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Abstract: PO0342

Meta-Analysis of the Impacts of Supplementation with Nutritional Vitamin D on Mineral and Bone Markers in Non-Dialysis CKD

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Gunnarsson, Joel, Quantify Research AB, Stockholm, Sweden
  • Cianciolo, Guiseppe, Universita di Bologna, Bologna, Emilia-Romagna, Italy
  • Lauppe, Rosa, Quantify Research AB, Stockholm, Sweden
  • Csomor, Philipp, Vifor Pharma Ltd, Glattbrugg, Zurich, Switzerland
  • Kaiser, Edelgard, Vifor Pharma Ltd, Glattbrugg, Zurich, Switzerland
  • Soro, Marco, Vifor Pharma Ltd, Glattbrugg, Zurich, Switzerland
  • Bover, Jordi, Fundacio Puigvert, Barcelona, Catalunya, Spain
Background

Secondary hyperparathyroidism (SHPT) is a critical component of mineral and bone disorder in chronic kidney disease (CKD-MBD), characterized by excessive parathyroid hormone (PTH) secretion and low levels of vitamin D. Nutritional vitamin D (NVD) supplements are frequently used to treat SHPT, especially in early CKD. The objective of this meta-analysis (MA) was to evaluate the impact of NVD supplements on PTH, vitamin D (25D), calcium (Ca), phosphate (P) and fibroblast growth factor 23 (FGF23).

Methods

Study level results were pooled using a fixed effect model with inverted-variance weighting. The impact of the NVDs was measured in two ways: as change versus placebo or ‘no treatment’ and as change within the NVD study arm (before versus after NVD supplementation).

Results

Overall changes in PTH from NVD supplementation were small when measured within the NVD study arms (pooled reduction of 10.53 pg/ml, 95 % confidence interval (CI): -16.33 to -4.73) but larger when compared to placebo/no treatment (reduction of 49.74 pg/ml, 95 % CI: -70.17 to -29.3).
NVDs tended to increase levels of 25D both within the NVD study arms (increase of 20.62 ng/ml, 95 % CI: 19.58 to 21.65) and when compared to placebo/no treatment (increase of 26.87 ng/ml, 95 % CI: 24.44 to 29.30). At the end of the study periods, average levels of 25D in the NVD study arms were >30 ng/ml in all but two RCTs and >50 ng/ml in only five of the included RCTs.
Ca levels increased statistically significant from supplementation with NVDs versus placebo/no treatment (increase of 0.23 mg/dl, 95 % CI: 0.12 to 0.34 mg/dl). Only small and statistically non-significant impacts were observed on levels of P and FGF23.

Conclusion

Our results suggest that the magnitude of 25D increase caused by NVD may be insufficient to effectively and consistently lower PTH. While supplementation with NVDs can be used to correct vitamin D insufficiency, the potential of NVDs to actively reduce PTH in ND-CKD patients with SHPT is limited.

Funding

  • Commercial Support