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At least 1,009 records · Page 56Linked to original sources
PubMed1984

[Regression of a massive hydronephrosis in familial central diabetes insipidus treated with Adiuretin].

A ten year old boy with hereditary pituitary diabetes insipidus presented with massive bilateral hydronephrosis, hydroureters and an extremely large bladder. Radiological investigations excluded a mechanical obstruction or vesicoureteral reflux. Treatment with the adiuretin analog DDAVP resulted in regression of the urinary tract changes after 5 months and an almost complete disappearance after 3 1/2 years. The urinary tract dilatation probably results from the large urine flows which exceed the capacity of the urinary tract causing a functional obstruction and residual urine.

Arginine Vasopressin↗
PubMed1982

[Wegener's granulomatosis causing diabetes insipidus].

Very few cases of Wegener's granulomatosis which were associated with diabetes insipidus have hitherto been described. Our patient was a young man with severe (also histological) changes in the nose and paranasal sinuses. Typical pulmonal involvement developed. The hypothalamus seemed not to be affected; hyperprolactinemia, as described by other authors, did not exist. A computerized tomography was normal with regard to the hypothalamus. Typically the disease responded well to cyclophosphamide. An affection of the anterior lobe of the hypophysis was not demonstrable; likewise the kidneys were unaffected.

Adolescent↗
PubMed1976

Effect of intraventricular perfusion of angiotensin II in conscious normal rats and in rats with hereditary hypothalamic diabetes insipidus.

1. Artificial cerebrospinal fluid was perfused through the cerebral ventricles of conscious rats. A basal secretion rate of 16 +/- 3 X 10(-15) mol of immunoreactive angiotensin II/min was calculated for intact rats. 2. Most of the immunoreactive angiotensin II consisted probably of the heptapeptide or pentapeptide angiotensin II fragments. 3. The pressor response to intraventricular perfusions of angiotensin II were normal in Long-Evans rats, virtually absent in rats homozygous for hereditary hypothalamic diabetes insipidus, irrespective of whether they were injected with vasopressin tannate or not, and intermediate in rats heterozygous for hypothalamic diabetes insipidus. 4. The results suggest that the pressor response to intraventricular angiotensin II is related to the release of vasopressin.

Angiotensin II↗
PubMed2006

Fabry disease and nephrogenic diabetes insipidus.

Fabry disease is a lysosomal storage disorder with kidney involvement. The initial manifestation of kidney disease is often impaired urinary concentrating ability in adolescence or young adulthood. We describe a boy diagnosed prenatally with Fabry disease who presented with polyuria, polydipsia, hypertension, hypokalaemia and proteinuria at 7 years of age. A formal water-deprivation test followed by vasopressin challenge confirmed nephrogenic diabetes insipidus. A renal biopsy revealed findings typical of Fabry disease. Angiotensin converting-enzyme therapy resulted in rapid improvement of symptoms, normalization of blood pressure and resolution of hypokalaemia and proteinuria. This child is the youngest reported Fabry disease patient with documented renal pathology and clinical manifestations of hypertension, proteinuria and nephrogenic diabetes insipidus.

Child↗
PubMed1996

Nephrogenic diabetes insipidus induced by lobenzarit disodium treatment in patients with rheumatoid arthritis.

Nephrogenic diabetes insipidus (NDI) occurred in a 43-year-old woman who had received lobenzarit disodium for the treatment of rheumatoid arthritis (RA). Her urine output was initially 3 l/day and urine osmolarity was 203 mOsm/l. Based on a sodium chloride loading test and a vasopressin loading test, she was diagnosed as having lobenzarit-induced NDI. Seven days after the cessation of the use of lobenzarit disodium, polydipsia and polyuria disappeared, and the vasopressin test showed a normal response. These findings suggest that lobenzarit induces a reversible form of NDI as a side effect. The reports of lobenzarit-induced NDI in Japan during the past seven years are also reviewed.

Adult↗
PubMed1997

Idiopathic hypothalamic diabetes insipidus, pituitary stalk thickening, and the occult intracranial germinoma in children and adolescents.

