[Abnormality of the ureters in dwarfism, infantilism and symptomatic diabetes insipidus (renal dwarfism)].
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Diabetes Insipidus↗
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Two distinct pathophysiological mechanisms in congenital nephrogenic diabetes insipidus.
V1 and V2 vasopressin receptor functions were studied in 2 patients with congenital nephrogenic diabetes insipidus. V1 receptor-mediated functions (increase in urinary prostaglandin E2 excretion and plasma cortisol levels) and Gs (guanine nucleotide-binding stimulatory protein) activity of erythrocyte membranes were normal in both patients. After infusion of 0.4 micrograms/kg dDAVP, a 57-yr-old male patient had no increase in plasma factor VIII coagulant, ristocetin cofactor, or fibrinolytic activity or change in von Willebrand factor multimers. In addition, he had no vasodilatory response to dDAVP, a response that occurs in normal subjects and patients with central diabetes insipidus. In contrast, a 25-yr-old female patient had normal hemostatic and vasodilatory responses to the infusion of dDAVP. These observations indicate that the cellular abnormalities in patients with congenital nephrogenic diabetes insipidus may be either at the V2 receptor or in the postreceptor (and Gs activity) cascade of events that mediate vasopressin-induced antidiuresis. Therefore, heterogeneity exists in the biochemical cause(s) of congenital nephrogenic diabetes insipidus in man.
Adult↗
Renal medullary adenylate cyclase in rats with hypothalamic diabetes insipidus.
The activities of enzymes related to the cellular action of vasopressin as well as the activities of other enzymes were studied in an animal model of hypothalamic diabetes insipidus. Rats with hereditary hypothalamic diabetes insipidus (homozygotes of Bratteboro strain) were found to have significantly lower renal medullary adenylate cyclase activity, either basal activity or activity stimulated by vasopressin, as compared with controls (heterozygotes of the same strain). There were no differences between the two strains in the activities of cyclic AMP phosphodiesterase, other hormone-sensitive adenylate cyclases, or the other renal medullary enzymes studied, which are apparently unrelated to the vasopressin action. The treatment of rats with hereditary hypothalamic diabetes insipidus with exogenous vasopressin increased the activity of renal medullary adenylate cyclase stimulated in vitro by maximal doses of vasopressin, but had no effect on the basal activity of adenylate cyclase or on the activity of cyclic AMP phosphodiesterase. This suggests that low adenylate cyclase activity in the renal medulla of rats with diabetes insipidus may be related to the subnormal concentrating ability observed in these animals.
3',5'-Cyclic-AMP Phosphodiesterases↗
Diabetes insipidus.
When the critically ill patient's clinical course is complicated by diabetes insipidus, a significant threat to the equilibrium of the body's delicate water and electrolyte balance ensues. Patients with diabetes insipidus are at significant risk of dehydration, hypernatremia, alterations in level of consciousness, and hemodynamic instability from hypovolemia. This article presents the causes of, and pathophysiologic alterations in, central and nephrogenic diabetes insipidus. Clinical manifestations and therapeutic management of both conditions in the critical care population are described.
Critical Illness↗
Antidiuretic action of chlorpropamide in diabetes insipidus patients and in normal subjects.
The antidiuretic action of chlorpropamide was studied in 10 diabetes insipidus patients sensitive to vasopressin and 15 normal subjects. After an oral load of water followed by sustained hydration through water ingestion in a volume equivalent to the urinary flow, chlorpropamide (4 mg/kg body weight) was intravenously administered as a single dose, either alone (34 experiments) or simultaneously with pitressin infusion (6 experiments). During the experiments, creatinine clearance as well as osmolal and plasma and urine electrolyte concentrations were measured. Several urine collection periods were made before and after the administration of chlorpropamide. In thes experimental conditions, chlorpropamide promoted a marked antidiuresis (p less than 0.01) in patients with diabetes insipidus and presented no antidiuretic effect (p greater than 0.01) in normal subjects, even with a double dose. However, if previously to the experiment, the normal individuals were dehydrated (mean weight loss of 4.8 per cent) or the diabetes insipidus patients were hydrated (mean weight gain of 6.4 per cent) a reverse behavior was observed: that is, the normal subjects did present (p less than 0.01) and the diabetes insipidus patients did not present (p greater than 0.01) antidiuresis to chlorpropamide. The results suggest that the state of hydration modulates the action of chlorpropamide in a way apparently independent of the antiduretic hormone.
Chlorides↗
[Diabetes insipidus in children--long-term follow-up study].
