Magnesium in CKD: more than a calcification inhibitor?

Abstract

Magnesium fulfils important roles in multiple physiological processes. Accordingly, a tight regulation of magnesium homeostasis is essential. Dysregulated magnesium serum levels, in particular hypomagnesaemia, are common in patients with chronic kidney disease (CKD) and have been associated with poor clinical outcomes. In cell culture studies as well as in clinical situations magnesium levels were associated with vascular calcification, cardiovascular disease and altered bone-mineral metabolism. Magnesium has also been linked to diseases such as metabolic syndrome, diabetes, hypertension, fatigue and depression, all of which are common in CKD. The present review summarizes and discusses the latest clinical data on the impact of magnesium and possible effects of higher levels on the health status of patients with CKD, including an outlook on the use of magnesium-based phosphate-binding agents in this context.

Fig. 1

Estimated survival probabilities in CKD patients with high (>2.2 mg/dL/>0.90 mmol/L), medium (1.8–2.2 mg/dL/0.74–0.90 mmol/L) and low (<1.8 mg/dL/<0.74 mmol/L) serum magnesium concentrations (adapted and reprinted from [2] with permission from Elsevier)

Fig. 2

Meta-analysis of prospective cohort studies examining magnesium intake and the risk of developing type 2 diabetes. M male, F female (adapted and reprinted from [63]. Copyright and all rights reserved. Material from this publication has been used with the permission of American Diabetes Association)

Fig. 3

Impact of phosphate binders on serum levels of the bone turnover marker β-CTX (beta-crosslaps). Time course of values at weeks 9 and 25 of the calcium acetate/magnesium carbonate group (n = 105) and of the sevelamer-HCl group (n = 99) is displayed in white and grey, respectively (adapted and reprinted from [28] by permission of Oxford University Press)