Phosphate overload accelerates vascular calcium deposition in end-stage renal disease patients.

Abstract

Cardiovascular disease is a major problem in end-stage renal disease (ESRD) patients, with calcification being one of the conspicuous features of arteriosclerotic vessels. In the present study, clinical analysis and in vitro cell culture were used to investigate factors promoting vascular calcification in ESRD patients. The aortic arch calcification score (AACS) was the method used to estimate vascular calcification by evaluation of the simple posterior-anterior view chest X-rays. Factors that relate significantly to vascular calcification and the AACS are the Ca x Pi, age, dialysis period, blood pressure, smoking and diabetes mellitus, but not total cholesterol or triglyceride. The Ca x Pi, which depends on the serum phosphate concentration, is the only specific factor with the possibility for correction in ESRD patients, and so control of serum phosphate concentration is an important factor for reducing vascular calcification. The effects of phosphate overload on calcium deposition in human vascular smooth muscle cells (hVSMCs) using a primary cell culture system were also investigated. hVSMCs were harvested from the radial artery in ESRD patients and it was found that they could secrete extracellular matrix with a high affinity for calcium in a high phosphate medium (Pi=5.4 mg/dl). Therefore, phosphate overload might stimulate the hVSMCs to accelerate the calcium deposition in ESRD patients. These results suggest that the control of phosphate excess is important for prevention of calcium deposition on arteriole walls in ESRD patients.