Association of Gitelman’s Syndrome and Focal Glomerulosclerosis

Dear Sir, Gitelman’s syndrome, also known as the hypocalciuric variant of Bartter’s syndrome or familial hypokalemia-hypomagnesemia, is a primary renal tubular disorder characterized by chronic hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria with normocalcemia, hyperreninemic hyperaldosteronism and normal renal function [1, 2]. It has been suggested that the primary defect is in the loop of Henle in Bartter’s syndrome and in the distal tubulus in Gitelman’s syndrome [3]. A 21-year-old male patient was admitted with complaints of lassitude, dizziness, syncopal attacks, occasional numbness in the hands and feet, and muscle cramps. Physical examination was not remarkable. Blood pressure was 90/60 mm Hg, plasma potassium levels ranged between 2.9 and 3.2 mEq/l. Serum magnesium and calcium levels were 1.5 and 9.8 mg/dl, respectively. On analysis of blood gases, pH was found to be between 7.495 and 7.528. Calcium excretion was 7.2 mg/day. The plasma renin level was 9.4 ng/ml (normal values <5.6 ng/ml) and the plasma aldosterone level was 325.3 pg/ml (normal values between 35 and 300 pg/ml). Serum urea (45 mg/dl) and creatinine (1.2 mg/dl) levels were normal. Considering these data this patient was diagnosed as having Gitelman’s syndrome. This syndrome is known as a benign disorder [1]. However, long-term hypokalemia may have some deteriorating effects on the kidney [4]. Apart from this point of view, with the informed consent of the patient, a renal biopsy was performed. The renal biopsy revealed focal glomerulosclerosis, and it was thought that this histopathologic diagnosis may be the result of long-term hypokalemia in Gitelman’s syndrome. Because focal glomerulosclerosis progresses to end-stage renal failure, this observation suggests that patients with Gitelman’s syndrome should be evaluated for the presence of this type of glomerulopathy.