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<p>Anticoagulant-related nephropathy (ARN) is a critical disease with clinical manifestations including acute kidney injury (AKI), which develops months after drug administration commences. The risk of ARN associated with direct oral anticoagulant agents (DOACs) is lower than that for warfarin, but there have been reports of ARN induced by DOACs other than dabigatran, such as edoxaban. We describe a patient with ARN caused by edoxaban, after the long-term use of warfarin and a switch from dabigatran, who had underlying IgA nephropathy with normal renal function. A 75-year-old man presented with AKI, with hematuria and proteinuria. He had never previously experienced urinary abnormalities or renal impairment. He was started on warfarin for atrial fibrillation 17&#xa0;years previously, then switched to dabigatran for 11&#xa0;years, and then edoxaban for 3&#xa0;years. Three months before admission, he developed melena and hematuria. On the basis of his medical history and renal pathologic findings, he was diagnosed with ARN complicated by IgA nephropathy, with interstitial lesions and marked arteriosclerosis. After discontinuing edoxaban and methylprednisolone pulse therapy followed by oral prednisolone, his proteinuria diminished, and his renal dysfunction and hematuria were ameliorated. ARN can develop at any time in association with any DOAC, even in patients with normal renal function, and may be associated with anticoagulant overdose and subclinical IgA nephropathy. Therefore, careful monitoring of renal function and urinalysis is necessary for the prevention and early recognition of ARN, and dose reduction or a change in anticoagulant should occur when anticoagulant overdose or ARN is suspected.</p>

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A case of anticoagulation-related nephropathy complicated by IgA nephropathy that developed following the long-term use of anticoagulants

  • 期刊论文

  • 发表日期：

    2025年8月8日

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  • Yuko Oyama,
  • Yoichi Iwafuchi,
  • Yumi Ito,
  • Naofumi Imai,
  • Ichiei Narita

摘要

Anticoagulant-related nephropathy (ARN) is a critical disease with clinical manifestations including acute kidney injury (AKI), which develops months after drug administration commences. The risk of ARN associated with direct oral anticoagulant agents (DOACs) is lower than that for warfarin, but there have been reports of ARN induced by DOACs other than dabigatran, such as edoxaban. We describe a patient with ARN caused by edoxaban, after the long-term use of warfarin and a switch from dabigatran, who had underlying IgA nephropathy with normal renal function. A 75-year-old man presented with AKI, with hematuria and proteinuria. He had never previously experienced urinary abnormalities or renal impairment. He was started on warfarin for atrial fibrillation 17 years previously, then switched to dabigatran for 11 years, and then edoxaban for 3 years. Three months before admission, he developed melena and hematuria. On the basis of his medical history and renal pathologic findings, he was diagnosed with ARN complicated by IgA nephropathy, with interstitial lesions and marked arteriosclerosis. After discontinuing edoxaban and methylprednisolone pulse therapy followed by oral prednisolone, his proteinuria diminished, and his renal dysfunction and hematuria were ameliorated. ARN can develop at any time in association with any DOAC, even in patients with normal renal function, and may be associated with anticoagulant overdose and subclinical IgA nephropathy. Therefore, careful monitoring of renal function and urinalysis is necessary for the prevention and early recognition of ARN, and dose reduction or a change in anticoagulant should occur when anticoagulant overdose or ARN is suspected.