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The VITAL study is a prospective cohort of community-dwelling adults [ 6].
However, no differences in plasma renin activity were observed between paricalcitol- and placebo-treated patients in the VITAL study [ 7].
In the VITAL study paricalcitol did not suppress PRA in patients with diabetic nephropathy, although albuminuria was reduced [ 4].
For all FAE recalculations that included the VITAL study, we used the data from the referenced publication.
The results of the VITAL study may define the effect of vitamin D and ω-3 PUFAs in the primary prevention of CVD.
The addition of vitamin D to a purified omega-3 compound is being investigated in the VITAL study (ClinicalTrials.gov Identifier: NCT01169259).
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Even so, there was a significant effect on 24 hour albuminuria similar to the 1 μg arm of the VITAL-study.
In the VITAL-study [ 9], iPTH was higher at baseline (9.6-11 9.6-11), with a significant reduction of apmol/lmately 30% in both treated groups.
In the VITAL-study performed by de Zeeuw et al [ 9], 281 patients with type 2 diabetes, nephropathy and stable ACEi/ARB-therapy, were randomized to 1 or 2 μg/d paricalcitol or placebo for 24 weeks.
Higher excretion of protein may be related to a higher level of renal inflammation – and anti-inflammatory and immuno-modulatory actions of VDRAs might explain why Fishbane et al. found a significant, and quite high, reduction in proteinuria with a 1 μg/d dose, while the 1 μg/d arm in the VITAL-study did not reach statistical significance.
The amount of urinary protein excretion at baseline differed substantially in these studies - it was approximately twice as high in the study-population of Fishbane et al. (proteinuria 2.6-2.7 2.6-2.7ompared to the diabetics of the VITAL-study (albuminuria 1.0-1.1 g/d).
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