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Case Reports
Journal Article
Lithium-induced nephrogenic diabetes insipidus.
Journal of the American Board of Family Practice 1999 January
BACKGROUND: Lithium can cause nephrogenic diabetes insipidus in up to 20 to 40 percent of patients currently taking the medication, and a subset of these patients will have a persistent concentrating defect long after lithium is discontinued. They are at risk for serious hypernatremia when fluid intake is restricted for any reason.
METHODS: MEDLINE as used to search the key words "nephrogenic diabetes insipidus" and "lithium" from 1990 to the present. A case report describes a patient who had been off lithium for 8 years and who developed hypernatremia after she was transferred to a new long-term facility and the staff attempted to control the patient's polydipsia. The diagnosis and treatment of nephrogenic diabetes insipidus are also discussed.
RESULTS: This case of persistent nephrogenic diabetes insipidus 8 years after discontinuing lithium is the longest ever reported. Certainly, a number of patients have varying degrees of persistent lithium-related nephrogenic diabetes insipidus. Although pathologic changes are associated with persistent nephrogenic diabetes insipidus, the exact mechanism of the persistent defect is unknown. The mechanism of acute lithium-induced nephrogenic diabetes insipidus while the patient is on lithium is related to changes in intracellular cyclic adenosine monophosphate.
CONCLUSIONS: Patients currently taking lithium and patients with a remote history of lithium treatment need to be monitored for signs and symptoms of nephrogenic diabetes insipidus. Physicians need to be aware of the potential for nephrogenic diabetes insipidus in these patients and care for them appropriately.
METHODS: MEDLINE as used to search the key words "nephrogenic diabetes insipidus" and "lithium" from 1990 to the present. A case report describes a patient who had been off lithium for 8 years and who developed hypernatremia after she was transferred to a new long-term facility and the staff attempted to control the patient's polydipsia. The diagnosis and treatment of nephrogenic diabetes insipidus are also discussed.
RESULTS: This case of persistent nephrogenic diabetes insipidus 8 years after discontinuing lithium is the longest ever reported. Certainly, a number of patients have varying degrees of persistent lithium-related nephrogenic diabetes insipidus. Although pathologic changes are associated with persistent nephrogenic diabetes insipidus, the exact mechanism of the persistent defect is unknown. The mechanism of acute lithium-induced nephrogenic diabetes insipidus while the patient is on lithium is related to changes in intracellular cyclic adenosine monophosphate.
CONCLUSIONS: Patients currently taking lithium and patients with a remote history of lithium treatment need to be monitored for signs and symptoms of nephrogenic diabetes insipidus. Physicians need to be aware of the potential for nephrogenic diabetes insipidus in these patients and care for them appropriately.
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