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tients [4] . This elegant observational analysis illustrates that patients with higher pulse pressure (PP) ( ≥ 65 mm Hg) (p = 0.01), left ventricular hypertrophy (LVMI ≥ 125 g/m 2 ) (p = 0.02), and higher VC (SVCS ≥ 3) (p = 0.008) have significantly lower serum Mg concentrations. In addition, Kaplan-Meier analysis shows that both all-cause and CV mortality were associated with a significant lower 48-month survival in HD patients with the level of serum Mg being lower than 1.15 mmol/l, thereby assigning Mg a role of a ‘renewed’ independent negative predictor of mortality. A growing body of evidence is suggesting a potential role for Mg in different diseases such as CKD-MBD, diabetes, low insulin resistance, poor endothelial reactivity, higher oxidative stress, increased intima-media thickness, vascular calcification, progression of CKD, and mortality [5] . Nevertheless, the maintenance of adequate intracellular Mg levels appears essential for life per se, considering that Mg is a fundamental co-enzyme of vital biochemical reactions just like Krebs cycle and glycolysis and it is essential for the maintenance of RNA and DNA stability. Thus, Mg may represent a cardinal biomarker and regulator of vascular aging in humans, with special emphasis in CKD patients. Furthermore, nephrologists are called to a growing comprehension of Mg physiology as a consequence of the renewed adoption of Mg as a phosphate

A Renewed Question in Haemodialysis Patients: Should We Correct Low Serum Magnesium Levels?