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PubMed2001

Molecular and cellular defects in nephrogenic diabetes insipidus.

The identification of the different molecular causes of congenital nephrogenic diabetes insipidus (NDI), a disorder characterized by renal insensitivity to the antidiuretic effect of arginine vasopressin, has been of indispensable importance for understanding the cellular processes involved in diuresis and antidiuresis. In most cases, NDI is X-linked and caused by mutations in the vasopressin type-2 receptor (V2R) gene. Mutations in the aquaporin-2 (AQP2) water channel gene are responsible for the autosomal recessive and rare dominant forms of NDI. By in vitro expression, it has been shown that the majority of V2R mutants and all AQP2 mutants found in recessive NDI are misfolded and retained within the endoplasmic reticulum (ER). Functional analysis of one of the mutations identified in dominant NDI showed that this mutant is properly folded and transported out of the ER, but is retained in the Golgi region. In addition, this mutant, in contrast to mutants found in recessive NDI, is able to heterotetramerize with wild-type AQP2. The resulting complex is hindered in its transport to the membrane, a finding that explains the dominant-negative effect of this mutation. Several new methodologies focused on the molecular defects causing NDI are presently being investigated in vitro and might eventually develop into useful therapeutic strategies.

Diabetes Insipidus, Nephrogenic↗
PubMed2003

A murine model of autosomal dominant neurohypophyseal diabetes insipidus reveals progressive loss of vasopressin-producing neurons.

Familial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant disorder caused by mutations in the arginine vasopressin (AVP) precursor. The pathogenesis of FNDI is proposed to involve mutant protein-induced loss of AVP-producing neurons. We established murine knock-in models of two different naturally occurring human mutations that cause FNDI. A mutation in the AVP signal sequence [A(-1)T] is associated with a relatively mild phenotype or delayed presentation in humans. This mutation caused no apparent phenotype in mice. In contrast, heterozygous mice expressing a mutation that truncates the AVP precursor (C67X) exhibited polyuria and polydipsia by 2 months of age and these features of DI progressively worsened with age. Studies of the paraventricular and supraoptic nuclei revealed induction of the chaperone protein BiP and progressive loss of AVP-producing neurons relative to oxytocin-producing neurons. In addition, Avp gene products were not detected in the neuronal projections, suggesting retention of WT and mutant AVP precursors within the cell bodies. In summary, this murine model of FNDI recapitulates many features of the human disorder and demonstrates that expression of the mutant AVP precursor leads to progressive neuronal cell loss.

Animals↗
PubMed1995

Posterior pituitary hematoma in a case of posttraumatic diabetes insipidus. Case report.

A 28-year-old man presented with diabetes insipidus (DI) 10 days after basilar skull fracture without brain injury. Magnetic resonance (MR) imaging revealed a hematoma in the posterior lobe of the pituitary gland but no lesions in the hypothalamus or pituitary stalk. The patient's DI continued for 2 months at which time transsphenoidal surgery was performed to decompress the cystic hematoma with persistent mass effect. The DI attenuated shortly after the surgery and the patient became completely free from DI 5 months later. Although hemorrhage into the posterior lobe is one of the frequent pathological changes in fatal head-injury victims and secondary DI in these cases has usually been thought to be acute and transient, the true incidence and natural course of the posterior pituitary hemorrhage and subsequent DI in nonfatal head-injury patients are totally unknown. In this article, the authors present the first demonstration on MR imaging of a posterior pituitary hematoma in a patient with head injury. The authors propose that serial MR imaging is an important diagnostic tool in patients with posttraumatic DI because some of them may harbor pituitary hematoma and because decompression surgery may prevent transition to permanent DI, especially in cases when the mass effect is persistent due to a cystic change in the hematoma.

Acute Disease↗
PubMed2002

Etiologies of central diabetes insipidus in children : 15 years experience in Songklanagarind hospital, Thailand.

Central diabetes insipidus (DI) is a rare disease in children. The authors retrospectively reviewed the records of children with central DI identified at Songklanagarind Hospital from 1985 to 2000. Of the total 29 patients identified, 16 patients were males and 13 were females. All patients received computed tomography or magnetic resonance imaging of the brain to differentiate the etiologies of central DI. The median age at diagnosis was 6.6 years (range 1.5-14.9). The etiologies of central DI were intracranial tumors in 7 patients (24.1%), histiocytosis in 3 patients (10.3%), septooptic dysplasia in 1 patient (3.5%), empty-sella syndrome in 1 patient (3.5%), pituitary abscess in 1 patient (3.5%), and idiopathic in 16 patients (55.1%). All patients with idiopathic central DI were followed-up for a median duration of 4.5 years (range 1.3-15.5). Three of 16 patients (18.8%) were found to have intracranial tumors at 1.3, 2.3, and 3.5 years of follow-up. It was also observed that the patients whose age at presentation was less than 5 years (histiocytosis was excluded) were less likely to have intracranial tumors than those older than 5 years, (0% vs 55%), with significant statistical difference (p<0.01). It is concluded that: 1) the common etiologies of central DI are intracranial tumor and idiopathic, 2) patients initially diagnosed with idiopathic central DI need to have long-term follow-up by magnetic resonance imaging to identify any occult intracerebral tumor.

Adolescent↗
PubMed1978

Treatment of central diabetes insipidus in adults and children with desmopressin.

