BACKGROUND: Long-term exposure to hypercalcaemia and hyperphosphataemia leads to media calcification and predicts mortality in patients with end-stage renal disease (ESRD). It is debatable whether this exposure is only a risk factor for arteriosclerosis, or also for superimposed atherosclerosis. Calcium-phosphate exposure is difficult to quantify, because it is variable in time and exerts its deleterious effects only after prolonged presence. METHODS: In 90 dialysis patients, calcium and phosphate values from the complete dialysis period were collected. From three-month averages, measures for calcium-phosphate exposure were derived after exclusion of transplant periods. Calcium-phosphate exposure was then related to intima-media thickness (IMT) and to ankle-brachial index (ABI) as markers of early atherosclerosis. RESULTS: Calcium-phosphate exposure was quantified in three ways using 1670 patient-quarters (i.e. three-months periods) covering 93% of the time on dialysis: averaged calcium-phosphate exposure, percentage of time with above-reference values, and burden of hypercalcaemia/hyperphosphataemia represented by this percentage multiplied by months on dialysis. No association was found with IMT. Patients with increased, not decreased, ABI had higher calcium-phosphate exposure throughout dialysis treatment: hyperphosphataemia burden was 31 (19 to 43) months for patients with ABI between 0.90 and 1.40 and 79 (58 to 100) months for patients with ABI >1.40 or incompressible ankle arteries (p<0.001). CONCLUSION: These findings do not support the hypothesis that calcium-phosphate exposure leads to atherosclerotic changes on top of arteriosclerosis in ESRD, and confirm its role in causing arteriosclerotic damage leading to increased arterial stiffness and incompressible ankle arteries. The used tool for quantifying calcium-phosphate exposure is easy to apply and can properly weigh the complete exposure during ESRD.
BACKGROUND: Long-term exposure to hypercalcaemia and hyperphosphataemia leads to media calcification and predicts mortality in patients with end-stage renal disease (ESRD). It is debatable whether this exposure is only a risk factor for arteriosclerosis, or also for superimposed atherosclerosis. Calcium-phosphate exposure is difficult to quantify, because it is variable in time and exerts its deleterious effects only after prolonged presence. METHODS: In 90 dialysis patients, calcium and phosphate values from the complete dialysis period were collected. From three-month averages, measures for calcium-phosphate exposure were derived after exclusion of transplant periods. Calcium-phosphate exposure was then related to intima-media thickness (IMT) and to ankle-brachial index (ABI) as markers of early atherosclerosis. RESULTS:Calcium-phosphate exposure was quantified in three ways using 1670 patient-quarters (i.e. three-months periods) covering 93% of the time on dialysis: averaged calcium-phosphate exposure, percentage of time with above-reference values, and burden of hypercalcaemia/hyperphosphataemia represented by this percentage multiplied by months on dialysis. No association was found with IMT. Patients with increased, not decreased, ABI had higher calcium-phosphate exposure throughout dialysis treatment: hyperphosphataemia burden was 31 (19 to 43) months for patients with ABI between 0.90 and 1.40 and 79 (58 to 100) months for patients with ABI >1.40 or incompressible ankle arteries (p<0.001). CONCLUSION: These findings do not support the hypothesis that calcium-phosphate exposure leads to atherosclerotic changes on top of arteriosclerosis in ESRD, and confirm its role in causing arteriosclerotic damage leading to increased arterial stiffness and incompressible ankle arteries. The used tool for quantifying calcium-phosphate exposure is easy to apply and can properly weigh the complete exposure during ESRD.