Association between baseline haptoglobin and early renal injury after pulsed-field ablation.

BACKGROUND

Pulsed-field ablation (PFA) has emerged as an effective modality for the treatment of atrial fibrillation. However, intravascular hemolysis and subsequent renal injury have been recognized as potential complications. Haptoglobin binds free hemoglobin and may influence susceptibility to hemolysis-related renal injury.

OBJECTIVE

This study aimed to determine whether baseline haptoglobin levels are associated with early renal injury after PFA and evaluate the feasibility of targeted haptoglobin supplementation.

METHODS

A total of 493 patients undergoing PFA were prospectively enrolled. Baseline haptoglobin and serial creatinine were assessed. Early renal injury (increase in creatinine of ≥0.2 mg/dL within 24 hours) was the primary exploratory endpoint; Kidney Disease: Improving Global Outcomes-defined acute kidney injury was the secondary endpoint. Primary analyses were performed in 481 patients without haptoglobin supplementation (analytical cohort), whereas 12 selected high-risk patients with low baseline haptoglobin and postprocedural hemoglobinuria received intravenous haptoglobin as a separate exploratory supplementation cohort.

RESULTS

Among 481 analytical cohort patients without supplementation, early renal injury occurred in 16 patients (3.3%) and decreased across increasing haptoglobin tertiles. Baseline haptoglobin was associated with early renal injury (odds ratio 0.985; P = .025; area under the curve 0.69). According to the Kidney Disease: Improving Global Outcomes criteria, 6 patients (1.2%) met the definition of acute kidney injury. Among patients with baseline haptoglobin of ≥80 mg/dL, haptoglobin decline correlated with PFA deliveries (r = 0.36; P < .001). In the exploratory supplementation cohort, hemoglobinuria resolved rapidly whereas renal function remained stable.

CONCLUSION

Lower baseline haptoglobin was associated with early renal injury after PFA, suggesting a role in susceptibility to hemolysis-related renal stress. Targeted supplementation appears feasible but requires validation.