Vascular changes in chronic renal disease patients with secondary hyperparathyroidism.

BACKGROUND: Secondary hyperparathyroidism (SHPT) and its metabolic consequences - high serum phosphate and calcium x phosphate (Ca x P) product - are associated with cardiovascular disease in chronic kidney disease (CKD). We evaluated the relationship between PTH, mineral metabolism, vascular reactivity and arterial stiffness in patients with CKD.
METHODS: The study included 31 CKD patients and 12 matched controls. Brachial artery diameter was recorded at baseline and after reactive hyperemia (flow-mediated vasodilation) and 0.45 mg of trinitrate, to analyze the flow-dependent and flow-independent responses. Large vessel stiffness was evaluated on the common carotid artery.
RESULTS: Compared with controls, both flow-mediated (5.8% +/- 4.3% vs. 11.6% +/- 5.4%; p<0.001) and flow-independent (11.7% +/- 7.6% versus 23% +/- 7.5%; p<0.001) vasodilation were reduced in CKD. Flow-mediated vasodilation was negatively correlated with PTH (r=-0.416, p<0.05) and age (r=-0.365, p<0.05) and positively with flow-independent vasodilation (r=0.483, p<0.01). Blood pressure, dialysis duration, hematocrit and serum levels of Ca, P, and Ca x P product, lipids, and medications did not influence flow-mediated function. Carotid distension correlated independently and negatively with age (r=-0.681, p<0.01) and Ca x P product (r=-0.496, p<0.01) but was not influenced by PTH.
CONCLUSION: In CKD, PTH adversely affects vascular reactivity, possibly by interfering with endothelial function, while large vessel distension is influenced by Ca x P product but not by PTH. This result suggests a dual mechanism of vascular aggression in SHPT: an endothelial effect mediated by PTH and a media/adventitial effect linked to alterations in mineral metabolism.