Vitamin D deficiency has been linked to many different pathologies, especially with morbidity and mortality in patients with chronic kidney disease.
The progressive loss of renal function leads to Calcitriol deficiency and homeostatic changes in calcium, phosphorus, FGF-23 and PTH, among others. All these changes can also influence vitamin D receptor ( VDR ) activation and the development of secondary hyperparathyroidism ( SHPT ).

The biologic actions of both vitamin D and its synthetic analogues are mediated by binding to the same VDR, acting on different genes.

There is a narrow relationship between low levels of calcitriol and secondary hyperparathyroidism.

The combined approach of VDR activation and phosphate restriction, among others, plays an important role in the early treatment of the chronic kidney disease-mineral and bone disorder ( CKD-MBD ).

The Spanish Society of Nephrology, in order to reduce the uniform and significant association with CKD-associated mortality, calcidiol and high phosphate levels suggests normalization of phosphate as well as calcidiol levels in both CKD and dialysis patients.
Moreover, it considers that, in addition to selective/non selective activation of VDR for the prevention and treatment of secondary hyperparathyroidism, VDR could be activated in dialysis patients by native Vitamin D or even low Paricalcitol ( Zemplar ) doses, independently of PTH levels, as some cohort studies and a recent meta-analysis have found an association between treatment with active vitamin D and decreased mortality in patients with CKD.( Xagena ).

Bover J et al, Nefrologia 2015;35:28-41

XagenaMedicine2015