A. Schmiedl et Po. Schwille, MAGNESIUM STATUS IN IDIOPATHIC CALCIUM UROLITHIASIS - AN ORIENTATIONAL STUDY IN YOUNGER MALES, European journal of clinical chemistry and clinical biochemistry, 34(5), 1996, pp. 393-400
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. Th
e two study groups comprised 12 male recurrent calcium urolithiasis pa
tients and 12 healthy male controls (mean age 31 and 29 years, respect
ively). In recurrent calcium urolithiasis, serum albumin and Mg of ery
throcytes 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 urolithias
is than controls. Further fractionation of serum and urinary Mg into i
ons and complexes in recurrent calcium urolithiasis subjects with iden
tical creatinine clearance revealed no statistical difference between
1) Mg ions and complexes filtered by renal glomeruli; 2) Mg ions and c
omplexes excreted in urine; 3) fractional Mg excretion. Median urine s
upersaturation with respect to calcium oxalate was insignificantly low
er (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 handli
ng. Thus, in recurrent calcium urolithiasis, a role of Mg deficiency i
n urine as a factor initiating stone formation may be ruled out, where
as a possible link between cellular Mg deficiency and the impairment o
f renal tubular functions involved in reabsorption of glucose and prot
eins, and in urine acidification, deserves further studies.