A follow-up study was carried out on 12 children with vasopressin sensitive diabetes insipidus. 1) Nine cases (75%) of 12 were finally diagnosed as having brain tumor in later course. There were 3 cases (25%) who could not be decided as having brain tumor during the follow-up period of more than 6 years. 2) There was one case who developed the overt signs of brain tumor 9 years after the onset of diabetes insipidus. Therefore, it seems necessary to follow-up cases with diabetes insipidus for at least 10 years before determining it as idiopathic type. 3) In cases with diabetes insipidus due to brain tumor, associated growth retardation, autonomic symptoms, behavior disorder, endocrine dysfunction and metabolic dysfunction were frequently observed. In the case where these symptoms become aggravated with lapse of time, these findings should be taken seriously as indicating brain tumor. 4) In the case showing either anterior or posterior focal slow waves in the EEG, if such focal slow waves aggravate with age, the findings should be considered as indicative of brain tumor. 5) We would like to emphasize the significance of brain tumor as the underlying pathology of childhood diabetes insipidus.
Astrocytoma↗
Adipsic diabetes insipidus following pituitary surgery for a macroprolactinoma.
Adipsic diabetes insipidus (ADI) is a rare condition in which thirst, an essential clinical feature for the prevention of hypernatraemic dehydration, is absent. We report the first case of adipsic diabetes insipidus to occur following surgery for a pituitary macroprolactinoma, with loss of both osmoregulated and baroregulated vasopressin release. Following extensive surgery for a vision threatening macroprolactinoma a 14-year-old boy developed profound hypernatraemia with absent thirst sensation. Detailed investigation, with hypertonic saline infusion and trimetaphan infusion, revealed absence of both osmoregulatory and baroregulatory release of vasopressin. We discuss the investigation and management of such patients and the physiology of hypothalamic-neurohypophyseal dysfunction in such patients.
Adolescent↗
Transient postpartum diabetes insipidus in twin pregnancy associated with HELLP syndrome.
Diabetes insipidus during pregnancy is an uncommon medical problem, and its cause is not entirely clear. We present a woman with twin pregnancy associated with HELLP syndrome, who developed diabetes insipidus during postpartum period. A hypertonic saline infusion study with measurement of plasma arginine vasopressin concentrations confirmed the diagnosis. She had mild response to 1-desamino-8-d-arginine-vasopressin (dDAVP) during the immediate postpartum period. On the 3rd postpartum day two doses of 100 microliters of dDAVP were administered, and her urinary volume gradually decreased. We could stop dDAVP on the 30th postpartum day. This exacerbation may result from increased vasopressinase activity caused by the excessive production in the placenta due to twin pregnancy, together with the insufficient degradation in the liver due to HELLP syndrome.
Adult↗
Impairment of bone status in patients with central diabetes insipidus.
The aim of the current study was to evaluate the biochemical parameters of bone metabolism and the bone mineral density (BMD) in patients with central diabetes insipidus, either treated or not treated with endonasal desmopressin. Eighteen patients with central diabetes insipidus and 18 sex- and age-matched healthy subjects entered the study. The patients were divided into 2 groups: patients who did not receive treatment with desmopressin for at least 1 yr (group 1), and patients chronically treated with desmopressin since the diagnosis of diabetes insipidus (group 2). Serum osteocalcin and urinary cross-linked N-telopeptide of type I collagen levels were measured in all patients and controls using RIA and enzyme-linked immunosorbent assay kits, respectively. BMD was measured at the lumbar spine (L1-L4) and at the femoral neck in all subjects, using a Hologic QDR 1000 analyzer (Hologic Inc., Waltham, MA). Serum osteocalcin concentrations were significantly lower, both in patients of group 1 and group 2, compared with healthy subjects (5.1 +/- 0.6 and 4.5 +/- 0.3 vs. 7.9 +/- 0.2 micrograms/L, P < 0.05), whereas urinary cross-linked N-telopeptide of type I collagen concentrations were similar in the three groups of subjects (72.8 +/- 2.2, 71.6 +/- 2.7, and 64.6 +/- 1.7 nmol bone collagen equivalent/mmol creatinine). BMD was significantly decreased in patients of groups 1 and 2, compared with controls, both at lumbar spine (0.84 +/- 0.06 and 0.87 +/- 0.04 vs. 1.01 +/- 0.02 g/cm2, P < 0.05) and femoral neck (0.78 +/- 0.06 and 0.80 +/- 0.04 vs. 0.93 +/- 0.02 g/cm2, P < 0.05). A significant inverse correlation was found between disease duration and BMD values, evaluated as T scores, both at lumbar spine (group 1: r = -0.952, P < 0.005; group 2: r = -0.921, P < 0.001) and at femoral neck (group 1: r = -0.914, P < 0.05; group 2: r = -0.683, P < 0.05). In conclusion, patients with central diabetes insipidus had a significant bone impairment, compared with healthy subjects. Replacement with endonasal desmopressin at standard doses was not able to prevent or reverse the bone impairment. These findings suggest that, in patients with central diabetes insipidus, bone status analysis is mandatory; and a bone-loss preventing treatment might be beneficial.
Administration, Intranasal↗
A case of Rathke's cleft cyst presenting with diabetes insipidus.
