Inflammation-associated clinical prognostic factors and primary patency after drug-coated balloon angioplasty for recurrent autogenous arteriovenous fistula stenosis: a single-center retrospective cohort study

Background Recurrent autogenous arteriovenous fistula (AVF) stenosis occurs in a vascular environment in which injury, neointimal hyperplasia and inflammation may coexist. Whether routine inflammatory or hematological markers contribute to clinical prognosis after drug-coated balloon (DCB) angioplasty remains uncertain. This retrospective study examines clinical outcomes and inflammation-related prognostic associations without assuming that inflammatory pathways were measured or causally established. Methods This single-center retrospective cohort comprised 357 patients treated between February 2023 and May 2026. The primary outcome was time from index DCB angioplasty to clinically driven target-lesion reintervention. Kaplan–Meier and Cox analyses used available follow-up; a separate clinical logistic model addressed failure within 12 months in 356 patients with complete model data. No non-DCB comparator or patient-level molecular measurements were available. Results Mean brachial-artery flow increased from 288.98 ± 139.37 to 980.92 ± 174.66 mL/min and minimal luminal diameter from 1.52 ± 0.50 to 5.21 ± 0.63 mm (both P < 0.001). Kaplan–Meier primary patency was 95.24%, 84.03%, 68.90%, and 55.40% at 3, 6, 9, and 12 months. In the extended Cox model (338 patients; 191 events), previous PTA count (HR 1.129 per procedure, P = 0.003) and lesion length (HR 1.105 per cm, P = 0.001) were associated with greater hazard; postprocedural flow (HR 0.889 per 100 mL/min, P = 0.014) and red-blood-cell count (HR 0.804 per 10 12 /L, P = 0.027) were associated with lower hazard. The five-fold cross-validated AUC of the clinical 12-month model was 0.706. Conclusion In this selected single-center cohort, recurrent AVF stenosis after DCB angioplasty was associated with previous PTA burden, lesion length, postprocedural flow, and red-blood-cell count. Routine blood-cell measures provide an exploratory inflammation-related clinical context but do not establish inflammatory mechanisms or validate a specific inflammatory biomarker. Independent validation and patient-level inflammatory measurements are required.