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PubMedDate not supplied

[Polyuric dilatation of the urinary tract in congenital nephrogenic diabetes insipidus. Clinical and diagnostic aspects. Presentation of a case and review of the literature].

Massive polyuria existing in congenital nephrogenic diabetes insipidus can cause a more or less severe dilatation of the urinary tract in absence of obstruction. Clinical and diagnostic aspects of this pathology are presented relating then with other types of diabetes insipidus. One case of bilateral severe dilatation with evolution towards renal atrophia is presented. Mechanical obstruction was discarded. The disease was refractory to urinary concentration tests and therapy to reduce urine volume. The possible etiopathological mechanisms of functional obstruction and surgical alternatives directed to preserve the kidney function are explained and discussed. The current literature is reviewed but the cases reported are few due to the low incidence of urological affectation. Presence of kidney atrophia is exceptional.

Adult↗
PubMed1975

Treatment of diabetes insipidus with carbamazepine.

Oral carbamazepine has been shown to have antidiuretic activity in seven out of nine patients with neurohypophyseal diabetes insipidus. At the doses used side-effects were not a major problem. In the eighth patient a carbamazepine and clofibrate combination was effective but in the ninth carbamazepine was without effect. It is suggested that carbamazepine should be used initially in neurohypophyseal diabetes insipidus if oral therapy is indicated, but the mode of its antidiuretic action is as yet unclear.

Adolescent↗
PubMed1978

Cyclic adenosine monophosphate excretion in urine of patients and carriers of congenital nephrogenic diabetes insipidus.

Urinary excretion of cyclic adenosine monophosphate (cAMP) is assessed in response to pitressin stimulation in three patients with nephrogenic diabetes insipidus, four carriers and seven controls. There is no significant difference in cAMP excretion between these groups when corrected for surface area, nor is there any significant increase in excretion after pitressin stimulation. There is very close correlation between urinary cAMP and both urinary concentration and urinary creatinine excretion. Urinary cAMP after pitressin stimulation does not discriminate between carriers of nephrogenic diabetes insipidus and control subjects.

Adult↗
PubMed1995

Urinary excretion of aquaporin-2 in patients with diabetes insipidus.

BACKGROUND: Urine-concentrating ability is regulated by vasopressin. Recently, the specific water-channel protein of the renal collecting duct, known as aquaporin-2, was cloned. However, it is not certain whether this molecule is responsive to vasopressin. METHODS: We measured the urinary excretion of aquaporin-2 and its response to vasopressin in 11 normal subjects and 9 patients with central or nephrogenic diabetes insipidus. The urine samples were collected during periods of dehydration and hydration and after the administration of vasopressin. Urine samples were analyzed for aquaporin-2 by the Western blot assay and immunogold labeling, and the amount of aquaporin-2 was determined by radioimmunoassay. RESULTS: Aquaporin-2 was detectable in the urine in both soluble and membrane-bound forms. In the five normal subjects tested, the mean (+/- SE) urinary excretion of aquaporin-2 was 11.2 +/- 2.2 pmol per milligram of creatinine after a period of dehydration, and it decreased to 3.9 +/- 1.9 pmol per milligram of creatinine (P = 0.03) during the second hour after a period of hydration. In the six other normal subjects, an infusion of desmopressin (1-desamino-8-D-arginine vasopressin) increased the urinary excretion of aquaporin-2 from 0.8 +/- 0.3 to 11.2 +/- 1.6 pmol per milligram of creatinine (P < 0.001). The five patients with central diabetes insipidus also had increases in urinary excretion of aquaporin-2 in response to the administration of vasopressin, but the four patients with X-linked or non-X-linked nephrogenic diabetes insipidus did not. CONCLUSIONS: Aquaporin-2 is detectable in the urine, and changes in the urinary excretion of this protein can be used as an index of the action of vasopressin on the kidney.

Adult↗
PubMed1978

Nephrogenic diabetes insipidus and Werdnig-Hoffmann disease in a child: an unusual association.

The unusual association of Werdnig-Hoffmann disease and nephrogenic diabetes insipidus in a 5-month-old child is described for the first time. The association is casual, considering the different pathways of genetical transmission in these two diseases. The possibility of identifying the heterozygote is discussed and it appears to be limited to nephrogenic diabetes insipidus.

