Pathophysiological Role of Magnesium in Familial Bartter's Syndrome.

Abstract

Westudied three siblings with Bartter's syndrome associated with hypomagnesemia;two of them showing marked hypomagnesemiaand the other mild hypomagnesemia.Urinary potassium, sodium and chloride excretions were determined and distal fractional chloride reabsorption and free water clearance on water loading test were comparedbefore and after magnesiumsupplementation. Baseline urinary potassium and magnesiumexcretions were elevated in spite of the decreased plasma levels, whereas distal fractional chloride reabsorption and free water clearance were depressed in all patients. Magnesiumrepletion resulted in significant decrease in urinary potassium, sodium and chloride and subsequent increase in plasma potassium in all patients. However,neither distal fractional chloride reabsorption nor free water clearance was affected. Hypomagnesemiamay contribute to urinary potassium wasting and aggravate urinary sodium and chloride wasting in familial Bartter's syndrome by a mechanism independent of the defect in free-water formation by the active reabsorption of chloride in Henle's loop. (Internal Medicine 33: 1-5, 1994)

Electrolyte Replacement in Bartter Syndrome With Abnormal Small Bowel: A Case Report

“…The current accepted pathophysiological mechanism is the reduction of potassium absorption back into the tubules causing an imbalanced electrochemical gradient. [4][5][6] In patients with kidney disease, electrolyte homeostasis can be maintained in part by absorption in the gastrointestinal tract. 7 Potassium and magnesium absorption in the small intestine do vary somewhat based on location.…”