MO279: Vitamin D Supplementation Attenuates Hyperandrogenemia-Associated Acute Kidney Injury in Female Sprague-Dawley Rats

Abstract BACKGROUND AND AIMS Polycystic ovary syndrome (PCOS) is closely related to the onset and development of metabolic abnormalities. However, the correlation between PCOS and kidney injury has not been clarified, and the underlying mechanism remains unknown. Vitamin D therapy has beneficial effects in women with PCOS and renal injuries. Therefore, this study was designed to explain the mechanisms responsible for kidney damages in a model of hyperandrogenic rats and the healing effects of vitamin D. METHOD Female Sprague-Dawley rats were randomly divided into five groups (n = 10): (i) control, (ii) sham, (iii) dehydroepiandrosterone (DHEA, 6 mg/100 g day-1 S.Q.), (iv) DHEA + vitamin D (1000 IU/Kg; 3 days/week), and (v) vitamin D. Plasma total testosterone, plasma creatinine (Cr), blood urea nitrogen (BUN), plasma and tissue levels of total oxidant status (TOS), total antioxidant capacity (TAC) and oxidative stress index (OSI), and histopathological changes of ovary and kidney were determined. RESULTS Plasma testosterone increased 9-fold in DHEA-treated rats compared with controls. They also had increased Cr, BUN, and severe renal tubular injury. Plasma and tissue TAC levels showed significant decreases, whereas TOS and OSI showed significant increases in the DHEA group. A significant injury in the glomerular and tubular parts of the kidney and ovarian follicular structure was observed in DHEA-administered rats. Vitamin D treatment attenuated TOS levels and significantly improved TAC levels. Kidneys and ovaries histopathological changes were significantly improved by vitamin D treatment. CONCLUSION Hyperandrogenemia causes systemic abnormalities through oxidative stress-related mechanisms, followed by obvious destruction to renal and ovarian tissues. Vitamin D supplementation attenuated these hyperandrogenemia-associated acute kidney injuries. FIGURE 1: Photomicrograph of renal tissue in experimental groups (Hematoxylin and Eosin staining). Renal section of control group with completely normal appearance in cortex (a) and medulla (b), renal section of DHEA-administered (6 mg/100 g day-1 SQ) group with brush border shedding of the proximal tubules (thin black arrow) and necrotic parts (yellow arrow head) in cortex (c), and casts inside the tubules (thick black arrow) in medulla (d) and renal section of DHEA + vitamin D group (received 1000 IU/Kg; 3 days/week, IM) with improved condition in cortex (C) and medulla (D), Magnification: ×400. DHEA = dehydroep