We report nine consecutive children and adolescents [five females and four males; aged 2 yr 8 months (m) to 18 yr 1 m] studied over the last 5 yr with idiopathic central diabetes insipidus. In addition to vasopressin deficiency, anterior pituitary hormone deficiencies were detected, either on evaluation at presentation or during follow-up studies over the following 3 yr. Four patients had an increased concentration of plasma PRL. One patient had multiple pituitary hormone deficiencies at diagnosis, and two others developed the same by 21 m of follow-up. Brain magnestic resonance imaging scans, performed at presentation, were originally interpreted as normal in four of nine patients, except for absence of the bright posterior pituitary signal; after retrospective review, two of nine were considered normal. All of the brain magnetic resonance imaging (MRI) scans showed positive findings by 14 m of follow-up. The first abnormal finding in all patients was isolated pituitary stalk thickening. Evaluation of cerebrospinal fluid (CSF) for hCG was positive in three of eight evaluated patients; the three positive CSF values were found at presentation and 3 and 9 m after presentation. All eight patients assessed were negative for CSF alpha-fetoprotein and cytology, and no patient had serum tumor markers. Transsphenoidal biopsy of the lesion in seven of nine patients showed a germinoma in six patients and inflammatory cells in one. The six patients with documented germinoma comprise 31% of the intracranial germinomas diagnosed in this age group at the University of California-San Francisco during the last 5 yr. The patient with mononuclear inflammatory cells on biopsy along with one other patient have had spontaneous resolution of their stalk thickening. So-called "idiopathic" central diabetes insipidus warrants close follow-up to determine the etiology, especially if anterior pituitary hormone deficiencies are detected. Normal brain MRI scans or scans that show isolated pituitary stalk thickening merit follow-up with serial contrast enhanced brain MRI for the early detection of an evolving occult hypothalamic-stalk lesion. CSF evaluation is recommended at presentation because elevated CSF hCG may precede MRI abnormalities.

Adolescent↗
PubMed1995

[A case of pulmonary eosinophilic granuloma and diabetes insipidus].

A 31-year-old man was admitted to our hospital because of a sudden onset of thirst, polyposia, and polyuria. Five years previously he had been admitted to our hospital because of a dry cough. On the first admission, the chest X-ray film had shown reticular shadows and bullous changes in both upper lung fields. Histological examination of a transbronchial lung biopsy specimen had revealed that the nodular lesion in the interstitium of the alveolar lesion consisted of an aggregate of many Langerhans cells with pale cytoplasm and partly convoluted nuclei. In addition, immunoperoxidase stain for S-100 protein had been strongly positive in numerous Langerhans cells in a bone biopsy specimen from a left mandibullar lesion, which is the same histological appearance as the lung lesion. A diagnosis of pulmonary eosinophilic granuloma had been made. The course after discharge was not progressive without treatment for 5 years, but the patient suddenly began to have thirst, polyposia, and polyuria. Dehydration, vasopressin tests, and the findings of MRI indicated diabetes insipidus due to a pathological change in the pituitary gland. Although diabetes insipidus is known to be a common complication of pulmonary eosinophilic granuloma, only 9 cases have been reported in Japan.

Adult↗
PubMed1991

Glucocorticoid-induced central diabetes insipidus in a case of malignant lymphoma.

A 37-year-old man was diagnosed as malignant lymphoma infiltrating in the central nervous system with hypopituitrism and secondary glucocorticoid deficiency. In this case, plasma arginine vasopressin (AVP) increased, but glucocorticoid administration decreased plasma AVP and increased urine volume with a reduction in urinary osmolality, indicative of the presence of glucocorticoid-induced diabetes insipidus. At the terminal stage, plasma AVP did not increase in response to the withdrawal of glucocorticoid and urine volume remained decreased, suggesting the presence of masked diabetes insipidus. Autopsy showed an infiltration of lymphoid cells around the cerebral ventricles and necrosis in the hypothalamo-hypophyseal system. These findings suggested that glucocorticoid might centrally play an important role in the regulation of AVP release, and its deficiency potentiated AVP release.

Adult↗
PubMed1992

Menière's disease in congenital nephrogenic diabetes insipidus: report of two twins.

Two cases, twins, affected by congenital nephrogenic diabetes insipidus (CNDI) with a high daily volume of dilute urine excretion and periods of compensatory high levels of antidiuretic hormone (ADH) simultaneously developed a fluctuating Menière-type hearing loss. It is well known that the kidney and the cochlea are linked by structural and anatomic characteristics, as well as by the physiologic mechanism of electrolytes and fluid regulation. The patients herein described seem to be paradoxical, because they suffered from hydropic hearing loss despite the pathophysiologic mechanism of CNDI and the possible role played by ADH in water regulation in the inner ear. The consequences on Menière's disease of the different therapeutic regimens followed by the two CNDI patients are discussed. To our knowledge these are the first cases of CNDI with Menière's disease described in the literature.

Audiometry, Pure-Tone↗
PubMed1991

Platelet vasopressin receptors in patients with congenital nephrogenic diabetes insipidus.

