Magnesium status in idiopathic calcium urolithiasis--an orientational study in younger males.

Abstract

With the aim of revealing a possible magnesium (Mg) deficiency in the aetiology of idiopathic recurrent calcium urolithiasis we studied the Mg content of red blood cells, serum total, protein-bound, ionised and complexed fractions of Mg, and urinary Mg after an overnight fast. The two study groups comprised 12 male recurrent calcium urolithiasis patients and 12 healthy male controls (mean age 31 and 29 years, respectively). In recurrent calcium urolithiasis, serum albumin and Mg of erythrocytes were significantly decreased, as was serum total and protein-bound Mg, whereas serum ultrafiltrable, ionised and complexed Mg were statistically indistinguishable from values in controls. Urinary Mg (per unit creatinine) in recurrent calcium urolithiasis (mean 0.188 vs 0.209 in controls; p = 0.386) was not statistically different, whereas urinary total protein, glucose, and pH were significantly increased. The renal clearances of Mg and glucose were positively correlated (r = 0.56; p < 0.01), with a steeper slope in recurrent calcium urolithiasis than controls. Further fractionation of serum and urinary Mg into ions and complexes in recurrent calcium urolithiasis subjects with identical creatinine clearance revealed no statistical difference between 1) Mg ions and complexes filtered by renal glomeruli; 2) Mg ions and complexes excreted in urine; 3) fractional Mg excretion. Median urine supersaturation with respect to calcium oxalate was insignificantly lower (1.5 vs 2.2), with respect to hydroxyapatite insignificantly higher (3.3 vs 1.8), than in controls. It is concluded that relatively young recurrent calcium urolithiasis patients exhibit a deficiency of Mg in erythrocytes and serum total Mg, but no alteration of renal Mg handling. Thus, in recurrent calcium urolithiasis, a role of Mg deficiency in urine as a factor initiating stone formation may be ruled out, whereas a possible link between cellular Mg deficiency and the impairment of renal tubular functions involved in reabsorption of glucose and proteins, and in urine acidification, deserves further studies.