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Vascular calcification (VC) is common in patients with diabetes and/or chronic kidney disease (CKD). It is strongly associated with cardiovascular morbidity and mortality. Hyperphosphatemia caused by CKD induces the transformation of vascular smooth muscle cells (VSMCs) into chondrocytes or osteoblast-like cells. Hyperglycemia may also accelerate VC. However, the exact mechanisms of this remain unclear. The effects of simultaneous hyperphosphatemia and hyperglycemia require investigation. CKD rat models are typically used to study VC, which are far removed from the clinical situations of patients with CKD. The present study cultured human aortic smooth muscle cells (HASMCs) in normal, hyperphosphatemic and/or hyperglycemic conditions for 14 days. Alizarin red staining, calcification content, VSMC differentiation marker gene expression, phenotypic osteoblast gene expression and type III sodium-dependent phosphate cotransporter-1 (Pit-1) protein expression was examined. Hyperphosphatemia and hyperglycemia had combined effects in promoting calcification, phenotypic transition and Pit-1 expression in cultured HASMCs. In the present study, the combined effects of hyperphosphatemia and hyperglycemia on the calcification and phenotypic transition of HASMCs were demonstrated. Hyperphosphatemia combined with hyperglycemia medium should be considered an appropriate experimental model to study VC in diabetic kidney disease (DKD). Pit-1 should be considered as a promising index of VC.

Combined effects of hyperphosphatemia and hyperglycemia on the calcification of cultured human aortic smooth muscle cells