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At least 685 records · Page 38Linked to original sources
PubMed1998

Pregnant woman with transient diabetes insipidus resistant to 1-desamino-8-D-arginine vasopressin.

We encountered a pregnant woman with transient diabetes insipidus which developed during the third trimester. A hypertonic saline infusion study did not concentrate the osmolality of urine. Her laboratory data showed hypokalemia, hyperreninemia, an increased concentration of plasma aldosterone and an increased urinary excretion rate of prostaglandin E2, which resembled hyperprostaglandin E-syndrome. T1-weighted magnetic resonance imaging of the posterior pituitary gland revealed decreased intensity. Polyuria reached 4-6 L daily, and urine osmolality remained dilute despite a lapse of four days since treatment with intranasal 1-desamino-8-D-arginine vasopressin (dDAVP: 10-25 microg every 12 h). The patient was conservatively managed without medical treatment, then delivered in the 38th week of pregnancy without complication. The osmolality of the patient's urine was higher than that of the plasma when tested 3 days postpartum. The abnormality of magnetic resonance imaging of the posterior pituitary gland disappeared at 6 months after delivery. We consider that subclinical nephrogenic diabetes insipidus in our patient was exacerbated during pregnancy.

Adult↗
PubMed1985

Water intoxication associated with nephrogenic diabetes insipidus secondary to lithium: case report.

In the psychiatric population, psychogenic polydipsia leading to water intoxication and nephrogenic diabetes insipidus secondary to lithium therapy are both well-recognized entities. A case is reported of the apparently unusual combination of these two conditions, where lithium probably not only has caused the nephrogenic diabetes insipidus, but might also have contributed to the state of psychogenic polydipsia.

Diabetes Insipidus↗
PubMed1978

Pharmacokinetics of 1-desamino-8-D-arginine vasopressin (DDAVP) in patients with central diabetes insipidus.

The pharmacokinetic parameters and biological duration of action of DDAVP were measured in five patients with central diabetes insipidus of differing severity. Plasma half-life correlated significantly with the duration of action (r = 0.89, P less than 0.05), 0ut there was no correlation between the severity of diabetes insipidus and either plasma half-life or duration of action of DDAVP.

Adult↗
PubMed1996

Partial central diabetes insipidus complicating nonketotic hyperglycemic hyperosmolar coma.

Nonketotic hyperglycemic hyperosmolar coma is an uncommon, but significant, complication of type II diabetes mellitus with a high overall mortality rate. Treatment of this entity is controversial but mandates aggressive fluid resuscitation and strict control of serum glucose levels. In the patient described, nonketotic hyperglycemic hyperosmolar coma complicated by diabetes insipidus was successfully treated with desmopressin acetate. To the authors' knowledge, this is the first reported case of nonketotic hyperglycemic hyperosmolar coma associated with partial central diabetes insipidus.

Aged↗
PubMed2007

A case of nephrogenic diabetes insipidus with a novel missense mutation in the AVPR2 gene.

We describe a pediatric case of nephrogenic diabetes insipidus (NDI) with a novel missense mutation in the arginine vasopressin receptor 2 (AVPR2) gene. The patient, a 3-year-old boy, had polyuria (4357 ml/day, 7230 ml/m(2)/day) and polydipsia. Water deprivation testing demonstrated no decrease of urine volume, and urinary volume did not respond to subcutaneous injection of 0.1 U/kg pitressin. Molecular genetic analysis demonstrated that the patient had an AVPR2 missense mutation involving substitution of phenylalanine for tyrosine at position 205 (Y205F). It was also found that the patient's mother was heterozygous for this Y205F mutation. Analysis of the intermolecular interaction of the Tyr-205 hydrogen group by molecular modeling showed that Tyr-205 was located in transmembrane domain (TM) 5, and that its hydroxy group formed a hydrogen bond with Leu-169 main-chain =O located in TM 4. The mutation of Tyr-205 to phenylalanine would cause loss of this hydrogen bond and decrease or change the interaction between these TM coils, thus affecting the ability of AVP to bind to the receptor. According to this molecular model of AVPR2, the Y205F mutation would cause nephrogenic diabetes insipidus.

Base Sequence↗
PubMedDate not supplied

Thickened pituitary stalk on MR images in patients with diabetes insipidus and Langerhans cell histiocytosis.

