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Paricalcitol regulatory effect on inflammatory, fibrotic and anticalcificating parameters in renal patiente. Far
Laura Salanova Villanueva1, Yohana Gil Giraldo1, Begoña Santos Sánchez-Rey1
1Nefrología, Hospital Universitario de la Princesa, Madrid, España.
Insights
Paricalcitol effectively regulated inflammation and mineral imbalances in chronic kidney disease (CKD) patients, improving key markers without altering calcium or phosphorus levels. This suggests potential benefits for cardiovascular risk in non-dialysis CKD patients.
Area of Science:
- Nephrology
- Endocrinology
- Cardiovascular Medicine
Background:
- Cardiovascular events are a leading cause of death in chronic kidney disease (CKD).
- Inflammation and mineral-bone disorder are linked to increased cardiovascular risk in CKD patients.
Purpose of the Study:
- To investigate the effects of paricalcitol on inflammatory, fibrotic, and mineral disorder parameters in non-dialysis CKD patients.
- To assess paricalcitol's regulation of key biomarkers associated with cardiovascular risk in CKD.
Main Methods:
- A prospective study involving 46 CKD stages III-V patients with elevated parathormone.
- Evaluation of mineral and bone metabolism, inflammatory, fibrotic, and anti-calcification markers over four months.
- Inclusion of novel markers like FGF-23, Klotho, BMP-7, and fetuin-A alongside traditional parameters.
Main Results:
- Paricalcitol increased soluble Klotho and calcidiol, while decreasing parathormone (PTH).
- Significant reductions in inflammatory markers (interleukin-6, TNF-α) and fibrosis markers (TGF-β) were observed.
- Positive regulation of anti-calcification marker fetuin-A and anti-fibrosis marker BMP-7, with stable FGF-23, calcium, and phosphorus levels.
Conclusions:
- Paricalcitol may benefit non-dialysis CKD patients by regulating inflammation and anti-calcification parameters.
- The treatment appears to preserve kidney function and offers potential benefits for mineral and endothelial disorders in CKD.
- Observed biomarker changes suggest paricalcitol's role in mitigating cardiovascular risk associated with CKD.
Backward:
Cardiovascular events are the major cause of morbidity and mortality in patients with chronic kidney disease (CKD). Inflammation and mineral-bone disorder are pathological conditions that have been associated with an increased cardiovascular risk.
Objective:
Show paricalcitol regulation overinflammatory, fibrotic and mineral disorder parameters in CKD.
Material And Methods:
Prospective Study in 46 CKD stages III-V patients without dialysis patients whith elevated parathormone in which we introduced paricalcitol. We evaluated classic and newest mineral and bone metabolism serum parameters (calcium, phosphorus, parathormone, fibroblast growth factor-23 [FGF-23], Klotho, calcidiol), inflammatory-fibrosis and anticalcifying parameters (interleukin-6 and 10, tumor necrosis factor-a [TNF- α], transforming growth factor-b [TGF-β],bone morphogenic protein-7 [BMP-7] and fetuin-A) for four months.
Results:
At the end of study soluble Klotho increased (p=.001), FGF-23 remained stable, calcium and phosphorus levels were not increased, calcidiol increased (p=.010) and PTH decreased (p=.002). Inflammation-fibrosis and calcification parameters showed positive regulation after paricalcitol treatment: interleukin-6 decreased significantly (p=.001) and also TNF-α did (p=.005), on the contrary, interleukin-10 and fetuin-A increased (p=.001 for both). Anti-fibrosis marker BMP-7 increased (p=.001) and TGF-b decreased (p=.001). We did not find significant changes in renal function.
Conclusions:
Paricalcitol treatment might be profitable in regulating inflammatory and anticalcificant parameters, unmodified calcium or phosphorus seric levels and preserving kidney function in renal patients with no dialysis. Our selected parameters could indicate paricalcitol effects in mineral and endothelial disorder related to renal disease.
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