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At least 631 records · Page 35Linked to original sources
PubMed1978

[Comparison of the diuretic and natriuretic effects of dopamine in control and diabetes insipidus dogs. Effect of propranolol].

The diuretic effect of dopamine is unchanged in the dog with diabetes insipidus but the natriuretic effect of dopamine is shorter. With the normal dog propanolol delays the dopamine-induced diuresis and natriuresis but the magnitude of this double effect is unchanged. In the dog with diabetes insipidus, propanolol suppresses the dopaminergic diuresis and reduces the natriuresis.

Animals↗
PubMed1997

Hyperuricemia as a clue for central diabetes insipidus (lack of V1 effect) in the differential diagnosis of polydipsia.

PURPOSE: In the differential diagnosis of patients with polyuria-polydipsia one must distinguish usually between primary polydipsia (PP) and central diabetes insipidus (CDI). The first situation is a state of volume expansion and the second of volume contraction. We evaluate whether serum uric acid determination could help to differentiate between the two conditions. PATIENTS AND METHODS: We analyzed the score of 13 consecutive patients with CDI, 7 patients with PP, and 7 patients with nephrogenic diabetes insipidus (NDI). Serum uric acid concentration was available during normonatremia without treatment with 1-desamino-8-D-arginine vasopressin (dDAVP), during mild dehydration and during treatment with dDAVP. In 8 of these patients plasma renin activity (PRA), urate, urea and creatinine clearances were also available. These data were also obtained in the patients with NDI. In 1 patient with CDI, we studied the effect on urate clearance of dDAVP, which stimulates exclusively the V2 receptors, and of triglycyl-lysine-vasopressin (TGLV), a potent V1-receptor agonist. RESULTS: Normonatremic polydypsic patients with CDI presented an increase in uric acid concentration (7.1 +/- 2.2 mg/dL), whereas in the PP group the value was decreased (3 +/- 0.75 mg/dL; P <0.001). All the normonatremic PP presented a serum uric acid concentration lower than 5 mg/dL, whereas all the normonatremic CDI patients, exept 1, presented a value higher than 5 mg/dL. In both groups blood urea concentration was decreased as a consequence of high renal clearances. The hyperuricemia of CDI was related to low uric acid clearances. Patients with hypernatremia and NDI presented a lower increase in serum uric acid concentration than those with similar levels of hypernatremia and CDI (NDI: 5.7 +/- 0.8 mg/dL and CDI: 7.9 +/- 2.3 mg/dL; P <0.05) and the NDI patients presented an urate clearance corrected for creatinine clearance which was significantly higher than in CDI (9% +/- 3% and 4% +/- 1.1%; P <0.01). When the patients with CDI were treated with dDAVP and normalyzed their PRA (0.9 +/- 0.4 ng/mL/h) we observed still mild hyperuricemia compared to controls (5.5 +/- 1.4 mg/dL and 4.3 +/- 0.9 mg/dL; P <0.01) and a low fractional excretion of filtered uric acid (6.5% +/- 1.7% compared to 8.2% +/- 2% in controls; P <0.05). Acute administration of dDAVP, stimulating the V2 receptors, in one patient with CDI, had no effect on urate clerance, while TGLV, which stimulates the V1 receptor, increased urate clearance. CONCLUSION: The presence of an serum uric acid concentration higher than 5 mg/dL in polyuric polydipsic patients is highly suggestive of CDI. Even when these patients are treated with dDAVP many of them remain hyperuricemic, and this seems to be the consequence of a lack of V1 receptor stimulation.

Adult↗
PubMed1999

[Ventriculostomy of the third ventricle and diabetes insipidus].

We report the case of a 2-year-old child who sustained a permanent diabetes insipidus following a third ventriculostomy for hydrocephalus from a Dandy-Walker syndrome. Ventriculostomy, used for therapy of non-communicating hydrocephalus, can cause complications such as diabetes insipidus. The latter has rarely been reported and is usually transient. Following ventriculostomy, a close postoperative surveillance is essential, especially in children.

Child, Preschool↗
PubMed2004

Lymphocytic hypophysitis with diabetes insipidus: improvement by methylprednisolone pulse therapy.

