PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “DIABETES INSIPIDUS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed2004

Clinical characteristics of eight patients with congenital nephrogenic diabetes insipidus.

Congenital nephrogenic diabetes insipidus (NDI) is characterized by the insensitivity of the distal nephron to arginine vasopressin. Clinical knowledge of this disease is based largely on case reports. For this study, we investigated the clinical findings of eight patients in terms of age at onset, age at diagnosis, main complaint, results of physical examination, the diagnosis, the effect of treatment, kidney function, and presence or absence of gene defects. The main complaints of all eight cases at initial examination were unknown fever, failure to thrive, and short stature. Polyuria and polydipsia are not always the chief complaints with congenital NDI. In one case, diabetes insipidus could be diagnosed based only on the results of a 5% hypertonic saline test. In six cases, we found abnormalities in the V2 receptor gene. Initially, trichlormethiazide therapy was shown to have a significant effect on polyuria; however, this effect decreased over time. In one patient with partial NDI, the addition of trichlormethiazide twice a day to 1-desamino-8-D-arginine vasopressin increased urine osmolality in the morning and caused nocturia to disappear. Results of 99mTc-diethylenetriamine pentaacetic acid kidney scintigraphy revealed a slight decrease in glomerular filtration rate in three patients. No patient experienced serious renal dysfunction.

Adolescent↗
PubMed2006

Transient postpartum diabetes insipidus associated with HELLP syndrome.

Diabetes insipidus in pregnancy has different causes. The association of diabetes insipidus with disturbances of liver function has been reported, however, diabetes insipidus has rarely been reported in HELLP syndrome. We present a 23-year-old primigravida with a singleton gestation complicated by HELLP syndrome who developed postpartum diabetes insipidus. Labor was induced promptly to terminate pregnancy because of intrauterine fetal death and liver dysfunction. 1-deamino-8-D-arginine-vasopressin was administered. Diabetes insipidus and liver dysfunction resolved within 2 weeks. Development of diabetes insipidus may result from increased vasopressinase activity mainly caused by deterioration of liver functions caused by HELLP syndrome. In pregnant women with liver disease as a result of any cause, the development of diabetes insipidus should be assessed with particular attention.

Adult↗
PubMed1983

Effects of desglycinamide-arginine-vasopressin (DG-AVP) on memory processes in diabetes insipidus patients and non-diabetic subjects.

The effects of desglycinamide9-arginine8-vasopressin (DG-AVP) on memory processes have been studied in patients with central diabetes insipidus (DI) and in non-diabetic control patients. Acute im injection of DG-AVP improved some aspects of short-term memory. Subchronic intranasal administration of DG-AVP facilitated short-term memory more consistently and in addition improved long-term memory. DG-AVP increased the attention, but only in the non-diabetic subjects. The effects of DG-AVP on memory processes persisted after discontinuation of treatment. DG-AVP did not affect the parameters for water and electrolyte metabolism, blood pressure and pulse rate neither in DI nor in the control patients. Thus, the memory effects of DG-AVP are probably mediated by a direct action on the central nervous system.

Adolescent↗
PubMed2001

A missense mutation encoding cys(67) --> gly in neurophysin ii is associated with early onset autosomal dominant neurohypophyseal diabetes insipidus.

Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is an inherited disorder in which progressive degeneration of magnocellular neurons of the hypothalamus impairs production of arginine vasopressin (AVP). ADNDI is caused by mutations in the arginine vasopressin-neurophysin II (AVP-NPII) gene. These mutations are hypothesized to trigger neurodegeneration via disruption of preproAVP-NPII processing. Affected individuals usually develop diabetes insipidus between 1 and 6 years of age. Here we report a novel mutation of the AVP-NPII gene in a family with unusually early presentation of ADNDI. The index case developed symptoms of diabetes insipidus at 1 month of age, her mother at 9 months of age, and the maternal grandfather in early childhood. Each was found to be heterozygous for the missense mutation 1665T > G encoding the amino acid substitution C67G within NPII. This mutation helps to define two homologous regions of the AVP-NPII precursor bounded by disulfide bridges between C13 and C27 and between C61 and C73 that have structural homology and contain the majority of amino acid substitutions associated with ADNDI. The early onset of symptomatic diabetes insipidus in this family suggests that the C67G substitution may be particularly deleterious to magnocellular neurons and may provide a valuable model for study of dominantly inherited neurodegeneration.

