Urinary Albumin-to-Creatinine Ratio Across Phenotypes of Polycystic Ovary Syndrome: A Phenotype-Based Evaluation.

Background/Aim: Albuminuria is a clinical marker associated with microvascular involvement and an independent predictor of cardiovascular risk. Polycystic ovary syndrome (PCOS) is associated with early metabolic and vascular abnormalities; however, whether albumin excretion differs across PCOS phenotypes remains unclear. This study aimed to evaluate the urinary albumin-to-creatinine ratio (U-ACR) across PCOS phenotypes and to examine its association with metabolic parameters. Materials and

Methods

In this cross-sectional study, 180 women aged 18-35 years with PCOS and 51 age-matched healthy controls were included. PCOS phenotypes were classified according to the Rotterdam criteria as Phenotype A (n = 96), Phenotype B (n = 19), Phenotype C (n = 35), and Phenotype D (n = 30). Insulin resistance was assessed using the homeostasis model assessment for insulin resistance (HOMA-IR). Urinary albumin and creatinine levels were measured in morning urine samples, and U-ACR was calculated.

Results

Age was comparable across all groups. Body mass index, waist circumference, diastolic blood pressure, and HOMA-IR were significantly higher in Phenotype A compared with controls and other phenotypes, reflecting a more adverse metabolic profile. Serum creatinine levels were similar across all groups. Despite this metabolic profile in Phenotype A, U-ACR was significantly elevated only in Phenotype B compared with controls (p = 0.018), and Phenotype D (p = 0.016). No significant correlations were observed between U-ACR and age, body mass index, or HOMA-IR. When participants were categorized according to U-ACR levels (<30, 30-299.9, and ≥300 mg/g creatinine), no significant differences in category distribution were observed between the total PCOS cohort, phenotype subgroups, and controls.

Conclusion

Among PCOS phenotypes, U-ACR elevation was observed exclusively in Phenotype B despite similar renal function markers. This finding, in the presence of a more adverse metabolic profile in Phenotype A, suggests a dissociation between metabolic burden and early microvascular involvement across PCOS phenotypes. These findings suggest a potential phenotype-specific pattern that warrants further investigation.