Arginine-vasopressin (AVP), interacts with at least two types of receptors: V1 receptors which mediate the aggregating effects of AVP on human blood platelets and other AVP actions on vascular smooth muscle and hepatocytes; and V2 receptors which mediate the antidiuretic effects on renal tubules. Congenital nephrogenic diabetes insipidus (CNDI) is a rare X-linked disorder in humans with abnormal renal and extrarenal V2-receptor responses. However, the V1 receptor responses are apparently normal, since in these patients blood pressure increases in response to AVP. To assess V1 receptor responses, binding studies (3H-AVP) were done on intact platelets obtained from 6 male patients with CNDI, 10 normal subjects and 4 patients with autosomal dominant central diabetes insipidus (ADCDI). The affinity constant (0.68 +/- 0.04 vs. 0.59 +/- 0.06 nM) and the number of specific binding sites per platelet (101 +/- 6 vs. 86 +/- 12) were similar in the normal subjects and the patients with CNDI. However, the number of binding sites per platelet was increased in the patients with ADCDI (189 +/- 12). Platelet aggregation induced by AVP was equivalent in the three groups. Platelet-fraction AVP was elevated in patients with CNDI and undetectable in patients with ADCDI. These results suggest that the structure and the function of V1 platelet receptor-effector pathway are normal in patients with CNDI.

Adolescent↗
PubMed2005

Etiologies of central diabetes insipidus in Thai children.

In order to determine the etiologies of central diabetes insipidus (DI) among Thai children, we retrospectively reviewed records of 67 patients (44 male and 23 female) between the age of 0.1 and 15.6 years (mean age 5.5 years) who were diagnosed with central DI at the Pediatric Endocrinology Unit, Siriraj Hospital, Bangkok, Thailand between 1996 and 2003. Etiologies were found to be central nervous system (CNS) malformations in 20 patients (29.8%), post resection of intracranial tumors and cysts in 17 patients (25.4%), intracranial tumors in 11 patients (16.4%), cerebral palsy of unknown cause in five patients (7.5%), infection in four patients (6%), and Langerhans cell histiocytosis in three patients (4.5%). In another seven patients (10.4%), the cause was considered to be idiopathic. This study revealed that CNS malformation was the most common etiology, followed by intracranial tumors and their treatment. A thorough investigation to rule out CNS lesions needs to be done before considering the diagnosis of idiopathic central DI.

Adolescent↗
PubMed1985

Peroral treatment of diabetes insipidus with a polypeptide hormone analog, desmopressin.

In the present study nine diabetes insipidus patients were treated with desmopressin (DDAVP) tablets. All patients had a significant reduction of their polyuria after a peroral dose of 50 micrograms DDAVP. During a 6-day trial, a peroral treatment with two or three daily peroral doses of DDAVP controlled their polyuria. A dose-response study in five of the patients indicated that peroral DDAVP doses as small as 10 micrograms have effects on renal concentrating ability. A log-linear relationship was found between DDAVP doses and maximal urine osmolalities and duration of antidiuresis. Measurements of plasma DDAVP concentrations after peroral DDAVP revealed a linear relationship between amounts of DDAVP absorbed and dose, but with great interindividual differences. The results indicate that graded renal response occur at plasma concentrations of DDAVP between 1 and 5 pg/ml. The results of this study and the assessment by the patients of the treatment indicate that peroral therapy with DDAVP may be an attractive alternative to traditional intranasal administration of the drug.

Administration, Oral↗
PubMed1995

Clinical phenotype of nephrogenic diabetes insipidus in females heterozygous for a vasopressin type 2 receptor mutation.

Nephrogenic diabetes insipidus (NDI) usually shows an X-linked recessive mode of inheritance caused by mutations in the vasopressin type 2 receptor gene (AVPR2). In the present study, three NDI families are described in which females show clinical features resembling the phenotype in males. Maximal urine osmolality in three female patients did not exceed 200 mosmol/kg and the absence of extra-renal responses to 1-desamino-8-D-arginine vasopressin was demonstrated in two of them. All affected females and two asymptomatic female family members were shown to be heterozygous for an AVPR2 mutation. Skewed X-inactivation is the most likely explanation for the clinical manifestation of NDI in female carriers of an AVPR2 mutation. It is concluded that, in female NDI patients, the possibility of heterozygosity for an AVPR2 gene mutation has to be considered in addition to homozygosity for mutations in the aquaporin 2 gene.

Adolescent↗
PubMed2001

Effects of diabetes insipidus mutations on neurophysin folding and function.

Mechanisms underlying the pathogenicity of diabetes insipidus mutations were probed by studying their effects on the properties of bovine oxytocin-related neurophysin. The mutations G17V, DeltaE47, G57S, G57R, and C67STOP were each shown to have structural consequences that would diminish the conformational stability and folding efficiency of the precursors in which they were incorporated, and factors contributing to the origins of these property changes were identified. Effects of the mutations on dimerization of the folded proteins were similarly analyzed. The projected relative impact of the above mutations on precursor folding properties qualitatively parallels the reported relative severity of their effects on the biological handling of the human vasopressin precursor, but quantitative differences between thermodynamic effects and biological impact are noted and explored. The sole mutation for which no clear thermodynamic basis was found for its pathogenicity was 87STOP, suggesting that the region of the precursor deleted by this mutation plays a role in targeting independent from effects on folding, or participates in stabilizing interactions unique to the human vasopressin precursor.

Amino Acid Sequence↗