Amino Acids↗
PubMed1978

Traumatic bitemporal hemianopsia and diabetes insipidus.

Bitemporal hemianopsia and diabetes insipidus are infrequently occurring complications of closed head injuries. Porter and Miller found 18 cases of posttraumatic diabetes insipidus among more than 5000 patients with nonfatal closed head injuries. Of these, five also manifested damage to the optic chiasm. In 1971 Laursen surveyed the literature regarding traumatic bitemporal hemianopsia and found associated diabetes insipidus in 26 of 50 patients for whom information on this was given. Both conditions were present in a patient seen at Walter Reed Army Medical Center.

Adult↗
PubMed1977

Diabetes insipidus following cardiorespiratory arrest.

Diabetes insipidus following cardiac arrest and hypoxemic encephalopathy occurred in two patients. In both, severe hypoxemic brain damage was followed within three days by clinical and laboratory features of diabetes insipidus, which were corrected by administration of exogenous vasopressin. Hypothalamic injury resulting in diabetes insipidus should be considered in the differential diagnosis of polyuria and dehydration occurring in critically ill patients who have suffered cardiorespiratory arrest.

Adult↗
PubMedDate not supplied

Vasopressin receptor mutations causing nephrogenic diabetes insipidus.

In congenital nephrogenic diabetes insipidus, the renal collecting ducts are resistant to the antidiuretic action of arginine vasopressin or to its antidiuretic analog 1-deamino[8-D-arginine] vasopressin (dDAVP). This is a rare, but now well described entity secondary to either mutations in the AVPR2 gene that codes for the vasopressin antidiuretic (V2) receptor or to mutations in the AQP2 gene that codes for the vasopressin-dependent water channel. A majority (> 90%) of congenital nephrogenic diabetes insipidus patients have AVPR2 mutations: Of 115 families with congenital nephrogenic diabetes insipidus, 105 families had AVPR2 mutations, and 10 had AQP2 mutations. When studied in vitro, most AVPR2 mutations lead to receptors that are trapped intracellularly and are unable to reach the plasma membrane. A minority of the mutant receptors reach the cell surface but are unable to bind vasopressin or to trigger an intracellular adenosine 3:5-cyclic phosphate signal properly. Most of the reported mutations are secondary to a complete loss of function of the receptor, and only a few mutations have been associated with a mild phenotype. These advances provide diagnostic tools for physicians caring for these patients because, when the disease causing mutation has been identified, carrier and perinatal testing could be done by mutation analysis.

Amino Acid Sequence↗
PubMedDate not supplied

Lithium-induced nephrogenic diabetes insipidus.

BACKGROUND: Lithium can cause nephrogenic diabetes insipidus in up to 20 to 40 percent of patients currently taking the medication, and a subset of these patients will have a persistent concentrating defect long after lithium is discontinued. They are at risk for serious hypernatremia when fluid intake is restricted for any reason. METHODS: MEDLINE as used to search the key words "nephrogenic diabetes insipidus" and "lithium" from 1990 to the present. A case report describes a patient who had been off lithium for 8 years and who developed hypernatremia after she was transferred to a new long-term facility and the staff attempted to control the patient's polydipsia. The diagnosis and treatment of nephrogenic diabetes insipidus are also discussed. RESULTS: This case of persistent nephrogenic diabetes insipidus 8 years after discontinuing lithium is the longest ever reported. Certainly, a number of patients have varying degrees of persistent lithium-related nephrogenic diabetes insipidus. Although pathologic changes are associated with persistent nephrogenic diabetes insipidus, the exact mechanism of the persistent defect is unknown. The mechanism of acute lithium-induced nephrogenic diabetes insipidus while the patient is on lithium is related to changes in intracellular cyclic adenosine monophosphate. CONCLUSIONS: Patients currently taking lithium and patients with a remote history of lithium treatment need to be monitored for signs and symptoms of nephrogenic diabetes insipidus. Physicians need to be aware of the potential for nephrogenic diabetes insipidus in these patients and care for them appropriately.

