Disease relevance of Diabetes Insipidus, Neurogenic

• Molecular basis of autosomal dominant neurohypophyseal diabetes insipidus. Cellular toxicity caused by the accumulation of mutant vasopressin precursors within the endoplasmic reticulum [1].
• Patients: Twenty-nine healthy controls and 113 patients with polyuria (15 with primary polydipsia; 86 with neurogenic diabetes insipidus [60 studied before, 28 during, and 10 after antidiuretic hormone treatment]; and 12 with nephrogenic diabetes insipidus) [2].
• Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI) [3].
• Additionally, the administration of a potent V1-receptor agonist (triglycyl-lysine-vasopressin) in a patient with central diabetes insipidus with preexisting dDAVP-induced hyponatremia produced a rapid increase of urate clearance [4].
• Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is a familial form of diabetes insipidus due to progressive vasopressin deficiency with onset typically at 1-6 yr of age [5].

Psychiatry related information on Diabetes Insipidus, Neurogenic

• 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 [6].
• Nine children aged 7 2/12 to 17 9/12 years with central diabetes insipidus were subjected to water deprivation and water loading during treatment with 1-deamino-8-D-arginine vasopressin (DDVAP) [7].
• Individual differences in the antidiuretic response induced by single doses of 1-deamino-8-D-arginine-vasopressin (DDAVP) in patients with pituitary diabetes insipidus [8].

High impact information on Diabetes Insipidus, Neurogenic

• In the normal subjects and the patients with central diabetes insipidus, dDAVP decreased mean arterial pressure (by 10 to 15 percent) and increased pulse rate (by 20 to 25 percent), renin activity (by 65 percent), and the release of coagulation factors (twofold to threefold) (all changes were significant, P less than 0.01) [9].
• All seven cases of severe neurogenic diabetes insipidus diagnosed by the indirect tests were confirmed by the vasopressin assay [10].
• DDAVP in the treatment of central diabetes insipidus [11].
• Familial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant disorder caused by mutations in the arginine vasopressin (AVP) precursor [12].
• Mutations in the arginine vasopressin (AVP) gene cause autosomal dominant familial neurohypophyseal diabetes insipidus (FNDI) [1].

Chemical compound and disease context of Diabetes Insipidus, Neurogenic

• Familial neurohypophyseal diabetes insipidus (FNDI) in humans is an autosomal dominant disorder caused by a variety of mutations in the arginine vasopressin (AVP) precursor [13].
• We used dDAVP, the 1-desamino-8-D arginine analogue of arginine vasopressin with high antidiuretic and low vasopressor potency, to treat 29 patients with neurogenic diabetes insipidus for up to 22 months [14].
• Efficacy of indapamide in central diabetes insipidus [15].
• Increases in plasma ACTH and cortisol after hypertonic saline infusion in patients with central diabetes insipidus [16].
• In conclusion, this study demonstrated that a 6-month treatment with alendronate in patients with central diabetes insipidus was effective in significantly improving BMD at the lumbar spine, which was significantly worsened in untreated patients [17].

Biological context of Diabetes Insipidus, Neurogenic

• Mutant vasopressin precursors that cause autosomal dominant neurohypophyseal diabetes insipidus retain dimerization and impair the secretion of wild-type proteins [18].
• Autosomal dominant neurohypophyseal diabetes insipidus with linkage to chromosome 20p13 but without mutations in the AVP-NPII gene [19].
• Effect of a short-term treatment with alendronate on bone density and bone markers in patients with central diabetes insipidus [17].
• We examined the nucleotide sequence of the arginine vasopressin-neurophysin II gene in three kindreds with autosomal dominant neurohypophyseal diabetes insipidus [20].
• Central diabetes insipidus and autoimmunity: relationship between the occurrence of antibodies to arginine vasopressin-secreting cells and clinical, immunological, and radiological features in a large cohort of patients with central diabetes insipidus of known and unknown etiology [21].

Anatomical context of Diabetes Insipidus, Neurogenic

• Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is an inherited disease caused by progressive degeneration of the magnocellular neurons of the hypothalamus leading to decreased ability to produce the hormone arginine vasopressin (AVP) [22].
• Association of arginine vasopressin-secreting cell, steroid-secreting cell, adrenal and islet cell antibodies in a patient presenting with central diabetes insipidus, empty sella, subclinical adrenocortical failure and impaired glucose tolerance [23].

Gene context of Diabetes Insipidus, Neurogenic

• Urinary excretion of AQP-2 was significantly increased by the single injection of AVP in patients with central diabetes insipidus [24].
• The urinary excretion of AQP-2 was one-eighth over in patients with central diabetes insipidus and three times greater in patients with impaired water excretion than that in normal subjects [24].
• A corticotropin-releasing hormone (CRH) test was performed on 7 patients with central diabetes insipidus (DI) and on 7 healthy subjects [25].
• Altered expression of COX-1, COX-2, and mPGES in rats with nephrogenic and central diabetes insipidus [26].
• This first report of familial CH with central diabetes insipidus may represent a previously unknown midline anomaly and provide new insights into the genetic control of pituitary and hypothalamic development [27].

Analytical, diagnostic and therapeutic context of Diabetes Insipidus, Neurogenic

• We examined plasma arginine-vasopressin concentrations by radioimmunoassay in two brothers, aged 6 and 7.5 years, with familial central diabetes insipidus inherited as an autosomal dominant trait [28].
• In this study, we analyzed plasma lipid and lipoprotein levels before and after treatment with 1-desamino-8-D-arginine vasopressin (DDAVP) in subjects with partial and complete central diabetes insipidus (DI) in order to determine how a shortage and supplement of this hormone affect plasma lipid metabolism [29].

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