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PubMed1980

Oxytocin: major corticotropin-releasing factor secreted from diabetes insipidus rat posterior pituitary in vitro.

In diabetes insipidus (DI) rats, electrical stimulation of the posterior pituitary lobes in vitro promotes the release of corticotropin-releasing factor (CRF). The CRF activity is abolished by preincubation of the posterior lobe media with thioglycolate. Oxytocin, which is released concomitantly into the medium (3.2 mIU/lobe/20 min), accounts for the complete CRF effect. Neural lobe extracts from DI and normal rats contain 40-70% more CRF activity than can be explained by their content in vasopressin and/or oxytocin. The discrepancy between released and extracted CRFs suggests that hypothetical CRFs or potentiating factors are not released from nerve endings or have to be present in high concentrations to manifest their effect.

Adrenocorticotropic Hormone↗
PubMed1987

Diabetes insipidus in children with brain death.

Central diabetes insipidus (DI) occurs in patients suffering from overwhelming CNS injuries leading to brain death. The purpose of this study was to describe the clinical presentation of DI in children with brain death. The medical records of 34 patients with a diagnosis of brain death were reviewed. Diuresis was present in 76% of patients; however, DI was only present in 38% of patients. On autopsy, the pituitary gland in six patients revealed varying degrees of edema, congestion, hemorrhage, and coagulative necrosis. We concluded that DI is present in many, but not all, patients who experience brain death and therefore, cannot be relied on solely as a marker of brain death.

Adolescent↗
PubMed1977

Uterine activity in diabetes insipidus.

In two nonpregnant women with cranial diabetes insipidus, myometrial activity under different hormonal conditions was studied by intrauterine pressure recording. Recordings were performed when the women were under the influence of their regular treatment with desaminocys1-D-arg8-vasopressin (DDAVP), and when they had fully developed symptoms of their disease. Uterine activity was similar to that found in normal women under the same hormonal conditions, and generally did not change when symptoms of lack of vasopressin appeared. Both DDAVP (15-20 microgram), given intranasally, and lysin vasopressin (0.2 IU), given intravenously, stimulated uterine activity, particularly in late secretory menstrual phase. It is suggested that endogenous vasopressin is of minor importance for the induction of spontaneous uterine activity in nonpregnant women.

Adult↗
PubMed2002

Utility of magnetic resonance imaging in the evaluation of the child with central diabetes insipidus.

Because of the association of central diabetes insipidus (CDI) and occult neoplasia, magnetic resonance imaging (MRI) is an important component of the diagnostic evaluation of a child with CDI. In more than 90% of these children, MRI (T1 weighted-image, without contrast) demonstrates an absence of the normal hyperintensity of the posterior pituitary. In one third of patients, the pituitary stalk is also thickened, suggesting infiltrative disease. Of those with a thickened stalk, the etiology of the CDI remains undetermined in about 60% of patients, whereas histiocytosis and occult germinoma each account for approximately 15-20% of patients. In contrast, germinoma is infrequent (3%) in children with CDI and an MRI showing a normal infundibular stalk, though histiocytosis still accounts for 15-20% of patients. In this paper, a diagnostic approach in children with CDI is proposed.

Adolescent↗
PubMed1977

Comparison of clofibrate and chlorpropamide in vasopressin-responsive diabetes insipidus.

Six patients with vasopressin-responsive diabetes insipidus (DI) received clofibrate and chlorpropamide, singly and in combination. Decrease in urinary output averaged (mean +/- SEM): (1) clofibrate 2 g/day, 47% +/- 6%; (2) chlorpropamide 250 mg/day 59% +/- 5%; (3) clofibrate 2 g/day plus chlorpropamide 125 mg/day, 54% +/- 7%; (4) clofibrate 2 g/day plus chlorpropamide 250 mg/day 61% +/- 4%. Water deprivation tests before and during treatment showed significantly higher basal, final, and peak urinary osmolalities (Uosm) and lower free water clearance (CH20) on chlorpropamide, singly and in combination: clofibrate raised Uosm less but significantly decreased CH2O. Water load tests before and during treatment showed that chlorpropamide, singly and in combination, markedly decreased maximal urinary flow, maximal CH2O, percentage water load excreted, and increased minimal Uosm; clofibrate significantly decreased maximal urinary flow and CH2O only. One patient responded only to combination therapy. Chlorporpamide caused serious hypoglycemia in three of six patients. Clofibrate had no significant side effects.