Lymphocytic hypophysitis is a rare inflammatory disorder in the pituitary gland. The lesion is usually confined to the adenohypophysis. Although the involvement of the posterior pituitary gland or the stalk is rare, such patients with diabetes insipidus have been reported. Surgery has been used to make the definitive diagnosis. Recent studies suggest, however, that the pathologic diagnosis may not be necessary always. We reported a case of Lymphocytic hypophysitis managed by methylprednisolone pulse therapy. A 50-year-old premenopausal woman with Lymphocytic hypophysitis and diabetes insipidus was treated with methylprednisolone pulse therapy. Her adenopituitary lesion disappeared and the diabetes insipidus resolved. The optimal management for patients with lymphocytic hypophysitis may be the high index of the suspicion prior to the extensive surgical resection. In addition, methylprednisolone pulse therapy may improve the clinical and MRI findings.

Anti-Inflammatory Agents↗
PubMed1979

Obstructive uropathy and nephrogenic diabetes insipidus in infants.

The syndrome of acute post-obstructive nephrogenic diabetes insipidus is a rare phenomenon. The lesion is acquired during the pre-diuretic phase, owing to antidiuretic hormone resistance of the distal tubule as well as a severe concentrating defect. The diuretic phase after relief of obstruction can result in a massive, sustained and life-threatening diuresis. Sodium restriction and thiazide diuretics produce a mild volume contracted state, enhancing sodium and water reabsorption, primarily in the proximal tubule and possibly in the distal tubule owing to aldosterone. The recognition and differentiation of this unique pyloric syndrome from other more common post-obstructive diuretic states are important for all urologists who are responsible for the care of children.

Chlorothiazide↗
PubMed1999

Plasma leptin levels in male patients with idiopathic central diabetes insipidus.

Leptin is known to regulate food intake and energy expenditure. Moreover, recent studies in rodents have shown that leptin in high doses decreases urine osmolality and increases water intake, together with renal sodium and water excretion. Since it is not clear whether leptin is involved in either the pathogenesis or in resulting metabolic abnormalities in diabetes insipidus, we measured leptin levels in 16 male patients with idiopathic central diabetes insipidus (DI) in comparison to a group of age- and BMI-matched male control subjects (no.=30). We found that plasma leptin concentration did not differ between patients with DI (4.45+/-3.24 microg/l) and healthy control group (3.69+/-2.81 microg/l; t test, p=0.41). Urine osmolality, plasma osmolality and urine volume of the patients with DI was not correlated to leptin. However, leptin was positively associated with body mass index (r=0.67; p=0.005). We conclude that leptin plasma concentrations are unchanged in diabetes insipidus. Furthermore, the lack of correlation between plasma leptin and urine osmolality, plasma osmolality or urine volume suggests that ADH deficiency does not have any impact on the plasma leptin levels.

Adult↗
PubMed1986

Nephrogenic diabetes insipidus presenting with infantile hypotonia. A report of 2 cases.

Nephrogenic diabetes insipidus usually presents with polyuria, polydipsia, fever, vomiting, dehydration and failure to thrive. However, in infancy polyuria may be absent because of dehydration and reduced glomerular filtration rate. In 2 cases the main presenting feature was hypotonia, with marked head lag. Family studies confirmed the X-linked mode of inheritance of the disease; in case 1 the disease appeared to have arisen as a new mutation in the mother, and in case 2 the carrier status was traced back to the great-grandmother. Pitfalls in the diagnosis and detection of the carriers are discussed. Treatment with thiazide diuretics and prostaglandin synthesis inhibitors is effective in reducing urine volumes and polydipsia. The early detection of the disease and adequate management may prevent such complications as megacystis, mega-ureter and hydronephrosis, with resulting renal failure. Mental and physical retardation may also be avoided.

Anorexia↗
PubMed1987

Vasopressin-resistant diabetes insipidus, liver dysfunction, hyperuricemia and decreased renal function. A case report.

A case of transient nephrogenic diabetes insipidus occurred in late pregnancy, the first associated with biopsy-proven hepatitis. Five previously reported cases occurred in pregnancy. All six patients demonstrated similar but transient signs, symptoms and laboratory abnormalities suggesting a syndrome peculiar to pregnancy. The characteristics of this syndrome are elevated liver function studies, decreased renal function, hyperuricemia and transient vasopressin-resistant diabetes insipidus.

