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Treatment of lithium-induced diabetes insipidus with amiloride.

A 63-year-old African-American woman was admitted to the hospital with urosepsis and altered mental status. She had a history of schizophrenia and was treated with olanzapine 5 mg/day and lithium carbonate 300 mg 3 times/day. During her hospital stay, her sodium level and serum osmolality increased and her urine osmolality decreased, whereas her lithium levels remained within normal limits. Based on these findings, the patient was diagnosed with diabetes insipidus secondary to lithium therapy and was treated successfully with amiloride. Clinicians have been aware of lithium toxicity for many years and traditionally have administered thiazide diuretics for lithium-induced polyuria and nephrogenic diabetes insipidus. Recently, amiloride, a potassium-sparing diuretic, has been reported as a successful treatment for nephrogenic diabetes insipidus.

Amiloride↗

Diabetes insipidus from sarcoidosis confined to the posterior pituitary.

A young white man with new-onset central diabetes insipidus was discovered to have a posterior pituitary mass on magnetic resonance imaging. No other radiological abnormalities were noted in the anterior pituitary, infundibulum or hypothalamus. No other endocrinopathies were present: laboratory investigations showed normal basal concentrations of anterior pituitary hormones, including prolactin. The patient was suspected to have sarcoidosis affecting the posterior pituitary, because of the discovery of pulmonary sarcoidosis during his diagnostic evaluation. His symptoms of polydipsia and polyuria responded promptly to intranasal administration of 1-desamino-8-D-arginine vasopressin (DDAVP). The patient demonstrated complete regression of the posterior pituitary mass after a course of corticosteroid therapy. However, his diabetes insipidus persisted and he continues to need DDAVP treatment, currently at 12 months of follow-up. The resolution of the neurohypophysial mass was compatible with the diagnosis of pituitary sarcoidosis and this precluded the need for a transsphenoidal biopsy or surgery.

Adrenal Cortex Hormones↗

DIABETES INSIPIDUS. TREATMENT WITH 8-LYSINE VASOPRESSIN IN A NASAL SPRAY.

Synthetic 8-lysine vasopressin administered as a nasal spray to three patients with diabetes insipidus resulted in excellent control in one. In the other two it was of some value as therapy supplemental to pitressin tannate in oil. The patient who was adequately controlled with "spray therapy" alone required the sprays every three hours during the day, but none during the night.

Aerosols↗

Lithium-induced nephrogenic diabetes insipidus.

We report a case of a 43 year-old female who presented with lithium-induced nephrogenic diabetes insipidus. This patient had history of bipolar disorder for which she had been taking lithium carbonate for last 16 years. Appropriate work up was done and she was diagnosed with nephrogenic diabetes insipidus, secondary to lithium toxicity, and was managed accordingly.

Adult↗

Aquaporin-2 water channel mutations causing nephrogenic diabetes insipidus.

Since the discovery of aquaporin water channels, insight into the molecular mechanism by which rapid osmotic water occurs across cell membranes has greatly improved. Aquaporin-2 is the vasopressin-responsive water channel in the collecting duct, and vasopressin control of water permeability in the collecting duct occurs in two ways: a short-term regulation and a long-term adaptation. In congenital nephrogenic diabetes insipidus, the kidney does not respond to vasopressin. Ninety percent of these patients carry a mutation in the gene coding for the vasopressin V2 receptor located on the X chromosome. Autosomal recessive and dominant forms of nephrogenic diabetes insipidus that are caused by mutations in the aquaporin-2 gene have now been described. This review focuses on recent insight in the molecular and cellular defect in autosomal nephrogenic diabetes insipidus.

Animals↗

Angiotensin stimulates oxytocin release: imparied response in rats with genetic hypothalamic diabetes insipidus.

Intracerebroventricularly (i.c.v.) administered angiotensin II (ANG II) at a dose of 100 ng caused a large increase in plasma oxytocin levels in Long Evans (LE) rats and in rats heterozygous for hypothalamic diabetes insipidus (HZ). In rats homozygous for diabetes insipidus (DI) even 100 fold higher doses of ANG II i.c.v. exerted only marginal effects on oxytocin release. The impaired responsiveness in DI rats was fully restored by prolonged treatment with a vasopressin (AVP) analogue. These data show that the decreased sensitivity of ANG II receptors in DI rats is due to the AVP defect and its metabolic consequences and can be reversed by AVP substitution.

Angiotensin II↗

Simultaneous occurrence of diabetes insipidus and ascites due to liver cirrhosis: clinical and pathophysiological studies.

Authors describe the simultaneous occurrence of ascites due to liver cirrhosis and diabetes insipidus in a patient with consistently normal urine volume. The diagnosis of diabetes insipidus has been proved by the water deprivation test combined with the administration of dDAVP as well as by serial determinations of plasma arginine vasopressin levels before and during infusion of hypertonic sodium chloride solution. Authors discuss the differential-diagnostic difficulties of the case and consider the mechanisms playing a role in the abolishment of diabetic polyuria by hepatic disease.

Aged↗