Abstract
The majority of end-stage renal disease including dialysis and kidney transplant patients are men. In contrast, the incidence of chronic kidney disease (CKD) is higher in women compared with men. In this review, we dissect the sex hormone levels and its effects on experimental models and patients with CKD. Sex hormones are clearly involved in CKD progression to end-stage renal disease (ESRD). A significant reduction in lipid peroxidation as a mechanism of renoprotection has been observed in kidneys of streptozotocin (STZ)-diabetic ovariectomized rats after estradiol administration. Furthermore, a G-protein-coupled estrogen receptor inhibits podocyte oxidative stress maintaining the integrity of the mitochondrial membrane. Sex hormone depletion has been shown to modulate RAS system and protect against kidney injury in the male STZ-diabetic model. In human primary proximal tubular epithelial cells, a proteomic study showed that dihydrotestosterone dysregulated metabolic, suggesting that the deleterious effect of androgens within the kidney maybe related to altered energy metabolism in renal tubules. Male gender is associated with worse CKD progression and this fact may be ascribed to sex hormone. Although male hormones exert a deleterious effect in terms of increasing oxidative stress, activating RAS system, and worsening fibrosis within the damaged kidney, female hormones exert a renoprotective effect.
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