Key result
Gonadal hormones and prolactin-derived vasoinhibins potentially drive sex-specific kidney damage and renal endothelial dysfunction.
Why the study?
Kidney damage is more severe in males than females with sexual hormones contributing, but the role of prolactin and its cleavage products (vasoinhibins) in renal endothelial dysfunction has not been sufficiently investigated.
This review highlights the role of sexual dimorphism, gonadal hormones, prolactin, and vasoinhibins in kidney pathophysiology and damage.
Alerts clinicians to consider sex-specific factors in kidney disease without practice change; leaves open targeted trials on vasoinhibins in renal endothelial dysfunction.
Kidney pathophysiology is influenced by gender. Evidence suggests that kidney damage is more severe in males than in females and that sexual hormones contribute to this. Elevated prolactin concentration is common in renal impairment patients and is associated with an unfavorable prognosis. However, PRL is involved in the osmoregulatory process and promotes endothelial proliferation, dilatation, and permeability in blood vessels. Several proteinases cleavage its structure, forming vasoinhibins. These fragments have antagonistic PRL effects on endothelium and might be associated with renal endothelial dysfunction, but its role in the kidneys has not been enough investigated. Therefore, the purpose of this review is to describe the influence of sexual dimorphism and gonadal hormones on kidney damage, emphasizing the role of the hormone prolactin and its cleavage products, the vasoinhibins.
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Franco-Acevedo et al. (2021) conducted a review in Kidney damage. Sexual dimorphism and gonadal hormones influence kidney damage, with prolactin and its cleavage products, vasoinhibins, potentially playing a significant role in renal endothelial dysfunction.