Adolescent↗
PubMed2006

[Nephrogenic diabetes insipidus in a large family].

Hereditary nephrogenic diabetes insipidus is a rare disease. We describe here three brothers with this disease from a big family consisting of 10 siblings. The case is undoubtedly X-linked because the sufferers are only boys, one of them with a different father. The illness was noticed rather late, namely, at the ages of approximately 7, 6 and 5 years. Possibly, this is a particular characteristic of this family, because the disease is usually diagnosed before the age of two years. In the oldest brother (at present 15 years old) epicystotomy was performed at the time of diagnosis because of polyuria, hydroureteronephrosis and bladder hypotonia; the intervention caused a urinary tract infection leading to chronic pyelonephritis and renal scarring. No urologic intervention was necessary in the younger brothers, because their illness was noticed and treatment started somewhat earlier. This case shows that polydipsia and polyuria should always be assessed properly to disclose their causes.

Adolescent↗
PubMed1990

Desmopressin and indomethacin therapy for nephrogenic diabetes insipidus in patients receiving lithium carbonate.

Individuals receiving lithium carbonate commonly have nephrogenic diabetes insipidus. There is no effective and practical treatment for this condition. We have found that large doses of desmopressin (DDAVP) may provide effective therapy without adverse effects. A recent report showed that indomethacin improved nephrogenic diabetes insipidus that had persisted after the lithium therapy was discontinued. We have provided additional evidence that indomethacin may be effective, even when treatment with lithium is continued. We also have shown that indomethacin together with desmopressin can markedly decrease polyuria, though indomethacin must be used with care because it may impair renal function.

Adult↗
PubMed2004

Myelodysplastic syndrome with central diabetes insipidus manifesting hypodipsic hypernatremia and dehydration.

Central diabetes insipidus (DI) is a rare but recognized complication of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) that is caused by leukemic infiltration to the hypothalamo-neurohypophyseal system. In rare patients in whom a wide region of the hypothalamus is involved, central DI results in hypodipsic hypernatremia and dehydration. Typical DI symptoms such as polydipsia, polyuria, and marked thirst are concealed in these cases, because the hypothalamic "thirst center" cannot send thirst stimuli to the cerebral cortex. Herein we describe a patient with MDS developing into AML, who presented with hypodipsic hypernatremia and dehydration. A diagnosis of central DI was made on the ground of a low level of serum anti-diuretic hormone (ADH) despite high serum osmolality. A magnetic resonance imaging study revealed attenuation of a physiological "bright spot" of the neurohypophysis. An induction course chemotherapy including regular-dose cytarabine and daunorubicin produced a rapid improvement of hypernatremia. The bone marrow aspirate after two courses of chemotherapy showed complete remission. At that point, ADH release and the "bright spot" were recovered. In order to correctly diagnose central DI in association with hematological malignancies, we should not overlook this atypical type of DI.

Dehydration↗
PubMed1993

A Null mutation in the vasopressin V2 receptor gene (AVPR2) associated with nephrogenic diabetes insipidus in the Hopewell kindred.

Congenital nephrogenic diabetes insipidus (DIR) is a rare X-linked hereditary disorder in which the renal collecting duct is unresponsive to arginine vasopressin; thus, the urine is consistently hypotonic to plasma. Recently, the association between the V2 receptor gene (AVPR2) and DIR has been proven. We have determined the gene sequence of four family members, from three generations, of a large North American family with CNDI who were originally part of the study used to formulate the Hopewell hypothesis. It had been proposed that a single DIR gene defect was introduced to North America by a member of an Ulster Scot kindred arriving on the ship Hopewell in 1761. DNA sequencing of the AVPR2 has identified a single base transversion from G-->A which changes tryptophan 71 to a stop codon in affected patients. This point mutation causes a truncation of the receptor leading to an essentially null allele. These data and other recently described mutations in the AVPR2 in North American pedigrees, descended from Ulster Scot ancestors and other origins, make the assertion of a founder effect proposed in the Hopewell hypothesis invalid.

