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Effects of calcitriol and paricalcitol on renal fibrosis in CKD

Laura Martínez-Arias1, Sara Panizo1, Cristina Alonso-Montes1

  • 1Bone and Mineral Research Unit, Hospital Universitario Central de Asturias, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Retic REDinREN-ISCIII, Oviedo, Spain.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|January 8, 2021
PubMed
Abstract

Insights

Paricalcitol treatment significantly reduced kidney fibrosis in chronic renal failure (CRF) by inhibiting the renin-angiotensin-aldosterone system (RAAS) and inflammation. This vitamin D receptor activator offers a promising therapeutic avenue for kidney disease progression.

Area of Science:

  • Nephrology
  • Pharmacology
  • Molecular Biology

Background:

  • Chronic kidney disease (CKD) involves renin-angiotensin-aldosterone system (RAAS) activation, renal inflammation, and fibrosis, worsening end-stage renal disease.
  • Low vitamin D receptor (VDR) levels and activators (VDRAs) exacerbate secondary hyperparathyroidism and renal fibrosis in CKD.

Purpose of the Study:

  • To investigate the anti-fibrotic effects of VDRAs, specifically paricalcitol and calcitriol, in a rat model of chronic renal failure (CRF).
  • To compare the efficacy of paricalcitol and calcitriol in mitigating renal fibrosis and associated pathological changes.

Main Methods:

  • A 7/8 nephrectomy model was employed to induce experimental chronic renal failure (CRF) in rats.
  • Animals were treated with paricalcitol and calcitriol at equivalent doses (3:1 ratio) for four weeks to assess anti-fibrotic effects.

Main Results:

  • CRF led to increased RAAS activation, renal inflammation, and interstitial fibrosis.
  • Paricalcitol treatment significantly reduced renal collagen I and interstitial fibrosis by inhibiting RAAS activation (modulating renin, ATR1, and ATR2 mRNA) and decreasing renal inflammation (reducing CD45, ADAM, TGF-β mRNA/protein, and preserving E-cadherin mRNA).
  • Calcitriol demonstrated similar trends but with less pronounced effects on most biomarkers.

Conclusions:

  • Paricalcitol effectively attenuated CRF-induced renal interstitial fibrosis.
  • The anti-fibrotic mechanism of paricalcitol involves combined inhibition of the RAAS, inflammation, and epithelial-to-mesenchymal transition.
Keywords:
CKDVDRAsepithelial/mesenchymal-transitioninflammatory infiltrationrenal fibrosis

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