Functional and histopathological kidney injury in hyperandrogenic female rats - a polycystic ovary animal model

Polycystic ovary syndrome (PCOS) is the most common reproductive disorder in premenopausal women. This syndrome is also associated with many metabolic and cardiovascular complications. These complications are major risk factors for renal injury and kidney disease. Therefore, this study aimed to investigate the types of functional and structural kidney injuries in a hyperandrogenic female rat model.

Female Sprague-Dawley rats were randomly divided into three groups (n=10 each): control, sham, and dehydroepiandrosterone (DHEA). Plasma total testosterone and kidney functional indices were measured using enzyme-linked immunosorbent assay (ELISA) and colorimetric techniques. Ovarian and renal histological changes were also evaluated qualitatively and quantitatively by Hematoxylin-Eosin (H&E) staining.

Plasma total testosterone in the DHEA group increased about 9-fold compared to the control and sham groups. There was also a significant increase in Cr, BUN, and absolute excretion of sodium ion. Insignificant increases in glomerular filtration rate (GFR), urine flow rate (V0), and absolute excretion of potassium ion were observed in DHEA group compared to other groups. However, significant damages were observed in the glomerular and tubular parts of the kidneys and the follicular parts of the ovaries in DHEA-receiving rats.

Hyperandrogenemia is likely to cause systemic abnormalities through a variety of mechanisms, followed by obvious destruction of kidney and ovarian tissues. Accordingly, DHEA administration provides a useful animal model for studying the mechanism of PCOS-mediated renal injury. Practical Implications. The present study Findings can be helpful in identifying the mechanism of PCOS-induced renal injury, especially in younger women.