The impact of Magnesium (Mg) on mineral metabolism in diabetic or non-diabetic patients with chronic kidney diseases (CKD)

Abstract

Renal handling of magnesium (Mg) is adaptive mechanism, but it’s affected when renal function declines. In moderate chronic kidney disease (CKD), loss of glomerular filtration is compensated by higher fractional excretion of Mg. In more advanced CKD however, (creatinine clearance <30 mL/min), overt hypermagnesemia develops frequently. Various studies show that increased serum Mg (sMg) lowers PTH, others do not prove the suggestion. Although the exact role of Mg in bone metabolism is unclear, it may have both positive and negative effects. The aim of this study is to investigate the impact of sMg on bone mineral metabolism in CKD patients with or without diabetes. 62 CKD patients (not receiving dialysis) were divided into two groups: 1 st group (32 CKD diabetic patients); 2 nd group (30 CKD patients without diabetes). Biochemical determinations were made, and the estimated glomerular filtration rate (GFR) was measured. Bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry. sMg was inversely correlated with sCa (P<0.02) and with parathyroid hormone (sPTH) (P<0.05), with alkaline phosphatase (AP) (P<0.02), and with phosphate (P) (P<0.01) in 1 st group (diabetic). The CKD diabetic patients had lower serum albumin (ALB) and a higher hypomagnesemia and osteoporosis than the nondiabetic patients. sMg inversely correlated with e-GFR in the CKD patients in both groups. sMg showed higher correlation with 25-hydroxyvitamin D in 2 nd non-diabetic group (P<0.01); diabetic patients with higher sMg had a lower iPTH. The lower sMg subgroup showed a higher incidence of osteoporosis than the moderate and higher sMg subgroups did. In conclusion, low sMg may impact iPTH and enlarge osteoporosis in CKD patients, particularly with diabetes.