Hypomagnesaemia, the kidney and the vessels

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The morbidity and mortality of chronic kidney disease (CKD) and dialysis patients remain excessive, despite increasing knowledge on the role of a multitude of cardiovascular risk factors. As a hallmark of this, randomized controlled trials (RCTs) in these populations failed to demonstrate survival benefit of interventions successfully targeted on well-accepted risk factors in the general population or on dialysis efficiency [1]. Extensive research has confronted the nephrology community with a complex and elusive network of pathophysiological pathways. In contrast, our knowledge of basic elements, such as magnesium, remains surprisingly scarce. Nevertheless, emerging evidence, be it mostly circumstantial, from in vitro and in vivo studies, indicates that hypomagnesaemia, or rather a magnesium deficit per se might convey nephrotoxicity together with negative cardiovascular effects. Alternatively, higher serum magnesium levels might be beneficial. This review aims to further critically appraise and outline this premise. Of importance, the interventional trials targeting magnesium status in CKD and dialysis patients are almost non-existent. Confounding by unmeasured residual subclinical disease and multicollinearity could subsequently hamper the interpretability of the observational evidence. Hypomagnesaemia might merely be considered a 'risk marker' rather than 'risk factor'. Future studies in the CKD and dialysis population therefore should meticulously address causality in order to allow the development of guidelines on optimal target values.