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Lithium-induced Nephrogenic Diabetes Insipidus with Concurrent Hyperosmolar Hyperglycemic State: A Case Report
摘要
Background: Diabetes insipidus (DI) is characterized by polyuria and polydipsia. Nephrogenic DI is confirmed by inadequate response to desmopressin and low urine osmolality during water deprivation test or by copeptin level above 21.4 pmol/L. Among the acquired causes of nephrogenic DI, lithium therapy is the most common etiology. Lithium-induced nephrogenic DI may lead to development of hyperosmolar hyperglycemic state (HHS) in patients with undiagnosed diabetes mellitus (DM). Methods: We report a case of lithium-induced nephrogenic DI with concurrent HHS and newly-diagnosed DM. Results: A 49-year-old man had schizoaffective disorder and took lithium regularly for years. He was admitted because of HHS. After resolution of HHS, severe polyuria, polydipsia and hypernatremia were still noticed. The urine osmolality was 102 mOsm/KgH_2O. The lithium level was 0.9 mmol/L at first. Water deprivation test revealed less than 50% increase in urine osmolality which was still below 300 mOsm/KgH_2O after desmopressin injection. Lithium-induced nephrogenic DI was suspected. Lithium was discontinued. Low-sodium diet and hydrochlorothiazide were administered. The urine output, renal function and serum sodium all improved. Conclusion: Clinical manifestations of DI and lithium toxicity should be closely monitored with check-up of blood sugar since untreated DI may lead to HHS. Lithium level should be obtained regularly. Lithium therapy results in nephrogenic DI by reducing aquaporin-2 expression, impairing urinary concentrating ability and decreasing response to aldosterone. Treatment includes early cessation of lithium, amiloride and combined therapy with thiazide and low-sodium diet. Lithium intoxication can be managed by fluid resuscitation, bowel irrigation and hemodialysis.