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BEST FORM OF MAGNESIUM FOR KIDNEY DISEASE TRIAL
So far, one double-blind, placebo-controlled randomised trial examined the efficacy of oral magnesium oxide (440 mg three times per week for 6 months) on endothelial function in HD patients. Furthermore, an observational cohort study, investigating 283 CKD patients, reported an association of high magnesium levels with less endothelial dysfunction. Similarly, a cohort study of 512 renal transplant recipients identified low magnesium levels as a predictor of PWV and thus of vascular stiffness, independent of clinically relevant covariates and especially in older patients. In addition, CKD patients with higher magnesium serum concentrations had a significantly lower pulse wave velocity (PWV). A prospective study in 47 HD patients revealed an association of magnesium serum concentration with the intima–media thickness of carotid arteries. The clinical relation between serum magnesium and vascular changes including calcification was assessed in several recent studies. This suggests that in CKD, local magnesium homoeostasis is disturbed and potentially aggravates vascular calcifications. In the context of these data, microcalcifications in human atherosclerotic lesions contain both calcium and magnesium (in the form of whitlockite and calcium phosphate/apatite) whereas CKD- accelerated calcification was associated with a predominant deposition of calcium phosphate/apatite. Inhibition of the Wnt/β-catenin signalling pathway was identified as one of the intracellular mechanisms by which the anti-calcifying effect of magnesium is achieved. Additionally, increasing magnesium concentrations improved cell viability and normalised the cellular release of proteins involved in vascular calcification. These studies suggested a potentially active intracellular role for magnesium ions in attenuating the vascular calcification process. The first in vitro evidence in human aortic VSMCs for a protective role of magnesium on phosphate-induced calcification was based on the observation that living cells are necessary for magnesium ions to exert its protective effect. Moreover, higher magnesium levels prevented calcification of bovine VSMCs, inhibited expression of osteogenic proteins, apoptosis and further progression of already established calcification. These results were extended by recent studies in which magnesium was shown to inhibit phosphate-induced calcification in vitro. Several cell culture and animal studies suggest a protective role of magnesium through multiple molecular mechanisms. These disturbances promote vascular calcification, whereby vascular smooth muscle cells (VSMCs) play a central role in the pathogenesis by undergoing an osteochondrogenic phenotype change in response to elevated phosphate levels. The progressive loss of kidney function is accompanied by elevated serum fibroblast growth factor 23 (FGF23) levels, a decrease in inorganic phosphate excretion and dysregulation of mineral and bone metabolism. The molecular mechanisms leading to vascular calcification in CKD patients are still under investigation, but there is consensus that it is an active, multifactorial, cell-mediated and dynamic process. The high prevalence of vascular calcification contributes significantly to this cardiovascular risk. Ĭardiovascular disease (CVD) is the leading cause of death in the CKD population. Furthermore, magnesium was identified as an independent risk factor for non-recovery of renal function in a cohort of critically ill patients with acute kidney injury. 1) and kidney function decline in CKD patients as well as mortality in haemodialysis (HD) patients. For instance, two cohort studies established hypomagnesaemia as a predictor of mortality (Fig. Given the growing interest in the molecule since then the literature on the role of magnesium in CKD has continued to accumulate substantially. In 2012, several reviews on magnesium metabolism and disorders in magnesium balance were published in a special issue of the Clinical Kidney Journal. While clinical issues regarding magnesium disorders had received surprisingly little attention until the 1990s, a shift in focus led to some clinical investigations, especially in patients with chronic kidney disease (CKD).
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Over 300 enzymes require the presence of magnesium for their catalytic action, including many enzymes utilising or synthesising ATP, or those that use other nucleotides to synthesise DNA and RNA. As the fourth most abundant cation in the body, magnesium fulfils an important role in multiple physiological processes.