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Vascular calcification in end‐stage renal disease
Author(s) -
Jablonski Kristen L.,
Chonchol Michel
Publication year - 2013
Publication title -
hemodialysis international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.658
H-Index - 47
eISSN - 1542-4758
pISSN - 1492-7535
DOI - 10.1111/hdi.12084
Subject(s) - medicine , cardiology , calcification , vascular smooth muscle , population , proinflammatory cytokine , arterial stiffness , myocardial infarction , kidney disease , endocrinology , blood pressure , inflammation , environmental health , smooth muscle
Vascular calcification is highly prevalent in end‐stage renal disease and independently predictive of future cardiovascular events and mortality. C alcification can occur in both the intimal and medial layers of vasculature, but medial calcification is the major form in end‐stage renal disease. Medial calcification increases large elastic artery stiffness and pulse‐pressure, promotes left ventricular hypertrophy, reduces perfusion of the coronary arteries, and ultimately promotes increased cardiovascular mortality via increased risk of myocardial infarction and heart failure. It results not from a passive deposition of calcium and phosphate due to increased circulating levels, but rather is an active cell‐mediated process involving vascular smooth muscle cell apoptosis and vesicle release, a shift in the balance of inhibitors and promoters of vascular calcification, and vascular smooth muscle cell differentiation from a contractile to osteochondrogenic phenotype. This phenotypic shift requires phosphate, as well as the uptake of phosphate by the sodium‐dependent phosphate cotransporter PiT ‐1, which is upregulated by proinflammatory cytokines and the uremic milieu. Further research is needed to determine if targeting these processes can ultimately reduce vascular calcification in this high cardiovascular risk population.