Chlorthalidone↗
PubMed2004

Three cases of diabetes insipidus complicating pregnancy.

Diabetes insipidus (DI) is a rare complication of pregnancy. In cases related to pregnancy, the condition is thought to result from enhanced placental clearance of arginine vasopressin secondary to placental vasopressinase production. In such cases careful monitoring of the patient's fluid balance during and after pregnancy is essential. If treatment is necessary, desmopressin is the drug of choice. In the present article, we present three cases of pregnancy complicated by DI.

Adult↗
PubMed1982

Effects of lysine-vasopressin and 1-deamino-8-D-arginine-vasopressin on memory in healthy individuals and diabetes insipidus patients.

Central diabetes insipidus (DI) patients showed impairments in short- and long-term memory functions, but not in attention and concentration, as compared to healthy individuals. A single i.m. injection or sub-chronic intranasal administration of either lysine-vasopressin (LVP) or 1-deamino-8-D-arginine-vasopressin (DDAVP) normalized the disturbed memory functions in DI patients. These peptides also improved memory functions in healthy individuals.

Administration, Intranasal↗
PubMed1998

Ovulation induction with pulsatile GnRH in a patient with anovulation of hypothalamic origin and central diabetes insipidus.

Patients with diabetes insipidus (DI) are at high risk for dehydration, hypernatremia and hemodynamic instability. Ovarian hyperstimulation syndrome (OHSS) likewise has negative effects on electrolyte balance. If ovulation induction is required in a patient with DI, there is thus a strong argument for avoiding techniques that increase the risk of OHSS. This paper reports the results of ovulation induction in a patient with anovulation of hypothalamic origin and central (vasopressin deficit) DI. Ovulation was induced with pulsatile gonadotropin-releasing hormone (GnRH), which induces single-ovule cycles and which does not increase the risk of OHSS. The patient successfully achieved pregnancy after seven ovulatory cycles.

Adult↗
PubMed1998

[Vasopressin type 2 receptor mutations in congenital diabetes insipidus].

Congenital nephrogenic diabetes insipidus is a rare inherited disorder, which is characterized by the inability of the kidney to concentrate urine due to unresponsiveness to antiduretic hormone arginine vasopressin. Defects must be present somewhere in a vasopressin signal transduction pathway in kidney collecting duct. Recent genetic analysis demonstrated that mutations in vasopressin type 2 receptor and water channel aquaporin 2 are responsible for x-linked and autosomal recessive form, respectively. Expression studies of mutant proteins showed that most of the mutations cause severe functional defects, which are compatible with clinical phenotypes. These advances help understanding of molecular mechanism underlying this disease and therefore improve diagnostic and therapeutic approaches.

Animals↗
PubMedDate not supplied

Perioperative anesthetic management for Cesarean section of a parturient with gestational diabetes insipidus.

PURPOSE: Gestational diabetes insipidus (GDI) is a rare endocrinopathy complicating about 4:100,000 deliveries. We present the case of a preterm parturient with GDI and severe hypernatremia (serum sodium concentration = 174 mmol.L(-1)) presenting for an urgent Cesarean section. CLINICAL FEATURES: Fluid resuscitation and desmopressin supplementation partially corrected the patient's homeostasis, allowing us to carefully titrate epidural anesthesia for an urgent Cesarean section. After delivery, the patient was transferred to the intensive care unit. The serum sodium concentration of the mother and the neonate was normalized over 48 hr and three days respectively. CONCLUSION: The careful perioperative management of GDI led to a favourable outcome of the mother and fetus.

Adult↗
PubMed1995

[Hereditary nephrogenic diabetes insipidus].

