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Table 1. Characteristics of the 62 non-dialysis CKD patients with or without diabetes  Discussion and Conclusion  of 4-7pmol/L, 7-10pmol/L, and 15-20pmol/L, respectively. The reference range of ALP was 50-130 (U/L) for laboratory used; vitamin D deficiency is defined as serum 25(OH)D<20ng/mL and vitamin D insufficiency - as 25(OH)D<30ng/mL. Bone mineral density at the both femoral necks and lumbar spine (L1-L4) was measured by dual- energy X-ray absorptiometry. Definition of CKD stages was based upon guidelines for the management of CKD.  Mg imbalance has been neglected in disorders of bone mineral metabolism of patients with CKD [1,3,7,8]. Our study may give an additional light for improvement of medical care in CKD patients, with and without diabetes. Low serum Mg levels may cause wrong increase of PTH and may further lead to bone diseases in CKD patients, especially with diabetes. For these patients, adequate Mg intake by diet or supplement may reduce the development of low turnover bone disease [2,8,12,13]. Oppositely, the inhibitory effect of a high sMg on PTH secretion may be offset by the stimulation produced through low serum Ca in moderate-severe CKD patients, who are not receiving dialysis [5,7,9]. These patients must maintain a sCa within optimal range and avoid consuming excess Mg and, to reduce the risk of low-turnover bone diseases [7,13-15]. A routine monitoring of sMg, and balancing sCa and sMg are important in the assessment and management of bone mineral disorders in CKD patients with or without diabetes.

Table 1 Characteristics of the 62 non-dialysis CKD patients with or without diabetes Discussion and Conclusion of 4-7pmol/L, 7-10pmol/L, and 15-20pmol/L, respectively. The reference range of ALP was 50-130 (U/L) for laboratory used; vitamin D deficiency is defined as serum 25(OH)D<20ng/mL and vitamin D insufficiency - as 25(OH)D<30ng/mL. Bone mineral density at the both femoral necks and lumbar spine (L1-L4) was measured by dual- energy X-ray absorptiometry. Definition of CKD stages was based upon guidelines for the management of CKD. Mg imbalance has been neglected in disorders of bone mineral metabolism of patients with CKD [1,3,7,8]. Our study may give an additional light for improvement of medical care in CKD patients, with and without diabetes. Low serum Mg levels may cause wrong increase of PTH and may further lead to bone diseases in CKD patients, especially with diabetes. For these patients, adequate Mg intake by diet or supplement may reduce the development of low turnover bone disease [2,8,12,13]. Oppositely, the inhibitory effect of a high sMg on PTH secretion may be offset by the stimulation produced through low serum Ca in moderate-severe CKD patients, who are not receiving dialysis [5,7,9]. These patients must maintain a sCa within optimal range and avoid consuming excess Mg and, to reduce the risk of low-turnover bone diseases [7,13-15]. A routine monitoring of sMg, and balancing sCa and sMg are important in the assessment and management of bone mineral disorders in CKD patients with or without diabetes.