MAGNESIUM AND CITRATE METABOLISM DISORDERS IN CHILDREN WITH COELIAC DISEASE

Abstract

Aim: Low urine citrate excretion may occur in coeliac patients with symptoms of Mg depletion, despite of normal plasma HCO3 and K levels. Aim was to evaluate the effect of Mg load dose on urine citrate excretion in 31 children, with coeliac disease without malabsorption syndrome. Methods: Mg loading test, serum Mg and K levels, urinary Mg and citrate excretion. Results: In 9 patients with Mg depletion confirmed with Mg loading test (Mg retention 66.9%) Mg infusion increased citraturia from 365.8 to 674.1 mg/1g creatinine (p = 0.0013). In 2 hypocitraturic patients the urine citrate excretion was increased from 23.3 to 504.1, and from 72.4 to 153.6 mg/1 g creatinine respectively. In the second patient with severe hypomagnesemia and hypokaliemia the test dose of Mg did not normalize citraturia. After 4 months of MgO administration the results normalized. In remaining 25 patients with normal results of Mg loading test (Mg retention 23.9%) i.v. administration of Mg increased urine citrate excretion from 448.9 to 706.8 mg/1g creatinine (p = 0.0008). Among 5 hypocitraturic patients the Mg depletion could be suspected in 3 children. Administration of Mg test dose increased citraturia from 219.4 to 515.9 mg/1g creatinine. Summary: Decreased citraturia was found in 7 out of 31 patients with coeliac disease. Five of them had biochemical symptoms of Mg depletion, and in their case the i.v. Mg loading test increased citraturia of more than 120% of the basic value. In remaining patients with normal citraturia, the i.v. Mg load led to marked increase of the urinary citrate excretion. Conclusions: Considerable increase of urine citrate excretion after Mg loading test suggests the link between Mg homeostasis and metabolism of citrate. Mg depletion may decrease citraturia directly, or secondarily, due to lower K stores, resulting in intracellular metabolic acidosis. Decreased diet Mg supply and/or defect of intestinal Mg absorption may lead to hypomagnesuria and secondary hypocitraturia, increasing the risk of calcium nephrolithiasis.