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Kidney Week

Abstract: SA-PO891

Beyond Blood: A Case Report on Anticoagulation-Related Nephropathy

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Kaur, Divmehar, Mount Auburn Hospital, Cambridge, Massachusetts, United States
  • Phipps, Elizabeth Ann, Mount Auburn Hospital, Cambridge, Massachusetts, United States

Group or Team Name

  • Mount Auburn Hospital.
Introduction

Anticoagulation related nephropathy (ARN) is thought to be a frequently undiagnosed complication of anticoagulant therapy. Typically manisfesting as gross hematuria and AKI in individuals on therapeutic anticoagulation doses, its diagnosis remains rare. Its confirmation through renal biopsy is tough, as it may be missed or underreported due to the presence of concurrent pathologies.

Case Description

A 76-year-old male with pertinent history of hypertension, BPH was started on Apixaban for a new diagnosis of atrial fibrillation. Soon after, his creatinine levels nearly doubled from their baseline of 1-1.3 within a year which prompted nephrology involvement. Initial work up showed microscopic hematuria with acanthocytes, raising suspicion for underlying nephropathy. Shortly, this progressed to gross hematuria and was initially attributed to severe BPH causing bilateral hydronephrosis found on renal ultrasound. However,the persistence of hematuria and AKI despite relieving post renal obstruction warranted a kidney biopsy which showed ATN, IgA nephropathy and numerous RBC casts.This raised suspicion for ARN, which was confirmed with improvement in renal function after stopping Apixaban.

Discussion

ARN is known to cause glomerular hemorrhage and occlusion of renal tubules with RBC casts.This is reflected in typical renal biopsy findings showing near complete occlusion of the tubular lumen by numerous RBC casts lacking Uromodulin.
Patients with underlying pathologies compromising the glomerular filtration barrier integrity such as IgA nephropathy (identified in our patient) are prone to develop ARN. Ongoing research is looking into thrombin driven activity of PAR-1(expressed in endothelial cells and podocytes) causing local inflammation at the filtration barrier, which along with free iron release (from trapped RBCs) may cause ARN.
These insights emphasize the need for further research to better understand ARN and improve patient management and outcomes.