Beneficial Effects of Selective Vitamin D Receptor Activation by Paricalcitol in Chronic Kidney Disease
Javier Donate-Correa, Virginia Domínguez-Pimentel, Mercedes Muros-de-Fuentes, Carmen Mora-Fernández, Ernesto Martín-Nunez, Violeta Cazana-Perez and Juan F. Navarro-González
Affiliation: Nephrology Service, University Hospital Nuestra Senora de Candelaria, 38010. Santa Cruz de Tenerife, Spain.
Keywords: Cardiovascular disease, inflammation, paricalcitol, vitamin D analogues, vitamin D receptor.
In chronic kidney disease patients, active vitamin D level progressively declines in the course of the disease.
This phenomenon is accompanied by elevation of parathyroid hormone, resulting in secondary hyperparathyroidism
(SHPT), increased phosphorus levels, and hypocalcemia. All these disorders are associated with high rates of cardiovascular
morbidity and mortality in these patients. Many vitamin D analogs have been approved for the treatment of SHPT in
renal patients. Currently, new and more selective vitamin D receptor activators (VDRAs) have been introduced in this
therapy with the aim of reducing SHPT without the hypercalcemia and hyperphosphatemia associated with the use of nonselective
VDRAs. In addition, amelioration in hypertension, albuminuria, insulin resistance, and inflammation have been
suggested as consequences of vitamin D receptor (VDR) activation. In this work, we summarize the beneficial effects attributed
to paricalcitol, the only selective, new generation VDRA, currently available in Europe and the USA, with proven
efficacy in the control of SHPT both in hemodialysis (HD) and pre-dialysis patients. Paricalcitol exerts less calcemic and
phosphatemic effects than other VDRAs and prevents deleterious bone resorption. Moreover, paricalcitol-based therapy
has been related to beneficial effects that could favor survival rates in chronic kidney disease patients. These benefits include
anti-inflammatory and antithrombotic effects, the inhibition of vascular smooth muscle cell proliferation, the reninangiotensin
system, vascular calcification, and regression of left ventricular hypertrophy, which could reduce the risk of
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