Effect of the administration of different forms of vitamin D on central blood pressure and aortic stiffness, and its implication in the reduction of albuminuria in chronic kidney disease

Abstract

Background and objectives

Vitamin D (vitD) participates in phospho-calcium metabolism and exerts multiple pleiotropic effects. There is tissue 1-α (OH)ase that converts 25-OH cholecalciferol (25 (OH) D) in calcitriol that exerts autocrine and paracrine effects. 25 (OH)D deficiency could limit these tissue effects of vitD. The administration of nutritional vitD and the activator of the vitD receptor, paricalcitol, may promote beneficial effects on vascular and renal function. The objective of this work was to study in subjects with chronic kidney disease (CKD) the effect that the administration of different forms of vitD has on arterial function and albuminuria, and the possible relationship between the modifications of these variables.

Patients and methods

We studied in 97 patients with CKD stages 3–4 the effect of the administration of cholecalciferol (group 2; n: 35) and paricalcitol (n: 31; group 3) on parameters derived from brachial blood pressure, aortic blood pressure and on aortic stiffness studied using carotid-femoral pulse velocity (Vp_c-f), and on albuminuria. A group of patients with stages 3–4 CKD who did not receive vitD therapy served as a control group (n: 31; group 1). All parameters were studied at baseline and after the follow-up period which was 7 ± 2 months.

Results

In the baseline phase, no differences were observed between the groups in brachial systolic blood pressure (bSBP), central systolic blood pressure (SBP), brachial pulse pressure (bPP), and central pulse pressure (pCP) or in aortic stiffness that was increased in all groups with a baseline Vp_c-f value of 10.5 (9.2–12.1) m/sec. The baseline albuminuria value in the grouped patients was 229 (43–876) mg/g (median (interquartile range)), with no differences between the groups.

Serum calcium and phosphorus increased significantly in those treated with cholecal-ciferol (native vitD) and paricalcitol (active vitD). Parathormone (PTH) values ​​decreased in those treated with paricalcitol. bPP and cPP decreased in all groups treated with native and active vitD. No significant changes in bPP and cPP were observed in the control group.

Vp_c-f did not change significantly in any of the groups, although the variation was quantitatively greater in group 3 (11.2 ± 2 vs. 10.7 ± 1.6 (p:0.06)). No differences were observed in the changes in Vp_c-f between the groups when adjusted to the baseline values ​​of estimated glomerular filtration rate (eGFR), albuminuria, PTH, vitD, brachial and central blood pressure parameters, and their changes with treatment.

Those who received treatment with native and active vitD presented a significant decrease in albuminuria of 17% (group 2) and 21% (group 3) compared to a 16% increase in the untreated group (group 1) (p:0 .01). A decrease in albuminuria ≥30% was observed more frequently in the groups treated with some form of vitD (group 2: 23%; group 3: 45%) than in the control group (13%) (p:0.03). The decrease in albuminuria observed in the groups treated with any of the forms of vitD did not vary when the baseline values ​​of the biochemical parameters of phosphorus-calcium metabolism, those of arterial function (PPb, PPc, Vp_c-f) or its modifications were introduced as covariates. There was no significant correlation between changes in Vp_c-f and albuminuria. In logistic regression, changes in arterial function parameters were also not explanatory for the ≥30% decrease in albuminuria.

Conclusions

In patients with CKD stages 3–4, treated with RAS blockers and with residual albuminuria, the administration of or paricalcitol reduces brachial and aortic pulse pressures, and albuminuria. The decrease in albuminuria does not seem to be mediated, at least not decisively, by changes in central hemodynamics or aortic stiffness.