Hereditary Nephrogenic Diabetes Insipidus and Bilateral Nonobstructive Hydronephrosis
| Title: | Hereditary Nephrogenic Diabetes Insipidus and Bilateral Nonobstructive Hydronephrosis |
|---|---|
| Authors: | Uribarri, Jaime; Kaskas, Marwan |
| Publisher: | Nephron |
| Date Published: | 1993 |
| Reference Number: | 144 |
We describe 2 cases of hereditary nephrogenic diabetes insipidus with massive bilateral dilatation of the urinary tract without any organic obstruction. A review of the literature revealed that dilatation of the urinary tract was present in 67% of the reported cases of nephrogenic diabetes insipidus which included a description of the urinary tract. This strong association between hereditary nephrogenic diabetes insipidus and nonobstructive hydronephrosis suggests a cause-and-effect relationship in which polyuria is responsible for the hydronephrosis.
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)
Upon reviewing the literature on NDI, the authors found there was significant dilation of the urinary tract recorded in 67% of NDI cases that included descriptions of the urinary tract.
In many instances, enlarged kidneys and bladders result from some sort of anatomical obstruction that impedes the flow of urine, e.g., an enlarged prostate or enlargement of the bladder neck. In these instances the excessive need to urinate is caused by the expansion of the kidney. The authors' study shows the kidney and bladder distention in the NDI cases they reviewed was not the result of anatomical obstruction. This suggests that NDI may cause the enlargement of the urinary tract due to the high urinary output NDI generates.
The authors reason that the rate of urinary flow is greater than the capacity of the kidneys and bladder, and this results in a functional obstruction when the kidneys and the bladder stretch because they can not empty all the urine they receive. As further support for their theory that excessive urination (polyuria) causes dilation of the urinary tract, the authors cite that enlarged urinary tracts have also been described in patients with pituitary diabetes insipidus and primary polydipsia, both of which induce excessive urination. The authors further reason that the urinary tracts of people with hereditary NDI, which manifests very early in life, have been subject to excessive urination over a long period of time beginning when the urinary tract may be more susceptible to expansion.
They note that in one of the cases they presented, the patient's urinary tract partially contracted from its expanded form when his urine out-put was reduced. The phenomena have been previously recorded in the literature and support their interpretation that excessive urination causes the expansion of the urinary tract.