[Effects of oral vitamin D3 supplementation in stage 3 chronic kidney disease subjects: insulin resistance syndrome and hormonal disturb interactions].

The 1-25-hydroxyvitamine D (1-25OHD) or calcitriol deficiency in chronic kidney disease (CKD) patients was associated with increases vascular calcification risk, nephrons reduction, bone deficit and cardiovascular mortality by atherosclerosis. The objective of this study was to investigate the pleiotropic effects of 200.000 IU (D200 group) every 3 months versus 30.000 IU (D30 group) every month dose vitamin D supplementation in stage 3 CKD patients. A cohort of 132 adult subjects was randomized into 2 groups according to dose vitamin D supplementation in deficient subjects (25OHD <50 nmol/L or <20 ng/mL). Serum 25OHD levels were assessed before and after 6 and 12 months of vitamin D supplementation. Patients were phenotyped for IRS according to NCEP/ATPIII. Glomerular filtration rate (GFR) by the MDRD formula. Insulin resistance was evaluated by the Homa-IR model. IRS clusters by Cobas Integra 400®. PTH, Cortisol and IGF-1 were determined by radioimmunologic methods. The 25OHD profile was analyzed by LC-MS/MS. Results showed that vitamin D supplementation increased serum 25OHD concentrations (>75 nmol/L or >30 ng/mL) in both groups; however, the supplementation benefits are more significant in D30 group than in D200 group. We noted a highlighted improvement of kidney function, an inhibition of GFR collaps, a safe reduction of proteinuria, a significant PTH and C-reactive protein (inflammation) levels attenuation, concomitantly with cortisolemia normalization and decreased IGF-1 depletion. Nevertheless, homocysteine and Lp(a) concentrations remain increased, not modulated by vitamin D treatment. This study shows that continuous low doses (30.000 IU every month) are recommended for intermittent high doses (200.000 IU every 3 months) vitamin D supplementation. Our study suggests that the serum 25OHD profile can be considered a reliable biomarker in the bioclinic CKD status to stage stabilization and inhibit its evolution.

RCT Entities:   Population Interventions Outcomes