Adult↗
PubMed1979

Vasopressin-resistant nephrogenic diabetes insipidus. A result of amphotericin B therapy.

Polyuria and polydipsia developed in two cases during amphotericin B therapy for deep mycoses. Neither patient could concentrate his urine in response to water deprivation or exogenous vasopressin. Other causes of vasopressin-resistant nephrogenic diabetes insipidus were not present. Three months after amphotericin B therapy had been discontinued, concentrating ability improved toward normal. A third patient was further observed and demonstrated normal diluting capacity but impaired free-water reabsorption, suggesting a distal tubular defect consistent with nephrogenic diabetes insipidus. Four months after discontinuing therapy, renal concentrating ability was normal. Amphotericin B can induce a reversible form of nephrogenic diabetes insipidus.

Amphotericin B↗
PubMed1996

Parasellar chronic inflammatory disease presenting Tolosa-Hunt syndrome, hypopituitarism and diabetes insipidus: a case report.

We describe a 60-year-old man with a history of Tolosa-Hunt syndrome associated with intermittent painful ophthalmoplegia and a visual disturbance on the left side, who presented with signs and symptoms of severe hypoadrenalism and diabetes insipidus. Magnetic resonance imaging demonstrated enlargement of the hypophysis and infundibulum and left cavernous sinus. An endocrinologic study revealed anterior pituitary dysfunction and diabetes insipidus. The patient underwent a transsphenoidal biopsy which revealed chronic inflammation in the hypophysis, mucosa of the sphenoid sinus, and dura mater. The patient was treated with steroids that decreased the size of the hypophysis and infundibulum, but the symptoms of anterior pituitary insufficiency and diabetes insipidus have persisted. The chronic inflammation of the hypophysis and infundibulum is thought to have spread from the cavernous sinus.

Anti-Inflammatory Agents↗
PubMed2001

Hyponatremia and polyuria in children with central diabetes insipidus: challenges in diagnosis and management.

Five patients with well-controlled, long-standing, central diabetes insipidus had acute development of dehydration, hyponatremia, and inappropriate natriuresis in the setting of polyuria resistant to exogenous antidiuretic hormone. Hyponatremia and dehydration worsened with fluid restriction or use of exogenous antidiuretic hormone. We discuss the challenges in diagnosis and management of probable salt wasting in children with central diabetes insipidus.

Adolescent↗
PubMed2005

A case of transient diabetes insipidus following cardiopulmonary bypass.

Cardiopulmonary bypass surgery has been linked with a number of postoperative complications. One of the frequently reported physiological alterations is the relative diuresis seen in the immediate post-op period. Rarely reported though is the development of full-blown diabetes insipidus in such patients. The etiology is unknown and has only been hypothesized in the past. We present the clinical course of a 54 year old male who developed transient diabetes insipidus post bypass surgery with subsequent recovery following exogenous vasopressin administration. The physiological alteration leading to the development of diabetes insipidus in a small fraction of bypass patients remains unknown. We propose that the variation in natriuretic peptide levels in the post-bypass period could account for the transient event.

Cardiopulmonary Bypass↗
PubMed1990

Transient diabetes insipidus in pregnancy complicated by hypertension and seizures.

A case is presented of a primigravida with transient diabetes insipidus, gestational hypertension, and multiple seizures resistant to magnesium sulfate and diazepam. After addition of phenytoin, no further seizures occurred. Transient diabetes insipidus in pregnancy has been previously associated with hypertension, liver dysfunction, and fetal distress. Considered with previous cases, it is suggested that seizures may frequently be part of this syndrome.

Adult↗
PubMedDate not supplied

[Diabetes insipidus in sarcoidosis of the lungs].

The paper is concerned with the little-investigated problem of diabetes insipidus in lung sarcoidosis patients with calcium metabolic derangement. An analysis of the literature and the author's data made it possible to reveal some clinical features, to assume new pathogenetic mechanisms of diabetes insipidus occurrence and to document effective therapy.

Adult↗
PubMed1964

DIABETES INSIPIDUS.

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Diabetes Insipidus↗