Pentosidine and Bone Properties in Autosomal Dominant Polycystic Kidney Disease

Background/Objectives: Altered bone metabolism and oxidative stress are features of autosomal dominant polycystic kidney disease (ADPKD). Pentosidine, an advanced glycation end-product and a marker of oxidative stress, has been proposed as an indicator of impaired bone health. This study aimed to evaluate whether pentosidine levels are altered in ADPKD and whether they are associated with bone characteristics in comparison with other chronic kidney disease (CKD) etiologies and healthy individuals. Methods: We conducted a cross-sectional analysis of three cohorts comprising 554 adults. Participants were categorized by CKD etiology and stage (G1-G5). ADPKD stages were classified according to the Mayo Imaging Classification (MIC). Plasma pentosidine was analyzed by HPLC and ELISA. Bone material strength index (BMSi) was assessed using a microindentation technique (OsteoProbe^®). Results: Plasma pentosidine was higher in ADPKD compared with other CKD etiologies in CKD stages G1-G4 (p = 0.023) and CKD 5D (p < 0.0001). Pentosidine was not associated with conventional bone biomarkers. However, in ADPKD individuals with preserved kidney function, higher pentosidine was associated with bone mineral density at the 1/3 radius and with BMSi. Conclusions: Pentosidine levels are consistently elevated in ADPKD compared with other CKD etiologies. Associations between pentosidine and measures of cortical bone properties suggest that pentosidine may contribute to skeletal alterations in ADPKD. These findings highlight a novel pathway linking oxidative stress and bone health.