B- CRF : Rheumatological and mineral complications
C- 05 : Hyperphosphatemia
E- 01 : Peripheral artery disease
Magnesium and cardiovascular complications of chronic kidney disease
Ziad A. Massy & Tilman B. Drüeke
Journal : Nature Reviews Nephrology
Year : 2015/ Month : July
Volume : 11
Pages : 432–442
doi:10.1038/nrneph.2015.74
ABSTRACT
Cardiovascular complications are the leading cause of death in patients with chronic kidney disease
(CKD). Abundant experimental evidence suggests a physiological role of magnesium in cardiovascular
function, and clinical evidence suggests a role of the cation in cardiovascular disease in the general
population. The role of magnesium in CKD–mineral and bone disorder, and in particular its impact on
cardiovascular morbidity and mortality in patients with CKD, is however not well understood.
Experimental studies have shown that magnesium inhibits vascular calcification, both by direct effects
on the vessel wall and by indirect, systemic effects. Moreover, an increasing number of epidemiologic
studies in patients with CKD have shown associations of serum magnesium levels with intermediate
and hard outcomes, including vascular calcification, cardiovascular events and mortality. Intervention
trials in these patients conducted to date have had small sample sizes and have been limited to the
study of surrogate parameters, such as arterial stiffness, vascular calcification and atherosclerosis.
Randomized controlled trials are clearly needed to determine the effects of magnesium
supplementation on hard outcomes in patients with CKD.
COMMENTS
The kidney is a major regulator of magnesium homeostasis. In patients with moderate chronic kidney
disease (CKD) serum magnesium levels are maintained within normal limits by an increase in fractional
excretion to compensate for the loss of glomerular filtration. As disease severity increases this
compensatory mechanism becomes insufficient, and overt hypermagnesaemia may develop in patients
with end-stage renal disease (ESRD).
Magnesium deficiency and/or hypomagnesaemia are often associated with hypocalcaemia and
hypokalaemia. Hypomagnesaemia can lead to impaired exercise capacity, sarcopenia and, in more
severe forms, general weakness, neuromuscular hyperexcitability with hyper-reflexia, carpopedal
spasm and seizure, whereas hypermagnesaemia owing to severe magnesium excess may induce loss
of deep tendon reflexes, respiratory paralysis, hypotension and loss of consciousness.
This review analyses in depth the present knowledge of magnesium disturbances in CKD patients and
try to define optimal nutritional recommandations for avoiding the magnesium impact on vascular
calcifications.
Ample evidence from experimental and clinical studies suggests a role for disturbed magnesium
metabolism in cardiovascular disease. In the advanced stages of CKD serum magnesium levels and
magnesium balance are often altered, and these alterations might contribute to the dramatic increase
in cardiovascular events and mortality observed in the CKD population.
The relative contribution of magnesium versus other more CKD-specific factors to the increase in
cardiovascular disease, however, remains uncertain. Several studies have reported associations of
serum magnesium levels with surrogate parameters of cardiovascular disease, and with hard
outcomes—including all-cause mortality—in patients with CKD. In addition small intervention studies
have suggested a potentially favourable role of oral magnesium supplementation in this population.
However, given the preliminary nature of these studies, a definitive statement as to a possible clinical
benefit of magnesium supplementation cannot be made at present.
Pr. Jacques CHANARD
Professor of Nephrology