Sinister Synergy: IgA Nephropathy and Apixaban

Introduction: IgA nephropathy is the most common glomerulonephritis worldwide, divided into primary and secondary types. Oral anticoagulants have been associated with acute kidney injury, although less well defined. We present a case of IgAN made more severe with the addition of Apixaban. Case Description: A 75-year-old male with history of recently diagnosed atrial fibrillation on Apixaban, systolic heart failure, and prior EtOH abuse who presented for evaluation of lower extremity edema. He developed rapid onset of stage 3 AKI (sCr 4mg/dL, baseline 1mg/mL) over one month and gross hematuria 1 week prior to presentation. Urinalysis revealed >50 RBCs; UPCR 1.8g/g. Urine microscopy revealed mixed cellular casts. Broad serological work up was negative. C3/C4 levels normal. Infectious work up was negative. US revealed mild liver contour changes concerning for mild cirrhosis. Renal biopsy with findings of IgAN (3+ IgA/C3 in the mesangium and tubular lumen, low mesangial expansion and endocapillary proliferation, no crescents), and numerous RBC casts. Findings were attributed to secondary IgAN with cirrhosis, with other findings suggestive of anticoagulant-related nephropathy. Given the rapid progression of his disease, patient was started on high-dose steroids. Apixaban was held with resolution of hematuria. Patient’s renal function subsequently improved and Apixaban was restarted. Discussion: We present a case of sIgAN complicated by the addition of anticoagulation. Our case is unique as the patient presented with rapidly progressive and severe renal injury, without characteristic findings of aggressive disease on biopsy. Our case highlights the role that anticoagulation can have worsening glomerular disease.IgA Mesangial StainingRBC Casts