Rathke's cleft cysts (RCCs) are considered to arise from the remnants of Rathke's pouch, an invagination of the stomodeum. They are classically described as benign epithelium lined intrasellar cysts containing mucoid material, and also found in 2-33% of routine autopsy series. The most common presenting symptoms are visual impairment, hypothalamic dysfunction, hypopituitarism and headache. Diabetes insipidus has been described in patients with RCC. Very few cases presented with only diabetes insipidus in adults. To our knowledge, our patient is the first case of RCC presenting with only diabetes insipidus in childhood. A 9-year-old girl presented with diabetes insipidus. The physical, neurological and endocrinological examinations were normal, except for diabetes insipidus. Magnetic resonance imaging scan revealed a hyperintense lesion with supra sellar extension in the posterior pituitary both on T1 and T2 weighted images. Subtotal excision of RCC was performed via transsphenoidal surgery. However, diabetes insipidus persisted after the surgery.
Child↗
A case of nephrogenic diabetes insipidus.
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Diabetes Insipidus↗
Hereditary nephrogenic diabetes insipidus and bilateral nonobstructive hydronephrosis.
We describe 2 cases of hereditary nephrogenic diabetes insipidus with massive bilateral dilatation of the urinary tract without any organic obstruction. A review of the literature revealed that dilatation of the urinary tract was present in 67% of the reported cases of nephrogenic diabetes insipidus which included a description of the urinary tract. This strong association between hereditary nephrogenic diabetes insipidus and nonobstructive hydronephrosis suggests a cause-and-effect relationship in which polyuria is responsible for the hydronephrosis.
Adult↗
[Nephrogenic diabetes insipidus].
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Diabetes Insipidus↗
[Hereditary idiopathic nephrogenic diabetes insipidus].
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Child↗
Transient diabetes insipidus and acute fatty liver of pregnancy.
OBJECTIVE: To review the association of transient diabetes insipidus and acute fatty liver of pregnancy. DESIGN: A retrospective study. SETTING: Six women presenting with polyuria and polydipsia in the third trimester or in the immediate postpartum period, referred over a two and a half year period; five out of six were primigravida. All had raised liver transaminases and biopsy-proven acute fatty liver of pregnancy. Four out of six also had pre-eclampsia. SUBJECTS: Tertiary referral centre. MAIN OUTCOME MEASURES: There were no maternal deaths and only one fetal death. Desamino-cys-1-D-arg-8-vasopressin administration produced a reduction in urine output in all five women to whom it was administered. In all cases symptoms had resolved by the end of the fourth postpartum week. Three of the women have had subsequent pregnancies uncomplicated by either transient diabetes insipidus or acute fatty liver of pregnancy. CONCLUSIONS: The association of transient diabetes insipidus and acute fatty liver of pregnancy appears more common than previously recognised. Both may be part of the spectrum of pre-eclampsia.
Acute Disease↗
Lithium-induced nephrogenic diabetes insipidus.
Two patients with severe lithium-induced nephrogenic diabetes insipidus are described. Although it is known lithium can cause diabetes insipidus, one should be especially alert in psychiatric patients, as the main defence mechanisms thirst and drinking behaviour may not function adequately in these patients. The major form of therapy in both patients consisted of drinking, a thiazide diuretic, as well as a protein and sodium restricted diet.
Aged↗
[Post-traumatic diabetes insipidus syndrome (author's transl)].
Post-traumatic diabetes insipidus was observed in 14 among 702 patients with severe trauma. The cause of the abnormal vasopressin secretion may be cerebral oedema, cerebral contusion near the hypothalamus, pull on the hypophyseal stalk by displacement or gross destruction of the brainstem. The hormonal hypofunction disappears once the cerebral damage has regressed. Treatment consists of exact balancing of water and electrolyte loss, using salt-free solutions. Drug treatment with vasopressin and with ADH-secretion stimulators has given unsatisfactory results, but should be used. Seven of the 14 patients died of their injuries. The symptoms of the diabetes insipidus syndrome regressed in the survivors.
Adult↗
[Central diabetes insipidus complicated with upbeat nystagmus and cerebellar ataxia].
A 34-year-old male presented with central diabetes insipidus accompanied by upbeat nystagmus and cerebellar ataxia. The patient without family history of above began to walk at the age of 2 years. Polyposia and polyuria were noted at the age of about 4 years. Dysbasia developed at the age of about 7 years. From the age of 30, lalopathy appeared together with various clinical symptoms including cataracts, disturbed intelligence, upbeat nystagmus, abnormal ocular movements, ataxic speech, cerebellar ataxia and reduction of the muscle tone of the limbs, and hypotonic polyuria. Abnormal laboratory findings included square wave jerks, upbeat nystagmus, and "bow tie" nystagmus by EOG, atrophy of the cerebellum and the brainstem by CT, a slight prolongation of the P300 latency, and a central diabetes insipidus pattern by water deprivation test and Carter-Robbins tests. There have been occasional reports of diabetes insipidus complicated by cerebellar ataxia, but in no earlier reports has diabetes insipidus been concurrent with abnormal ocular movements such as upbeat nystagmus. A degenerative disease primarily of the posterior lobe of the hypophysis, hypothalamus, cerebellum, and brainstem was suspected.
Adult↗