1 Department of Nephrology and Hypertension, Rabin Medical Center, Petah Tikua 49372, 2 Department of Urology, Hillel Yaffe Hospital, Hadera, Israel and 3 Affilitated with the Rappaport Faculty of Medicine, the Technion, Haifa, Israel
Correspondence and offprint requests to: Asher Korzets, Department of Nephrology and Hypertension, Rabin Medical Center, Petah Tikua 49372, Israel. Email: aradmt{at}012.net.il
Keywords: central diabetes insipidus; hydronephrosis; polyuria
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Case report |
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Relevant past history included compulsive water drinking from the age of 18. On examination the patient weighed 62 kg and he was normotensive. Urinalysis was normal. After insertion of a urethral catheter it was noted that the patient voided 78 l of urine daily (even after i.v. fluid replacement was stopped). Despite this post-obstructive diuresis renal function did not improve. Repeated urine osmolarity throughout this period was
100 mosm/kg/day.
A water deprivation test was carried out (Table 1) and a diagnosis of central diabetes insipidus (CDI) was made. Further investigations at this stage included negative antithyroid, antiparietal and antinuclear antibodies. MRI of the brain, before and after gadolinium injection, was normal with no thickening of the pituitary gland or the infundibulum.
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Presently (December 2003) the patient is asymptomatic apart for mild nocturia, he remains normotensive and on daily oral desmopressin (0.15 mg). Daily diuresis is 3 l/day and renal function is stable (serum creatinine 1.5 mg/dl).
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Discussion |
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Prolonged polyuria as a cause of bilateral, non-obstructive hydronephrosis was first described by Osler in 1892 [2]. Since then, excessive urine flows and extensive dilatation of the urinary tract have been most frequently documented in young children with nephrogenic diabetes insipidus, often hereditary and X-linked [310] but also in patients with CDI [6,7,11] and psychogenic polydipsia [7,8,12,13]. Apparently, persistently large urine volumes can lead to urinary bladder distension and hypertrophy, with subsequent intramural obstruction of the distal ureters [6,7,10,11]. In time, bladder contractility is compromised, ureteric peristalsis diminishes and large residual urine volumes worsen this functional obstructive uropathy [7,8,13]. Also, because of social embarrassment, these patients often self-cause urine retention and this only acts to exaceberate the obstructive uropathy even further [3,6].
Although many patients have undergone surgical procedures in an aim to alleviate this functional obstruction [4,9,14], treatment should be essentially medical. It should be based on correct and early diagnosis of the cause behind the polyuria, teaching of the patient as to the importance of frequent voiding [7,14], the possible use of non-steroidal anti-inflammatory drugs and thiazides in nephrogenic diabetes insipidus [6,15] and the importance of desmopressin in CDI [2,6,7,15]. Drugs capable of interfering with water homeostasis should be avoided, as should anticholinergic drugs with their undesired ability to impair bladder contractility [13].
Correct therapy, even after a short period of time, can lead to a marked improvement in renal tract dilatation. This will occur more often in those children diagnosed early on and who have had urinary tract dialatation for only relatively short periods of time. However, urinary tract dilatation, presumably of many years duration, can also be improved [47,10,14].
Although chronic renal failure is infrequent in these patients [4,68,10,14], it can occuras was so graphically demonstrated in four schizophrenic patients with psychogenic polydipsia who were concurrently using anticholinergic drugs [13].
The patient presented is relatively unique because of a number of points. First, he presented at a late age after routine blood tests revealed mild chronic renal failure. If this patient had remained undiagnosed and untreated, renal failure would, most probably, have progressed unabated. Secondly, he has CDI, with only three other patients with CDI presenting with hydronephrosis and hydroureters [6,7,11]. All patients were relatively young (presenting ages 1221 years) and all had many years of polyuria. Measured residual urine volume was large in two of the three patients in which it was measured [6,11]. In all three patients desmopressin therapy reduced urine volume and led to marked radiological improvement in hydronephrosis. In the one patient with renal failure, this also improved after only 1 month of therapy (reduction in serum creatinine from 1.3 to 0.9 mg/dl).
The management of diabetes insipidus in adults was well reviewed by Singer et al. in 1997 [15]. In patients with CDI, treatment must be individualized. Desmopressin should be initially given to the patient just prior to bedtime, in order to ensure a reduction in nocturnal diuresis. Furthermore, it is important to permit brief, intermittent polyuric episodes. Ideally, this should be accompanied by designing a desmopressin schedule such that polyuria recurs predictably before one of the scheduled daily doses, preferably so as not to disrupt sleep [10].
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Teaching points |
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Acknowledgments |
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Conflict of interest statement. None declared.
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References |
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