Stage 3 acute kidney injury secondary to haemolysis after high-burden pulsed field ablation in a patient with normal baseline renal function: a case report

Pulsed field ablation (PFA) causes intravascular haemolysis via irreversible electroporation of erythrocytes. Clinically significant acute kidney injury (AKI) has been reported predominantly in patients with pre-existing chronic kidney disease. However, the relationship between pulse burden and haemolysis-induced renal injury in patients with normal baseline renal function remains incompletely characterized.

A 76-year-old woman with persistent atrial fibrillation and normal baseline renal function [creatinine 89 µmol/L (normal: 44–80 µmol/L); estimated glomerular filtration rate >60 mL/min/1.73m²] underwent high-burden PFA (72 pulses; Farawave™, Boston Scientific) over a 75-min procedure including all four pulmonary veins, left atrial roof, and posterior wall. Within 48 h, she developed haemoglobinuria, a haemoglobin fall from 132 to 83 g/L (normal: 120–160 g/L), lactate dehydrogenase (LDH) 597 U/L (normal: 135–214 U/L), and undetectable haptoglobin (normal: 0.3–2.0 g/L). Creatinine peaked at 720 µmol/L (KDIGO Stage 3 AKI). Serial LDH declined to 304 U/L by Day 8 of admission, consistent with haemolytic resolution. No intraoperative contrast was used; alternative contributors to AKI, including contrast nephropathy and nephrotoxic medications, were excluded. Full renal recovery was achieved with intravenous hydration and urinary alkalinization (discharge creatinine: 112 µmol/L, Day 17).

Haemolysis-induced pigment nephropathy may cause severe AKI after high-burden PFA, even in patients with normal baseline renal function. When ablation extends beyond pulmonary vein isolation, periprocedural intravenous hydration and early post-procedural urine inspection may be considered; prompt hydration with urinary alkalinization can achieve full renal recovery.