Our aim was to study the U0126 vitamin D deficiency in a murine model of CKD progression after AKI induced by ischemia/ reperfusion. In our experimental ischemia/reperfusion injury model, we found renal hypertrophy, increased levels of blood pressure and proteinuria in both ischemic animal groups. Furthermore, we observed enlargement of the interstitial area, including increased infiltration of ED1 positive cells and presence of fibrosis, and phenotypic modification of renal tubular cells. Vitamin D deficiency contributed to the elevation of plasma PTH and decrease of plasma FGF-23 levels as well as for important chronic tubulointerstitial changes. In addition, we found increased expression of cytokine TGF-b1 and decreased expression of VDR receptor and Klotho protein in vitamin D-deficient animals submitted to ischemia/reperfusion injury. Our results clearly show that animals fed the vitamin D-free diet presented undetectable levels of 25D. The plasma level of 25D reflects vitamin D intake from foods and supplements, as well as cutaneous synthesis. In addition to calcium and phosphorus, another important compound related to vitamin D synthesis is PTH level. Our results showed high levels of PTH in VDD, mainly in VDD+IRI group. These alterations were expected since the lack of vitamin D reduces intestinal calcium absorption, leading to a lower level of calcium and higher production of PTH by the parathyroid gland. PTH, in turn, acts on bone tissue in order to attenuate the decrease in serum calcium and the increase in phosphorus excretion. We also investigated the role of vitamin D on blood pressure control. In our study, ischemic and vitamin D deficient rats showed higher levels of blood pressure. This alteration was accompanied by an increased mRNA expression of some RAS compounds, including renin, angiotensinogen and ACE. Further more, we found increased levels of plasma aldosterone in VDD, IRI and VDD+IRI groups. So, our data reinforce an important role of vitamin D in blood pressure control. In fact, strong evidences from studies conducted in humans and animals show that vitamin D can be related to a decrease in the reninangiotensin activity. Also, it has been demonstrated that vitamin D deficiency can led to an upregulation of the RAS, changes in the endothelium, and vascular smooth cells as well. Li et al demonstrated that VDR knockout mice showed increased renin expression and hypertension, and these changes were suppressed by an analogue of vitamin D. Studies have shown that vitamin D deficiency is associated with increased prevalence of proteinuria in adult population, a marker of CKD progression. Our results showed a progressive and significant increase of proteinuria among the studied groups. In addition, it was noteworthy that vitamin D deficiency enhanced proteinuria in VDD and VDD+IRI. However, the mechanisms by which proteinuria leads to reduced levels of vitamin D in the body or vice versa are not fully understood.