Abstract
Patients with advanced chronic kidney disease exhibit an increase in cardiovascular mortality. Recent works have shown that low levels of magnesium are associated with increased cardiovascular and all-cause mortality in hemodialysis patients. Epidemiological studies suggest an influence of low levels of magnesium on the occurrence of cardiovascular disease, which is also observed in the normal population. Magnesium is involved in critical cellular events such as apoptosis and oxidative stress. It also participates in a number of enzymatic reactions. In animal models of uremia, dietary supplementation of magnesium reduces vascular calcifications and mortality; in vitro, an increase of magnesium concentration decreases osteogenic transdifferentiation of vascular smooth muscle cells. Therefore, it may be appropriate to evaluate whether magnesium replacement should be administered in an attempt to reduce vascular damage and mortality in the uremic population In the present manuscript, we will review the magnesium homeostasis, the involvement of magnesium in enzymatic reactions, apoptosis and oxidative stress and the clinical association between magnesium and cardiovascular disease in the general population and in the context of chronic kidney disease. We will also analyze the role of magnesium on kidney function. Finally, the experimental evidence of the beneficial effects of magnesium replacement in chronic kidney disease will be thoroughly described.
Highlights
Magnesium has been shown to influence pulse pressure (PP) in patients with chronic kidney disease (CKD) Stages 2–4, defined in terms of the estimated glomerular filtration rate (GFR) according to the formula derived from the Modification of Diet in Renal Disease Study (MDRD) [66]
Magnesium levels diminished according to the progression of CKD and were significantly associated with increased PP (OR = 0.550; 95% CI, 0.305–0.727, p = 0.016)
Dey et al found a relationship between hypomagnesemia and dyslipidemia in patients in CKD Stages 2–5; in particular, Mg levels were found to be significantly associated with total, HDL, LDL and non-HDL cholesterol; in addition, all these parameters correlated with CKD severity [71]
Summary
Magnesium (Mg) is one of the most abundant cations in organisms [1], and it is involved in a number of physiological processes such as enzymatic reactions and membrane and structural functions [2]. Mg (60–65%), buffering changes in Mg level; tissue compartments, mainly skeletal muscle, represent approximately 35% of total Mg, whereas only 1–2% Mg is present in the extracellular fluid [1]. Three different organs are responsible for Mg homeostasis: intestine, where absorption takes place; takes place; bone, responsible storage; and kidneys, controllingIntestinal. Magnesium reabsorption takes place in the various parts of the Magnesium reabsorption takes place in thepassive variousparacellular parts of thetransport nephronoccurs through different mechanisms: nephron through different mechanisms: in the proximal tubule passive paracellular transport occurs in the proximal tubule and the thick ascending limb, and the thick ascending limb, where 10–25% and 70% of Mg is absorbed, respectively.
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