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)

Kato et al., report on a 32-year-old man admitted to their hospital complaining of chronic, excessive urination and thirst. A year earlier he had surgery to remove tumors from his small intestine. Now examination revealed that both of the patient's ureters (the tubes which carry urine from the kidney to the bladder) were obstructed because of more tumors in his small intestine. Examination revealed the patient also had nephrogenic diabetes insipidus (NDI).

NDI can be acquired many ways. NDI observed in the presence of ureteral obstruction is rare. The patient was treated with trichlorothiazide and this decreased his urine output. Later he received diclofenac sodium along with trichlorothiazide and this further reduced his urine output. In addition, the physicians inserted a catheter through the patients skin and into the bottom of his kidney to relieve his obstruction, a process that continued for six months. A month after this surgical procedure, the patient was taken off the drugs and his urine output continued to gradually decrease.

Studies show that ureteral obstruction can cause prostaglandin E2 (PGE2) to increase in the kidney. PGE2 inhibits the antidiuretic action of the antidiuretic hormone, arginine vasopressin (AVP). However, the authors did not measure the patient's PGE2 so they could not confirm this as the cause of the patient's NDI. However, they did show that surgical treatment for ureteral obstruction is effective in reducing urine output in NDI patients with ureteral obstruction.