Diabetes Insipidus↗
PubMed1987

Transient diabetes insipidus and preeclampsia.

A woman with triplet gestation had polydipsia and polyuria during pregnancy. She subsequently had preeclampsia for which she was delivered. The presumed diabetes insipidus was transient, resolving by postpartum day 5. The association of preeclampsia and diabetes insipidus may be confusing to the practitioner. Careful attention to fluid status and consideration of this abnormality will lead to the best outcome when hypertension is accompanied by polydipsia and polyuria.

Adult↗
PubMedDate not supplied

Metastatic adenocarcinoma presenting with central diabetes insipidus.

The case of a previously healthy 63-year-old female with metastatic adenocarcinoma to the hypothalamus presenting with central diabetes insipidus is presented. The patient was found to have metastatic disease isolated to her hypothalamus on brain magnetic resonance imaging as well as a water deprivation test consistent with central diabetes insipidus. The patient had a decrease in symptoms of polyuria and polydypsia as well as a decrease in urine volumes after treatment with intranasal vasopressin. Even though a rare occurrence, physicians should consider metastatic adenocarcinoma in patients with recent-onset polyuria and polydypsia.

Adenocarcinoma↗
PubMed1986

Management of cranial diabetes insipidus with oral desmopressin (DDAVP).

The effect of oral administration of desmopressin (DDAVP) solution was investigated in six patients with cranial diabetes insipidus of varying aetiology. All patients experienced a prompt and prolonged antidiuresis. Nine patients have been managed with oral DDAVP tablets for up to 5 months and all preferred this route of administration to intranasal application using a rhinyle. Oral DDAVP gives excellent and convenient control in cranial diabetes insipidus.

Administration, Oral↗
PubMed1989

Clinical experience with desmopressin: efficacy and safety in central diabetes insipidus and other conditions.

Because of its selective antidiuretic activity, desmopressin is recognized as the drug of choice for central diabetes insipidus. Compared with previously available treatments, it has a greatly enhanced therapeutic profile, allowing more specific antidiuresis without adverse reactions. Its selective antidiuretic activity is used with advantage in the treatment of nocturnal enuresis and as a diagnostic test of tubular function. Desmopressin is available for intranasal and parenteral administration; antidiuretic doses range from 10 to 40 micrograms intranasally and from 2 to 4 micrograms intravenously or subcutaneously. For its hemostatic effect, a single infusion of desmopressin at a dose of 0.3 microgram/kg has been used in most studies. Well-documented evidence shows that desmopressin is safe and efficacious as a selective antidiuretic agent for the treatment of central diabetes insipidus and nocturnal enuresis and as a diagnostic test of tubular function. Even at the 15-fold higher doses used in bleeding disorders, desmopressin appears to be well tolerated.

Adult↗
PubMed2001

Role of sodium depletion in acute antidiuretic effect of bendroflumethiazide in rats with nephrogenic diabetes insipidus.

The mechanisms underlying the acute antidiuretic response to bendroflumethiazide (BFTZ; 0.25 mg/h for 3 h) in rats with nephrogenic diabetes insipidus (NDI) was investigated. NDI was induced in conscious chronically instrumented female Wistar rats either by chronic lithium administration (40-60 mmol Li/kg of diet for 4 weeks) or by acute infusion of V2 antagonist OPC-31260 (0.2 mg/h). Renal clearance experiments were performed in conscious rats instrumented with permanent catheters. During experiments total body water content was held constant by i.v. replacement of urine production (V) with 150 mM glucose. One group in addition received i.v. replacement of urinary sodium losses. In both models of NDI, BFTZ-induced antidiuresis was associated with a decrease in the delivery of tubular fluid to the distal nephron, as measured by lithium clearance (C(Li)). Both the antidiuresis and the decrease in C(Li) could be prevented by sodium replacement. BFTZ did not affect distal water handling as measured by V/C(Li). BFTZ did not induce antidiuresis in normal rats with water diuresis. It is concluded that in rats with NDI, thiazide-induced antidiuresis can be entirely explained by a fall in distal delivery of tubular fluid related to sodium depletion. This contrasts the response in rats with central diabetes insipidus, where thiazides in addition increase distal water reabsorption.

Animals↗