Transient Nephrogenic Diabetes Insipidus Accompanied by Possible Psychogenic Polydipsia

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Title: Transient Nephrogenic Diabetes Insipidus Accompanied by Possible Psychogenic Polydipsia
Authors: Sone, MD PhD, Hirohito; Kawai, Koichi; Nishi, Masaaki; Shimakura, Shuya; Bannai, Chieko; Kawakami, Yasushi; Odawara, Masato; Matsushima, Teruhiko; Okuda, Yukichi; Yamashita, Kamejiro
Publisher: Hormone Research
Date Published: January 01, 1995
Reference Number: 80
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A 50-year-old Japanese man had been suffering from polydipsia and polyuria for 2 months without any other specific symptoms. His daily urinary output reached 5 liters. On admission, no abnormalities of the kidneys, heart,thyroid, adrenals, pituitary or hypothalamus were detected by laboratory tests and MRI of the head. Purepsychogenic polydipsia was ruled out because his urine volume did not decrease sufficiently with 18 h of waterdeprivation and the subsequent injection of aqueous vasopressin. Plasma arginine vasopressin (AVP) levels against plasma osmolality remained within the normal range during the test. These results indicated that diabetes insipidus in this case was caused by renal insensitivity to AVP. The symptoms disappeared spontaneously, and marked improvement was observed in a second water deprivation test 1 month later, although the maximum urine concentration was still subnormal. The combination of both latent insufficiency of AVP secretion and impairment of the renal countercurrent system induced by psychogenic polydipsia was speculated as a possible mechanism for the transient nephrogenic diabetes insipidus in this case.

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)

Case Report
A fifty-year-old man experienced dry mouth and upper abdominal pains similar to heart burn on 11/10/92. A few days later he was extremely thirsty and urinated a lot (once every 2 hours, even during the night). These symptoms deteriorated after 11/25; he urinated every thirty to sixty minutes and felt tired. A check of his family history revealed nothing exceptional including neither head traumas nor recent drug use (prescribed by a doctor or otherwise). He was admitted to the hospital.

During his three-week stay, we administered various tests and treated his symptoms with drugs. Two drugs, cimetidine--a gastric antacid--and teprenone, relieved his upper abdominal discomfort. His urine excretion rate gradually decreased to 1.5 litres per day without any other specific therapies, such as water deprivation or administration of vasopressin or desmopressin. He was temporarily discharged because his urine rate became almost normal and the urine osmolality (density and concentration of various things) increased significantly, both indicating that his kidneys were working better.

A month after his discharge (in February), we readmitted him to study the development of his transient polyuria (non-genetic excessiveurination). Further tests showed that his condition continued to improve. Those symptoms have not returned.

Discussion
Based on the results of the first water deprivation test, his polyuria could be diagnosed as NDI. His psychogenic polydipsia (excessive thirst) seemed to be induced by his upper abdominal discomfort.

A question that arises in this case is why did this patient develop acquired NDI? Many patients with psychogenic polydipsia do not develop acquired NDI. In times of severe dehydration, the body secretes arginine vasopressin (AVP) in order to retain as much water as possible. The water deprivation tests revealed that this man's body could not do this. His inability to secrete AVP may have contributed to his acquired NDI.

Even though this man's polydipsia can be corrected, we still do not know why he cannot concentrate urine as necessary (i.e., why his kidneys won't retain all the water they need).