The author's patient also showed impairment of his glomerular filtration rate, though studies disagree as to whether or not lithium does result in this sort of impairment.
The authors close by remarking how the normal, generous intravenous administration of sodium and water produced the excessive urination and high blood sodium which led to the diagnosis of NDI. This points to the importance of checking to see whether the normal rehydration procedures are appropriate for all patients.