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An Unusual Case of Lithium-Induced Nephrogenic Diabetes Insipidus
Venkateshwara Reddy Malreddy1, Laxmi M Balmuri2
1Internal Medicine, Manchester Royal Infirmary, Manchester, GBR.
Abstract:
We report a case of a 53-year-old woman with bipolar affective disorder on long-term lithium therapy who presented with confusion, acute right lower quadrant abdominal pain, fever, vomiting, and increased urinary frequency, with suspected urinary sepsis. Initial assessment revealed very high C-reactive protein (CRP), severe hyperglycemia, and acute kidney injury (AKI Stage 3). She was treated for urinary sepsis as computed tomography (CT) imaging demonstrated bilateral pyelonephritis, and Escherichia coli was isolated from blood cultures. Lithium was withheld initially due to renal impairment. As she met diagnostic criteria for hyperosmolar hyperglycemic state (HHS), she was treated as per the hospital hyperosmolar hyperglycemic state protocol. Glycemic control improved with appropriate fluid resuscitation and insulin administration. When renal function improved, lithium was restarted due to behavioral deterioration, following which she developed polyuria, severe hypernatremia, and persistently elevated serum osmolality. Due to severe agitation, she required intensive care unit (ICU) support for clinical and biochemical monitoring. Despite the resolution of hyperglycemia, persistent polyuria and hypernatremia prompted suspicion of diabetes insipidus (DI). Elevated serum sodium, high serum osmolality, and low urine osmolality were consistent with the diagnosis of DI. Normal brain imaging, elevated baseline co-peptin, and no response to desmopressin excluded central diabetes insipidus (CDI) and supported nephrogenic diabetes insipidus (NDI) secondary to chronic lithium use. She was treated with thiazide diuretics, with significant improvement in her urine output and stabilization of serum sodium. Lithium was discontinued, and referral to psychiatry was arranged. This case highlights the diagnostic challenge in differentiating osmotic diuresis of HHS from lithium-induced NDI and emphasizes the need for clinical suspicion of NDI in patients on lithium therapy presenting with polyuria and electrolyte disturbances.
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