«RESULTS: BGP is a Pi-donor that requires enzymatic cleavage in order to release Pi. As Pi exposure is one of the decisive factors in the calcificationprocess, the Pi concentration of the cell culture supernatant was assessed after 2, 8 and 14 days of treatment (Fig. 1). 10 mM BGP treatment resulted in gradual increase in Pi concentration over time, reaching 4.6 ± 0.3 mM after 14 days. 2 mM Mg2+ supplementation led to significantly higher Pi concentration of 7.6 ± 0.8 mM after 14 days. In contrast, BGP treatment in cell-free conditions did notlead to increased Pi concentration under the same conditions (data not shown).»
Introduction: Chronic kidneydisease (CKD) is associated with high cardiovascular morbidity and mortality. Recent evidence suggests that increases in both serum and intracellular magnesium (Mg) can slow or even prevent the development of vascular calcification seen in CKD. Serumcalcification propensity (T50) is a novel functional test, which is associated with all-causemortality in CKD and measures the ability of serum to delay the formation of crystalline nanoparticles. Theoretically, increasing serum Mg should improve T50 and thereby reduce the propensity towards ectopic calcification.
Methods: We conducted a randomizedplacebo-controlled double-blinded clinical trial to investigate the safety of 2 different doses of oral Mg supplementation in subjects with CKD stages 3 and 4 as well as their effects on intracellular Mg and T50. Thirty-six subjects with CKD stages 3 and 4 were randomized to one of 3 groups (placebo, elemental Mg 15 mmol/d or elemental Mg 30 mmol/d) given as slow-release Mg hydroxide and followed for 8 weeks.
Results: Thirty-four subjects completed the trial. Intracellular Mg remained stable throughout the trial despite significantincreases in both serum and urine Mg. T50 increasedsignificantly by 40 min from 256 ± 60 (mean ± SD) to 296 ± 64 minutes (95% confidence interval, 11-70, P < 0.05) in the Mg 30 mmol/d group after 8 weeks. No serious adverse events related to the study medication were reported during the study.
Discussion: Oral Mg supplementation was safe and well tolerated in CKD stages 3 and 4 and improved T50, but did notincrease intracellular Mg. Further studies are needed to investigate the long-termeffects of Mg supplementation in CKD stage 3 and 4 and whether improvement in calcification propensity is related to clinical endpoints.
Patients and methods: Seventy-two stable hemodialysispatients were randomly allocated to two groups: 36 administered a regimen containing magnesium carbonate plus calciumacetate as a phosphate binder (Mg group), while the rest 36 received calciumacetate alone (Ca group). The presence and the progression of arterial calcifications were evaluated in plain X-rays using a simple vascular calcification score. The duration of the follow-up period was 12 months.
Results: Thirty-two patients of the Mg group and 27 of the Ca group completed the study. The mean time average values of the biochemical laboratories did not differ between the two groups, except serum Mg: 2.83 + 0.38 in the Mg group versus 2.52 + 0.27 mg/dl in the Ca group, p = 0.001. In 9/32 (28.12 %) patients of the Mg group and in 12/27 (44.44 %) patients of the Ca group, the arterial calcifications were worsened, p = 0.276. Moreover, in 4/32 (15.6 %) patients of the Mg group and in 0/27 (0 %) patients of the Ca group, they were improved, p = 0.040. The multivariate logistic regression analysis revealed that serummagnesium was an independent predictor for no progression of the arterial calcifications, p = 0.047.