Parathyroid hormone and mineral metabolism do not have significant impact on pulse pressure in patients undergoing peritoneal dialysis.

BACKGROUND

Pulse pressure, a surrogate for arterial stiffness, has been shown to have substantial impact on predicting patient mortality. Excess cardiac risk in the end-stage renal disease population could be mediated by elevated arterial stiffness, which might in turn result from secondary hyperparathyroidism and abnormal calcium metabolism.

METHODS

A cross-sectional study was carried out to examine a possible relationship between pulse pressure and secondary hyperparathyroidism among 126 prevalent patients undergoing continuous ambulatory peritoneal dialysis.

RESULTS

The mean values for calcium and intact parathyroid hormone level were 2.48 mmol/l and 50.5 pmol/l, respectively. No correlation was found between pulse pressure and the plasma PTH levels (r = -0.15, p = 0.11) or calcium-phosphorus product (r = -0.08, p = 0.38). In a multivariate regression analysis, on the other hand, elevated pulse pressure was directly associated with age (2.1 mmHg per 10-year increase) and the presence of diabetes mellitus (6.9 mmHg) (both p < 0.001). Pulse pressure was also inversely associated with hemoglobin level.

CONCLUSION

The magnitude of arterial pulse pressure in a peritoneal dialysis population was not significantly affected by parathyroid disease and alterations in mineral metabolism with end-stage renal disease. In agreement with similar observations in hemodialysis populations, it is postulated that abnormalities in conduit vessel stiffness (as measured by pulse pressure) are substantially caused by atherosclerosis, in which intimal calcification (as distinct from medial calcification in the context of hyperparathyroidism) plays a more important role.