Abstract
Vascular calcification (VC) is common in dialysis and non-dialysis chronic kidney disease (CKD) patients, even in the early stage of the disease. For this reason, it can be considered a CKD hallmark. VC contributes to cardiovascular disease (CVD) and increased mortality among CKD patients, although it has not been proven. There are more than one type of VC and every form represents a marker of systemic vascular disease and is associated with a higher prevalence of CVD in CKD patients, as shown by several clinical studies. Major risk factors for VC in CKD include: Increasing age, dialysis vintage, hyperphosphatemia (particularly in the setting of intermittent or persistent hypercalcemia), and a positive net calcium and phosphate balance. Excessive oral calcium intake, including calcium-containing phosphate binders, increases the risk for VC. Moreover, it has been demonstrated that there is less VC progression with non-calcium-containing phosphate binders. Unfortunately, until now, a specific therapy to prevent progression or to facilitate regression of VC has been found, beyond careful attention to calcium and phosphate balance.
Highlights
Cardiovascular disease (CVD) is the most common cause of death in patients with chronic kidney disease (CKD) [1]
High circulating calcitriol levels caused by loss of Fibroblast Growth Factor 23 (FGF23) function are not detrimental per se, but the toxicity is rather greatly caused by hyperphosphatemia and hypercalcemia, both induced by increased vitamin D activity
calcifying cells (CCCs) have been associated with coronary artery disease and calcific aortic stenosis, in both advanced CKD and diabetes [34,35,36]
Summary
Cardiovascular disease (CVD) is the most common cause of death in patients with chronic kidney disease (CKD) [1]. PiT-2 [12], which upregulates genes associated with matrix mineralization [5,7,12,13] Hypercalcemia and hyperphosphatemia both increase the release of matrix vesicles, resulting in the deposition of hydroxyapatite in the extracellular matrix [14,15]. Many of the factors that cause medial calcification (hyperphosphatemia, hypercalcemia, and hyperparathyroidism) probably worsen intimal calcification. Elevated circulating levels of FGF23 lead to phosphate-wasting disorders, and strongly suppresses renal 1α-hydroxylase expression, causing a reduction of the synthesis of the vitamin D hormone 1α,25-dihydroxyvitamin D3 in kidney proximal tubules [18]. High circulating calcitriol levels caused by loss of FGF23 function are not detrimental per se, but the toxicity is rather greatly caused by hyperphosphatemia and hypercalcemia, both induced by increased vitamin D activity
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