Journal Article

Hyperphosphataemia as a cardiovascular risk factor – how to manage the problem

Jorge B. Cannata‐Andía and Minerva Rodríguez‐García

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 17, issue suppl_11, pages 16-19
Published in print November 2002 | ISSN: 0931-0509
Published online November 2002 | e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/ndt/17.suppl_11.16
Hyperphosphataemia as a cardiovascular risk factor – how to manage the problem

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Hyperphosphataemia is a frequent and important cardiovascular risk factor in patients with chronic kidney disease (CKD). High phosphate levels may influence vascular calcifications by two separate mechanisms: by worsening secondary hyperparathyroidism, which in turn facilitates calcification, and by promoting calcium phosphate deposition in pre‐formed endothelial plaques and in the arterial wall. Recent studies have shown that hyperphosphataemia induces the proliferation and differentiation of endothelial vascular cells into osteoblast‐like cells, promoting vascular calcification. High phosphate levels also increase the risk of mortality in patients with CKD. To reduce the negative impact of high phosphate, serum phosphate levels should be <5 mg/dl and serum calcium <10 mg/dl. This allows the calcium×phosphate product to be maintained at ⩽50 mg2/dl2, reducing the risk of vascular, valvular, and extraskeletal calcification. A multiple‐factor approach can be used to reduce serum phosphate: (i) decrease bone resorption by maintaining adequate serum parathyroid hormone levels; (ii) reduce phosphorous intake in the diet, (iii) use phosphate binders efficiently; and (iv) avoid under‐dialysis. The patient's diet should be high in nutrition but with the lowest possible phosphorous content. Doses of phosphate binders should be tailored to individual dietary habits and must be taken during meals in a dose proportional to the phosphorous content of the meal. Because of the risk of increased extraskeletal calcification, calcium‐containing phosphate‐binder intake should not exceed 2–3 g/day. Sevelamer hydrochloride, a non‐calcium and non‐aluminium phosphate binder with a potency similar to that of calcium salts has shown beneficial effects on lipid profiles. Better control of serum phosphate is achieved in patients on continuous ambulatory peritoneal dialysis than in those on haemodialysis. Removal of phosphate is directly correlated with duration and frequency of dialysis sessions. Thus, it is advisable not to reduce the duration of dialysis sessions to <4 h three times per week.

Keywords: cardiovascular; chronic kidney disease; hyperphosphataemia; secondary hyperparathyroidism; vascular calcification

Journal Article.  0 words. 

Subjects: Nephrology

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