Renal manifestations and implications in polycystic ovary syndrome; an analytical review

Abstract

Insulin resistance in polycystic ovary syndrome (PCOS) contributes to renal dysfunction through multiple interconnected mechanisms. In PCOS, insulin resistance leads to compensatory hyperinsulinemia, which exacerbates metabolic disturbances including hyperandrogenism and systemic inflammation. These factors collectively promote renal injury. Meanwhile, insulin resistance in PCOS promotes hypertension and endothelial dysfunction, which impair renal microcirculation. Hyperinsulinemia increases sodium retention and activates the renin-angiotensin-aldosterone system (RAAS), further elevating blood pressure and causing glomerular hyperfiltration and damage. Insulin resistance also contributes to dyslipidemia and oxidative stress, accelerating atherosclerosis and renal vascular injury. Moreover, insulin resistance worsens hyperuricemia by reducing renal uric acid excretion, which is a direct nephrotoxic factor. Persistent hyperuricemia leads to inflammation and fibrosis within the kidneys, potentially progressing to chronic kidney disease (CKD). In addition, systemic low-grade inflammation and oxidative stress driven by insulin resistance and PCOS-related hyperandrogenism also induce renal tissue injury through inflammatory cytokines and apoptotic pathways, contributing to impairment in renal function.