Modification of the natural vasopressin molecule to form desmopressin acetate (DDAVP) resulted in a compound with prolonged antidiuretic activity and virtual elimination of vasopressor activity. Twenty-one patients with central diabetes insipidus who ranged in age from 3 to 68 years were treated with DDAVP, which was administered intranasally in a dosage ranging from 10 microgram every 12 hours to 20 microgram every eight hours. Effective control of symptoms was obtained in all cases. There were no consequential toxic effects. As previously reported, DDAVP appears to be the preferred drug for the management of central diabetes insipidus. Biochemical alteration of hormones may enhance desired therapeutic activity and eliminate toxic effects. The development of DDAVP is an example of the potential for development of useful therapeutic peptides.

Adolescent↗
PubMed2006

Diabetes insipidus.

Water balance is precisely regulated by vasopressin, thirst and the kidneys; plasma osmolality is maintained within a narrow range, despite large variations in normal water intake and loss. Disruption of these finely balanced mechanisms is common, however, and can be precipitated by various disease states. Diabetes insipidus is a disease process with several underlying pathogenic mechanisms--all ultimately resulting in excretion of large volumes of dilute urine. This review will discuss the pathophysiology, diagnosis and treatment of diabetes insipidus, with emphasis on disorders of osmoregulation following neurosurgery of the pituitary and hypothalamus.

Animals↗
PubMed1993

Reduction of exogenous vasopressin RNA poly(A) tail length increases its effectiveness in transiently correcting diabetes insipidus in the Brattleboro rat.

Magnocellular hypothalamic neurons in Brattleboro rats can accumulate, transport, and translate exogenous [Arg8]vasopressin (AVP) mRNA after injection in the hypothalamo-hypophysial tract in amounts sufficient to reverse transiently the animals' characteristic diabetes insipidus. In the present study, different preparations of hypothalamic RNA extracted from normal rats or synthetic AVP RNA were injected into the lateral hypothalamus of Brattleboro rats. Poly(A)- RNA and poly(A)+ RNA from which tails were removed by RNase H digestion were much more effective than poly(A)+ RNA in expressing AVP in the magnocellular hypothalamic neurons and in raising urine osmolarity. Synthetic AVP RNA lacking a poly(A) tail also produced a very potent dose-dependent diabetes insipidus reversal. Our results suggest that a short or absent poly(A) tail may facilitate the accumulation, transport, or expression of exogenous AVP mRNA by magnocellular neurons.

Animals↗
PubMed1998

Hyperosmolar nonketotic coma precipitated by lithium-induced nephrogenic diabetes insipidus.

A 45-year-old man, with a 10-year history of manic depression treated with lithium, was admitted with hyperosmolar, nonketotic coma. He gave a five-year history of polyuria and polydipsia, during which time urinalysis had been negative for glucose. After recovery from hyperglycaemia, he remained polyuric despite normal blood glucose concentrations; water deprivation testing indicated nephrogenic diabetes insipidus, likely to be lithium-induced. We hypothesize that when this man developed type 2 diabetes, chronic polyuria due to nephrogenic diabetes insipidus was sufficient to precipitate hyperosmolar dehydration.

Antimanic Agents↗
PubMed1988

[Familial nephrogenic diabetes insipidus with chronic hypernatremia and cerebral calcifications].

The authors report on the unusual evolution of two brothers suffering from nephrogenic diabetes insipidus after a 25-year follow-up. The polyuro-polydipsic syndrome was clinically well tolerated, without acute complications even during infancy. However, despite the lack of water restriction and the presence of thirst sensation, the children remained chronically hypernatremic. An intellectual deficiency was present, with a dysmorphic syndrome unrelated to a biochemically determined central nervous system disorder, or an X fragility. Calcifications of basal ganglia and frontal lobes were discovered on a cerebral computed tomography performed at 16 and 18 years. This syndrome may represent a specific entity.

Adult↗
PubMedDate not supplied

Behavioral and medical treatment of chronic polydipsia in a patient with schizophrenia and diabetes insipidus.

OBJECTIVE: This case report describes a novel outpatient behavioral treatment intervention for chronic polydipsia. The program was used in an effort to reduce excessive fluid intake in a woman with chronic paranoid-type schizophrenia who also had a diagnosis of diabetes insipidus. METHODS: The 12-session individual behavioral intervention incorporated self-monitoring, stimulus control, coping skills training, and reinforcement components. RESULTS: The patient engaged fully in the treatment program, and she successfully restricted her fluid intake. Her diabetes insipidus could therefore be treated with desmopressin, a medication that requires fluid restriction, and she experienced a concomitant reduction in polyuria and urinary incontinence. CONCLUSIONS: The outpatient behavioral intervention demonstrated promising outcomes in a chronically mentally ill patient whose polydipsia had underlying psychogenic and physiological components. This case highlights the efficacy of combining behavioral and medical interventions.

Ambulatory Care↗
PubMed1979

The effects of elevated circulating prolactin in rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain).

Administration of ovine or rat PRL to animals, including man, has resulted in decreased urine volume and increased urine osmolality. Contamination of PRL preparations with vasopressin is the most likely explanation for the apparent antidiuretic effect. In this study, diabetes insipidus rats lacking vasopressin(homozygous Brattleboro rats) had extra anterior pituitary glands implanted under the kidney capsule, resulting in hyperprolactinemia. The urine of such rats was not more concentrated than that of unoperated littermates or sham-operated littermates with diabetes insipidus. In fact, hyperprolactinemic male rats produced even less concentrated urine than control rats. Furthermore, the hyperprolactinemic rats responded to exogenous vasopressin in a manner similar to normoprolactinemic rats. These studies provide strong evidence against an antidiuretic action of PRL in mammals.

Animals↗