Reduced kidney function causes an impairment of mineral metabolism, especially regarding phosphate and calcium. The classic review “Cardiovascular risk in chronic kidney disease: the CKD–mineral bone disorder (CKD-MBD)” describes how high levels of phosphate can stimulate vascular smooth muscle cells to transform into cells that promote vascular calcification.
Another key paper entitled “Role of Uremic Toxins in Early Vascular Ageing and Calcification” explained that uremic toxins, including indoxyl sulfate, drive vascular calcification through osteogenic changes in the vessel wall.
A related mechanistic review in PubMed describes how elevated phosphate and calcium directly drive vascular calcification through VSMCs’ undergoing apoptosis, releasing calcifying vesicles, and taking on bone-like properties.
These mineral imbalances are central to the CKD–mineral bone disorder (CKD‑MBD) and contribute to bone disease (renal osteodystrophy) and arterial stiffness. In people with end-stage kidney disease, a BMC Nephrology study demonstrated that there was an association between abnormal bone turnover-as determined by bone biopsy-and arterial calcification.