The MR images of four female patients with acute onset of central diabetes insipidus and pathologically confirmed Langerhans cell histiocytosis were evaluated retrospectively for evidence of lesions in the hypothalamic-pituitary axis. The examinations were conducted on a 1.5-T MR system with thin-section sagittal and coronal T1-weighted (short TR/short TE) and T2-weighted (long TR/long TE) images. Three patients underwent T1-weighted MR after IV administration of gadopentetate dimeglumine. Compared with 20 normal subjects who were evaluated with the same MR protocol, three of the four patients had a symmetrically thickened pituitary stalk that demonstrated homogeneous signal enhancement following contrast administration. The high signal intensity of the posterior lobe, which was seen in normal subjects on T1-weighted sagittal images, was absent in all four patients. Two patients had associated abnormalities on either chest films or imaging studies of the temporal bone and two patients had isolated CNS Langerhans cell histiocytosis. The combination of a thickened pituitary stalk and absent posterior pituitary hyperintensity, while nonspecific for Langerhans cell histiocytosis, should nevertheless prompt further studies, such as chest films, bone scanning, or temporal bone CT, to attempt to narrow the differential diagnosis. Gadopentetate dimeglumine, in particular, may be a useful adjunct in the MR examination of the patient with diabetes insipidus.

Adolescent↗
PubMed1998

Recurrent central diabetes insipidus secondary to cryptococcal meningitis.

Meningitis is often associated with hyponatremia due to inappropriate secretion of antidiuretic hormone, and diabetes insipidus is associated with bacterial meningitis. This article describes a patient with acquired immunodeficiency syndrome who experienced recurrent episodes of central diabetes insipidus in association with recurrent fungal meningitis. Desmopressin was effective in controlling the polyuria until the episodes of meningitis resolved.

AIDS-Related Opportunistic Infections↗
PubMed1994

Acquired nephrogenic diabetes insipidus secondary to distal renal tubular acidosis and nephrocalcinosis associated with Sjögren's syndrome.

A 52-year-old woman was referred to our hospital because of 16-year history of polyuria and polydipsia. Hyposthenuria, hyperchloremic metabolic acidosis and the inabilities to acidify the urine after acid-loading test and to concentrate the urine in responses to water-deprivation and antidiuretic hormone administration allowed us to diagnose renal tubular acidosis and nephrogenic diabetes insipidus. Radiographic examinations revealed bilateral nephrocalcinosis. The patient was also found to have clinical and laboratory findings characteristic for Sjögren's syndrome. Thus the longstanding, poorly monitored distal renal tubular acidosis associated with Sjögren's syndrome was considered to result in very rare renal complications-nephrocalcinosis and nephrogenic diabetes insipidus. In patients with renal tubular acidosis and/or nephrogenic diabetes insipidus of unknown etiology, therefore, Sjögren's syndrome should be considered as one of primary disorders.

Acidosis, Renal Tubular↗
PubMed1989

Diabetes insipidus caused by lymphocytic infundibuloneurohypophysitis.

Pathologic examination at autopsy of a 74-year-old man with central diabetes insipidus revealed that he had a chronic lymphocytic inflammation limited to the infundibulum, stalk, and posterior lobe of the pituitary gland. No meningitis, sarcoidosis, or granulomas were detected, though there was evidence of chronic pancreatitis. In addition, neuronal loss with gliosis was observed bilaterally in the supraoptic and paraventricular nuclei. The unusual localized inflammatory brain lesion was considered to be responsible for the diabetes insipidus.

Aged↗
PubMed1996

Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy.

Foscarnet is used as therapy of cytomegalovirus (CMV) infection in immunosuppressed subjects. We present a patient with human immunodeficiency virus infection under treatment with foscarnet for CMV retinitis who complained of thirst and polyuria. Laboratory data showed hypernatremia with increased plasma osmolality and metabolic hyperchloremic acidosis. A water deprivation test demonstrated a nephrogenic diabetes insipidus. Other laboratory studies, including urine pH, anion gap, titratable acidity, and bicarbonate, showed a distal tubular acidification defect. All abnormalities were transient, with recovery a few days after foscarnet withdrawal. No cases of renal acidosis, and only one case of nephrogenic diabetes insipidus, has been previously reported as a complication of foscarnet treatment. Our patient developed both nephrogenic diabetes insipidus and renal tubular acidosis with a temporal pattern that demonstrated a link between foscarnet therapy and these abnormalities.

AIDS-Related Opportunistic Infections↗