024). We also measured markers of mineral metabolism as prior study results demonstrating relationship with total 25(OH)D have been inconsistent. Findings revealed inverse correlation between total 25(OH)D and iPTH (r = −0.360; p = 0.018) in nephrotic patients. More
importantly, iPTH levels demonstrated stronger inverse correlation with bioavailable 25(OH)D levels (r = −0.428; p = 0.004). No correlation was found with FGF −23, calcium and phosphorus levels. Conclusion: It is concluded that bioavailable 25(OH)D is a better measure of vitamin D status with respect BMD and mineral metabolism in patients of nephrotic syndrome. KUSUNOKI YASUO1, MATSUI ISAO1, HAMANO TAKAYUKI2, SHIMOMURA AKIHIRO1, MORI DAISUKE1, NAKANO CHIKAKO1, OBI YOSHITSUGU1, INOUE KAZUNORI1, TSUBAKIHARA YOSHIHARU2, ISAKA YOSHITAKA1, RAKUGI HIROMI1
1Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine; 2Department of Comprehensive Kidney Disease Research, learn more Osaka University Graduate School of Medicine Introduction: Several interventional studies both in animals and humans have revealed that active vitamin D (1,25(OH)2D) and its analogs protect the kidney from various injuries. However, in most observational studies, not 1,25(OH)2D but low serum 25-hydroxyvitamin D (25(OH)D), a precursor of active vitamin D, correlates with poor renal outcomes. In addition to its deficiency, excess of 25(OH)D has been revealed selleck chemical to be harmful in NHANESIII. Although it is well established that 1,25(OH)2D is the most active form among vitamin D metabolites, these observations suggest that 25(OH)D may have some direct biological effects. Methods: Our aim is to test whether 25(OH)D has direct effects. We used 25(OH)D-1α-hydroxylase knockout mice (CYP27B1 KO mice) in order to separate effects ID-8 of 25(OH)D from 1,25(OH)2D. Mice at age 7 weeks were randomly divided into two groups, control and vitamin D group. Vehicle or 25(OH)D at
a dose of 100 ng/g BW was injected subcutaneously every two days prior to unilateral ureteral obstruction (UUO) at age 8 weeks. The kidneys harvested at age 9 weeks were analyzed. Results: While serum 25(OH)D was 4.5 ± 0.4 ng/mL in control group, toxic range was achieved in the group vitamin D(334.5 ± 52.1 ng/mL). In the group vitamin D serum calcium and phosphate were slightly elevated, but remained within physiological ranges. Real time PCR analyses revealed that vitamin D excess upregulates mRNA for collagen I, III, and fibronectin in UUO-kidneys, but not in contralateral kidneys. Histological analyses confirmed that vitamin D excess exacerbates renal fibrosis in the UUO-kidneys. Inflammatory cytokines, such as tumor necrosis factor-α and monocyte chemotactic protein-1, were also upregulated in the UUO-kidneys of the group vitamin D. All these data indicated that vitamin D excess may be harmful for kidney disease. Conclusion: Vitamin D excess exacerbated renal fibrosis.