Amino Acid Sequence↗
PubMed2004

Perioperative management of diabetes insipidus in children [corrected].

Managing children with diabetes insipidus (DI) in the perioperative period is complicated and frequently associated with electrolyte imbalance compounded by over- or underhydration. In this study the authors developed and prospectively evaluated a multidisciplinary approach to the perioperative management of DI with a comparison to 19 historical control children. Eighteen children either with preoperative DI or undergoing neurosurgical operations associated with a high risk for developing postoperative DI were identified and managed using a standardized protocol. In all patients in whom DI occurred during or after surgery, a continuous intravenous infusion of aqueous vasopressin was initiated and titrated until antidiuresis was established. Intravenous fluids were given as normal saline and restricted to two thirds of the estimated maintenance rate plus amounts necessary to replace blood losses and maintain hemodynamic stability. In all children managed in this fashion, perioperative serum sodium concentrations were generally maintained between 130 and 150 mEq/L, and no adverse consequences of this therapy developed. In the 24-hour period evaluated, the mean change in serum sodium concentrations between the historical controls was 17.6 +/- 9.2 mEq/L versus 8.36 +/- 6.43 mEq/L in those children managed by the protocol. Hyponatremia occurred less frequently in the children managed with this protocol compared with historical controls.

Adolescent↗
PubMed1997

Atherosclerosis, aortic stenosis and sudden onset central diabetes insipidus.

The majority of cases of central diabetes insipidus are still pathogenetically unclear (idiopathic). Atherosclerotic cholesterol emboli might be partly responsible for some of these idiopathic cases. A 54-year-old woman with known aortic valve stenosis and a history of a transitory ischemic attack presented with sudden-onset polyuria and polydipsia of up to eight l/d, which had started acutely with headaches. She had been treated with lithium for 3 years because of cyclothymic depression. Plasma sodium was in the upper normal range (142-148 mmol/l). Hypertonic saline infusion during lithium therapy revealed a normal threshold of thirst and resetting of vasopressin secretion (osmotic threshold > 300 mosmol/l), whereas vasopressin reserve was normal. Lithium withdrawal led to an even greater delay of vasopressin release upon hypertonic saline infusion (> 310 mosmol/l). Pituitary function tests revealed a normal anterior pituitary function. MR imaging of the hypothalamo-hypophyseal region showed a normal hypothalamic region and a highly intensive neurohypophyseal signal in the T1-weighted image. The patient responded well to desmopressin. We suggest that in this rare case clinical symptoms as well as biochemical findings like impairment of AVP release might be related to a minor structural hypothalamic damage by a vascular lesion, caused, for example, by an atheromatous (cholesterol) embolism in the hypothalamic region responsible for integration of osmoreceptor function and AVP-secretion. The patient's atherosclerosis and aortic stenosis might be responsible for this event.

Aortic Valve Stenosis↗
PubMed2004

Course and clinical impact of magnetic resonance imaging findings in diabetes insipidus associated with Langerhans cell histiocytosis.

BACKGROUND: Diabetes insipidus (DI) is the most frequent sequela in Langerhans cell histiocytosis (LCH). The clinical relevance and therapeutic impact of brain magnetic resonance imaging (MRI) findings in LCH patients with LCH during the disease course is unclear. PROCEDURE: In this retrospective study, we reviewed 113 brain MRIs from 59 DI patients, in 17 of these serial follow up MR-examination findings were correlated to the clinical course and therapy. RESULTS: At DI diagnosis, 71% patients showed a thickened stalk, in 24% the stalk was still thickened on MRIs done more than 5 years after DI onset, and in two patients the stalk was already thickened several months before DI onset. The changes of the pituitary stalk thickness were highly variable and did not clearly correlate with the treatment. Regression of pituitary thickness on MRI did not concur with clinical recovery of DI, which persisted in all but one patient with initially partial DI. The occurrence of anterior pituitary hormone deficiencies appeared to be linked to a thickening of the stalk at DI diagnosis. LCH-lesions in the craniofacial bones were seen in 75% DI patients, and 76% of DI patients with follow up MRIs done 5 years or longer after DI diagnosis had parenchymal neurodegenerative brain changes. CONCLUSIONS: Our study indicates that repeated MR-examinations in DI patients are of limited value for assessing a response to therapy in the pituitary stalk, but are important for the monitoring of craniofacial bone lesions and for the detection of parenchymal CNS disease.

