T Y Chan1. 1. Department of Clinical Pharmacology, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong.
Abstract
OBJECTIVE: To describe 2 patients with severe indapamide-induced hyponatremia and hypokalemia and to discuss the incidence and mechanisms of diuretic-induced hyponatremia and hypokalemia. CASE SUMMARY: Two women aged 60 and 62 years presented with severe hyponatremia (plasma sodium concentrations of 103-104 mmol/L) and hypokalemia (plasma potassium concentrations of 1.6-2.2 mmol/L) 5-6 weeks after they received indapamide 2.5 mg/d therapy for arterial hypertension. Central nervous system symptoms of hyponatremia were observed in both patients. One patient experienced severe postural hypotension, a plasma potassium concentration of 1.6 mmol/L, and electrocardiographic abnormalities consistent with hypokalemia. Hyponatremia was initially mistaken in this patient for the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Both patients recovered completely after withdrawal of indapamide therapy and correction of the hyponatremia and hypokalemia. DISCUSSION: Previous studies of administration of indapamide 2.5 mg/d for 10-24 months in hypertensive patients showed a low incidence (0.6-1.2%) of hypokalemia severe enough to require withdrawal of drug therapy. Serum sodium concentrations were unaltered in these studies. All case reports, except 1, of indapamide-induced electrolyte disturbances described only hypokalemia. CONCLUSIONS: Indapamide can cause both severe hypokalemia and hyponatremia. The predominant clinical features can be a result of severe hyponatremia. The latter can have diverse clinical presentations and may be mistaken for SIADH. As with other diuretics, plasma sodium and potassium concentrations must be monitored during indapamide therapy, especially in patients at risk for hyponatremia and hypokalemia.
OBJECTIVE: To describe 2 patients with severe indapamide-induced hyponatremia and hypokalemia and to discuss the incidence and mechanisms of diuretic-induced hyponatremia and hypokalemia. CASE SUMMARY: Two women aged 60 and 62 years presented with severe hyponatremia (plasma sodium concentrations of 103-104 mmol/L) and hypokalemia (plasma potassium concentrations of 1.6-2.2 mmol/L) 5-6 weeks after they received indapamide 2.5 mg/d therapy for arterial hypertension. Central nervous system symptoms of hyponatremia were observed in both patients. One patient experienced severe postural hypotension, a plasma potassium concentration of 1.6 mmol/L, and electrocardiographic abnormalities consistent with hypokalemia. Hyponatremia was initially mistaken in this patient for the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Both patients recovered completely after withdrawal of indapamide therapy and correction of the hyponatremia and hypokalemia. DISCUSSION: Previous studies of administration of indapamide 2.5 mg/d for 10-24 months in hypertensivepatients showed a low incidence (0.6-1.2%) of hypokalemia severe enough to require withdrawal of drug therapy. Serum sodium concentrations were unaltered in these studies. All case reports, except 1, of indapamide-induced electrolyte disturbances described only hypokalemia. CONCLUSIONS:Indapamide can cause both severe hypokalemia and hyponatremia. The predominant clinical features can be a result of severe hyponatremia. The latter can have diverse clinical presentations and may be mistaken for SIADH. As with other diuretics, plasma sodium and potassium concentrations must be monitored during indapamide therapy, especially in patients at risk for hyponatremia and hypokalemia.