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Clinical |
Home Peritoneal Dialysis Unit,1 University Health Network and University of Toronto, Toronto, Ontario, Canada; Department of Nephrology,2 Guangxi People's Hospital, Guangxi, P. R. China; Al-Fatah University,3 Tripoli Central Hospital, Tripoli, Libya
Correspondence to: D.G. Oreopoulos, Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario M5T 2S8 Canada.dgo{at}teleglobal.ca
Secondary hyperparathyroidism is present in most patients with end-stage
renal disease and has been linked to uremic bone disease, vascular
calcification, and mortality. Current literature suggests an association
between hypomagnesemia and cardiovascular disease in the general population.
We reviewed all published studies on the relationship between serum magnesium
and parathyroid hormone and the relationship between serum Mg and vascular
calcification in dialysis patients. Of these, 10 of 12 studies of patients on
hemodialysis and 4 of 5 studies of patients on peritoneal dialysis showed a
significant inverse relationship between serum Mg and serum intact parathyroid
hormone. Hyperparathyroidism develops in peritoneal dialysis patients dialyzed
with a solution containing normal calcium (1.25 mmol/L) and low Mg (0.25
mmol/L), even though serum calcium is maintained at a normal level. Four of
the hemodialysis studies and one of the peritoneal dialysis studies indicated
that there is an inverse relationship between serum Mg and vascular
calcification in these patients. Potential benefits have been attributed to
magnesium carbonate as a phosphate binder and it may possibly be an effective,
less toxic, less expensive phosphate binder. We believe that the role of Mg in
secondary hyperparathyroidism and vascular calcification merits further
investigation.
KEY WORDS: Magnesium; parathyroid hormone; vascular calcification; phosphate control.
Received 13 June 2005; accepted 3 October 2005.
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