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Excerpt
Polyuria is a common side effect associated with lithium therapy, with 5% to 20% of patients developing nephrogenic diabetes insipidus [1]. This disease state is characterized by the formation of hypotonic urine in the presence of plasma hyperosmolality and results from the inability of the kidney to respond to vasopressin. The failure of deamino-8-D-arginine vasopressin (dDAVP), a synthetic analog of vasopressin, to reduce urine volume is a key component in the diagnosis. Nephrogenic diabetes insipidus may be congenital or acquired. More commonly, it is acquired and is due to renal or urinary tract abnormalities, electrolyte disturbances, or drugs, especially lithium and demeclocycline [2]. Reports have shown that lithium concentrations within the therapeutic range can result in nephrogenic diabetes insipidus in 12% to 30% of patients. The associated signs and symptoms usually dissipate after discontinuation of lithium but can remain for approximate 1 yr [3,4]. Previous studies [5,6] showed amiloride and hydrochlorothiazide to be beneficial in improving polyuria, but side effects and gradual onset make these agents of little value in an acute situation. Recent case reports [1,7-11] showed that the use of indomethacin resulted in rapid improvement in symptoms associated with nephrogenic diabetes insipidus. We describe a case in which a patient being treated for bipolar affective disorder received chronic lithium carbonate therapy and suffered from nephrogenic diabetes insipidus. The patient did not respond to indomethacin but had dramatic improvement in urine output and urine osmolality after receiving intravenous ketorolac.
