Background. Low serum magnesium has been associated with an increased cardiovascular risk in the general population and in dialysis patients. Our aim was to analyze the influence of serum magnesium on overall mortality and cardiovascular outcomes in patients with advanced CKD not yet on dialysis. Methods. Seventy patients with CKD stages 4 and 5 were included. After a single measurement of s-magnesium, patients were followed a mean of 11 months. Primary end-point was death of any cause, and secondary end-point was the occurrence of fatal or nonfatal CV events. Results. Basal s-magnesium was within normal range ( ？mg/dL), was lower in men and in diabetic patients , and was not different between patients with and without cardiopathy. Magnesium did not correlate with PTH, calcium, phosphate, albumin, inflammatory parameters (CRP), and cardiac (NT-proBNP) biomarkers but correlated inversely ; with the daily dose of loop diuretics. In univariate and multivariate Cox proportional hazard models, magnesium was not an independent predictor for overall mortality or CV events. Conclusions. Our results do not support that serum magnesium can be an independent predictor for overall mortality or future cardiovascular events among patients with advanced CKD not yet on dialysis. 1. Introduction Magnesium is predominantly an intracellular cation. Serum magnesium concentration does not reflect total body magnesium content since 60% is found in the skeleton, 39% intracellular and only 1% extracellular [1]. Magnesium (Mg) plays an important role in the regulation of vascular tone and heart rhythm [2, 3]. Magnesium deficiency has been reported to promote inflammation, and it decreases the specific immune response [4]. Magnesium also reduces total peripheral resistance by stimulation of nitric oxide synthesis [5] and is a potent inhibitor of vascular calcification [6–8]. In the general population, it seems that hypomagnesaemia may play a significant role in the development of cardiovascular disease [9, 10]. The gastrointestinal tract, the skeleton, and the kidneys are integrally involved in normal magnesium homeostasis. Renal failure is the most common cause of hypermagnesemia, which is usually mild and asymptomatic. In CKD, when GFR falls to below 30？mL/min, urinary Mg excretion may be insufficient to balance intestinal Mg absorption leading to chronic Mg overload [11]. However, some conditions can lead to negative Mg balance even in these patients, such as excessive intake of diuretics, reduced gastrointestinal intake, and a low Mg concentration of dialysate [12, 13].
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