Adolescent↗
PubMed1997

Identification and characterization of aquaporin-2 water channel mutations causing nephrogenic diabetes insipidus with partial vasopressin response.

Congenital nephrogenic diabetes insipidus (NDI) is a rare disease caused most often by mutations in the vasopressin V2 receptor (AVPR2). We studied a family which included a female patient with NDI with symptoms dating from infancy. The patient responded to large doses of desmopressin (dDAVP) which decreased urine volume from 10 to 4 I/day. Neither the parents nor the three sisters were polyuric. The patient was found to be a compound heterozygote for two novel recessive point mutations in the aquaporin-2 (AQP2) gene: L22V in exon 1 and C181W in exon 3. Residue Cys181 in AQP2 is the site for inhibition of water permeation by mercurial compounds and is located near to the NPA motif conserved in all aquaporins. Osmotic water permeability (Pf) in Xenopus oocytes injected with cRNA encoding C181W-AQP2 was not increased over water control, while expression of L22V cRNA increased the Pf to approximately 60% of that for wild-type AQP2. Co-injection of the mutant cRNAs with the wild-type cRNA did not affect the function of the wild-type AQP2. Immunolocalization of AQP2-transfected CHO cells showed that the C181W mutant had an endoplasmic reticulum-like intracellular distribution, whereas L22V and wild-type AQP2 showed endosome and plasma membrane staining. Water permeability assays showed a high Pf in cells expressing wild-type and L22V AQP2. This study indicates that AQP2 mutations can confer partially responsive NDI.

Amino Acid Sequence↗
PubMed2005

Causes of reversible nephrogenic diabetes insipidus: a systematic review.

BACKGROUND: In nephrogenic diabetes insipidus (NDI), the kidney is unable to produce concentrated urine because of the insensitivity of the distal nephron to antidiuretic hormone (arginine vasopressin). In settings in which fluid intake cannot be maintained, this may result in severe dehydration and electrolyte imbalances. The risk for conversion of reversible to irreversible NDI seems to be a potential complication. This review summarizes the reversible causes of acquired NDI to facilitate earlier recognition and more effective treatment by clinicians. METHODS: Two reviewers independently searched MEDLINE, Experta Medica (EMBASE), and ISI bibliographic databases. Human studies that described NDI caused by drugs, substances, or metabolic disturbances were included. To evaluate the causal role of the risk factor, data were abstracted according to Koch's postulates. RESULTS: One hundred fifty-five studies published between 1957 and March 2004 described 30 risk factors. Of 155 studies, 58 studies provided a "definite" diagnosis of NDI; 83 studies, a "probable" diagnosis; and 14 studies, a "possible" diagnosis. Nine factors were considered "definite" causes of NDI; 15 factors, "probable" causes; and 6 factors, "possible" causes. The most reported risk factors were lithium (84 studies), antibiotics (16 studies), antifungals (11 studies), antineoplastic agents (9 studies), antivirals (8 studies), and metabolic disturbances (8 studies). Duration of NDI reversal, as well as conversion to irreversible symptoms, seemed to depend on the duration of exposure. CONCLUSION: Most risk factors for reversible NDI were medications, and their identification and removal resulted in resolution of the condition. Long-term treatment with lithium seemed to result in irreversible NDI.

Anti-Infective Agents↗
PubMed2000

Neonatal mortality in an aquaporin-2 knock-in mouse model of recessive nephrogenic diabetes insipidus.