Congenital nephrogenic diabetes insipidus (NDI) is a rare inherited disorder characterized by the inability of the kidney to concentrate urine in response to vasopressin (AVP). Following the recent characterization of the cDNA and genomics sequences encoding the human V2 receptor to AVP (AVPR2), X-linked NDI has been found to be due to mutations in the AVPR2 gene that maps to the chromosome Xq28 region. To date more than 30 mutations, insertions or deletions have been reported in independent families, without any significant differences in the phenotypic expression of the disease. The AVPR2 is a member of the superfamily of 7 transmembrane domain, G protein-coupled receptor, linked to cyclic AMP second messenger system. Other types of inheritance have been described in NDI, and recently, a mutation of the aquaporin-2 gene, encoding a water channel of the renal collecting duct, has been reported in an autosomal recessive form of NDI.

Diabetes Insipidus, Nephrogenic↗
PubMed1987

Diabetes insipidus in pregnancy.

Diabetes insipidus (DI) and pregnancy may coexist and, when they do, present challenging diagnostic and therapeutic problems. Women with preexisting central DI usually experience increased thirst and require additional hormone replacement. Women with nephrogenic DI have an increased water turnover. Of interest is a group of women with transient DI of gestation. In some of these patients, central DI is brought to the fore by increases in water turnover during pregnancy as well as increments in the metabolic clearance of arginine vasopressin (AVP), especially near term. Others have a "vasopressin-resistant" form of the disease, which in one case followed by us appeared to be due to marked increments in circulating cystine-aminopeptidase (vasopressinase). This patient's DI was resistant to pitressin, but she concentrated her urine when given dDAVP. Her vasopressinase levels 2 weeks postpartum were still several-fold those of normal term gravidas. Her DI remitted, and she concentrated her urine appropriately 2 months postpartum. This article reviews the different forms of DI peculiar to pregnancy.

Arginine Vasopressin↗
PubMed1994

Inheritance of mutations in the V2 receptor gene in thirteen families with nephrogenic diabetes insipidus.

Congenital nephrogenic diabetes insipidus (NDI) is an X-linked recessive disease characterized by insensitivity of the distal nephron to the antidiuretic effect of arginine vasopressin. The hypothesis that the defect underlying NDI might be a dysfunctional renal vasopressin V2 receptor has recently been proven by the identification of mutations in the V2 receptor gene in NDI patients. We examined thirteen unrelated Dutch NDI families and identified thirteen distinct and unique mutations. These included nine missense mutations, two nonsense mutations and two small deletions and were found in the extracellular domains II, III and IV, the intracellular domains II and IV and in the transmembrane loops I, II, IV and V of the vasopressin type 2 receptor. In the families with multiple NDI patients the mutated gene cosegregated with the disease. Our data suggest a higher mutation frequency in male than in female gametes. No discrepancies between carrier detection by means of DNA analysis with closely linked polymorphic markers and the definite diagnosis based on sequencing data were found.

Alleles↗
PubMed1998

Identification of a novel nonsense mutation and a missense substitution in the vasopressin-neurophysin II gene in two Spanish kindreds with familial neurohypophyseal diabetes insipidus.

Familial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant disease caused by deficiency in the antidiuretic hormone arginine vasopressin (AVP) encoded by the AVP-neurophysin II (AVP-NPII) gene on chromosome 20p13. In this study, we analyzed two families with FNDI using direct automated fluorescent, solid phase, single-stranded DNA sequencing of PCR-amplified AVP-NPII DNA. In one of the families, affected individuals presented a novel nonsense mutation in exon 3 of the gene, consisting in a G to T transition at nucleotide 2101, which produces a stop signal in codon 82 (Glu) of NPII. The premature termination eliminates part of the C-terminal domain of NPII, including a cysteine residue in position 85, which could be involved in the correct folding of the prohormone. In the second family, a G279A substitution at position -1 of the signal peptide was observed in all affected individuals. This missense mutation, which replaces Ala with Thr, is frequent among FNDI patients and is thought to reduce the efficiency of cleavage by signal peptidases.

Adolescent↗