Sina Salem Ahim
1 
, Abnoos Mokhtariardekani
2 , Houshang Sanadgol
3 , Shiva Hosseinian
4 , Mehrdad SalekShahabi
5 , Ali Emadzadeh
6 , Zohreh Sanjarian
7 , Atena Abbasszade
8 , Zahra Hamidi Madani
9* 1 Fasa University of Medical Sciences, Fasa, Iran
2 Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Science, & Physiology Research Center, Kerman University of Medical Sciences, Kerman, Iran
3 Department of Nephrology, Hasheminejad Kidney Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
4 Emergency Medicine Management Research Center, Iran University of Medical Sciences, Tehran, Iran
5 Department of Medicine, Faculty of Medicine, Islamic Azad University, Tabriz Branch, Tabriz, Iran
6 Department of Internal Medicine, MMS.C., Islamic Azad University, Mashhad, Iran
7 Department of Midwifery and Reproductive Health, Student Research Committee, School of Nursing and Midwifery, Isfahan University of Medical Sciences, Isfahan, Iran
8 Student Research Committee, Faculty of Nursing and Midwifery, Kerman University of Medical Sciences, Kerman, Iran
9 Department of Obstetrics and Gynecology, Reproductive Health Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
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.
Implication for health policy/practice/research/medical education:
Insulin resistance in polycystic ovary syndrome (PCOS) contributes to renal dysfunction by causing metabolic and hemodynamic changes including hypertension, hyperuricemia, oxidative stress, and inflammation, all of which damage kidney structure and function over time.
Please cite this paper as: Salem Ahim S, Mokhtariardekani A, Sanadgol H, Hosseinian Sh, SalekShahabi M, Emadzadeh A, Sanjarian Z, Abbasszade A, Hamidi Madani Z. Renal manifestations and implications in polycystic ovary syndrome; an analytical review. J Renal Inj Prev. 2026; 15(1): e38711. doi: 10.34172/jrip.2026.38711.