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Kidney Week

Abstract: FR-PO0483

Anticoagulant-Related Nephropathy: A Diagnostic Challenge in the Setting of Leukocytoclastic Vasculitis

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Joseph, Megan S., University of Florida, Gainesville, Florida, United States
  • Irfan, Zoha, University of Florida, Gainesville, Florida, United States
  • Canales, Muna T., University of Florida, Gainesville, Florida, United States
Introduction

Anticoagulant-related nephropathy (ARN) is an underrecognized cause of acute kidney injury (AKI) driven by glomerular hemorrhage and tubular obstruction from red blood cell (RBC) casts. Although it has been mostly described with warfarin, there is growing recognition that direct oral anticoagulants (DOACs) may also play a role.

Case Description

A 65-year-old man with atrial fibrillation, type 2 diabetes, and significant peripheral vascular disease on long-term dabigatran presented with a painful, progressive rash involving his lower extremities and trunk. Skin biopsy confirmed leukocytoclastic vasculitis thought related to dabigatran by dermatology. ANCA serologies were negative. Dabigatran was replaced by apixaban, and his rash improved over several weeks.
Approximately one month later, he was admitted with dysuria, retention, and gross hematuria. His serum creatinine (SCr) rose from 0.8 mg/dL to 4.2 mg/dL. Methicillin-resistant Staphyolococcus Aureus urinary tract infection with bacteremia was diagnosed and treated with antibiotics. AKI was thought to be related to obstruction and ATN from sepsis. SCr declined to 3.3 mg/dL on discharge
One week later, SCr rose to 5.3 mg/dL with non-nephrotic range proteinuria. ANA and ANCA serologies were negative, and complements were normal. Kidney biopsy demonstrated acute tubular injury with numerous intratubular RBCs/casts; IFTA was 40%. Of 14 glomeruli, one had a small necrotizing lesion by light microscopy; the remainder were normal. Immunofluorescence was negative, and EM showed one glomerulus with a crescent. Given the degree of hematuria out of proportion to glomerular findings, we suspected anticoagulant-related nephropathy. However, the presence of rare glomerular inflammation raised the question of negative pauci-immune vasculitis (primary or infection-related) vs anticoagulant-related vasculitis. Apixaban was discontinued, and he received 2 weeks of empiric corticosteroids but ultimately required dialysis.

Discussion

ARN can be difficult to recognize when multiple competing causes of AKI are present, given increasing evidence that DOACs may cause ARN.
ARN should be considered in patients with AKI and gross hematuria receiving DOAC therapy, especially when the clinical picture is unclear.