Hereditary non-X-linked nephrogenic diabetes insipidus (NDI) is caused by mutations in the aquaporin-2 (AQP2) water channel. In transfected cells, the human disease-causing mutant AQP2-T126M is retained at the endoplasmic reticulum (ER) where it is functional and targetable to the plasma membrane with chemical chaperones. A mouse knock-in model of NDI was generated by targeted gene replacement using a Cre-loxP strategy. Along with T126M, mutations H122S, N124S, and A125T were introduced to preserve the consensus sequence for N-linked glycosylation found in human AQP2. Breeding of heterozygous mice yielded the expected Mendelian distribution with 26 homozygous mutant offspring of 99 live births. The mutant mice appeared normal at 2-3 days after birth but failed to thrive and generally died by day 6 if not given supplemental fluid. Urine/serum analysis showed a urinary concentrating defect with serum hyperosmolality and low urine osmolality that was not increased by a V2 vasopressin agonist. Northern blot analysis showed up-regulated AQP2-T126M transcripts of identical size to wild-type AQP2. Immunoblots showed complex glycosylation of wild-type AQP2 but mainly endoglycosidase H-sensitive core glycosylation of AQP2-T126M indicating ER-retention. Biochemical analysis revealed that the AQP2-T126M protein was resistant to detergent solubilization. Kidneys from mutant mice showed collecting duct dilatation, papillary atrophy, and unexpectedly, some plasma membrane AQP2 staining. The severe phenotype of the AQP2 mutant mice compared with that of mice lacking kidney water channels AQP1, AQP3, and AQP4 indicates a critical role for AQP2 in neonatal renal function in mice. Our results establish a mouse model of human autosomal NDI and provide the first in vivo biochemical data on a disease-causing AQP2 mutant.

Animals↗
PubMed2001

[Perioperative management of a child with congenital nephrogenic diabetes insipidus].

The key point in perioperative management of a patient with congenital nephrogenic diabetes insipidus is fluid and electrolytes management. Since the urine of these patients consists mainly of solute free water, replacement fluids should be fluids which provide free water. A 2-year-old girl with congenital nephrogenic diabetes insipidus was scheduled for dental extraction. Her daily fluid intake was 10 liter. She had a history of recurrent fever, polyuria and polydipsia since 2 months of age. Her previous perioperative course for gastric volvulus at another hospital was complicated with postoperative hyponatremia and convulsion. A venous line was secured the day before surgery and 5% dextrose in water was infused at a rate of 12 ml.kg-1.hr-1. Intraoperative infusion was mainly with 5% dextrose in water combined with maintenance fluid. Five hours after surgery oral intake was started. Her intraoperative electrolytes levels were low (Na 133 mEq.l-1, K 2.8 mEq.l-1), but otherwise her perioperative course was uneventful.

Anesthesia, Inhalation↗
PubMed2003

[Improvement of diabetes insipidus after allogeneic bone marrow transplantation in a patient with myelodysplastic syndrome].

A 45-year-old male was diagnosed as having myelodysplastic syndrome (RAEB) in March 2001. He was admitted to our hospital because of cellulitis in his left lower limb in May. The blood cell count showed pancytopenia and immature myeloid cells were seen in the peripheral blood. Bone marrow aspiration showed the proliferation of myeloblasts (11.2%) and complex karyotypic abnormalities were detected including the long arm deletion of chromosome 7. The patient developed polyuria and polydipsia after admission and was diagnosed as having central diabetes insipidus. He was treated with DDAVP and the polyuria disappeared. In November, he underwent unrelated allogeneic bone marrow transplantation after conditioning with total body irradiation and cytarabine. After transplantation DDAVP was no longer required. Central diabetes insipidus has been reported as a rare complication of leukemia or myelodysplastic syndrome, but the underlying mechanism remains unclear. The complete remission of diabetes insipidus after bone marrow transplantation suggests that the infiltration of leukemic cells into the pituitary gland caused the diabetes insipidus in this case.

Bone Marrow Transplantation↗