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Brentuximab-Induced Acute Interstitial Nephritis: A Case Report
Matthew Patterson1, Pouneh Dokouhaki2, Chance S Dumaine1
1Division of Nephrology, Department of Medicine, University of Saskatchewan, Saskatoon, Canada.
Brentuximab vedotin is a combination monoclonal antibody to anti-CD30 conjugated to the anti-tubulin agent monomethyl auristatin E. It is approved for the treatment of mycosis fungoides, Hodgkin's lymphoma, and systemic anaplastic large cell lymphoma. Brentuximab has been associated with a number of potential adverse reactions; however, reports of renal complications are rare. A 73-year-old male with mycosis fungoides was admitted to hospital with acute kidney injury following his third cycle of brentuximab. The patient's serum creatinine (SCr) was 122 µmol/L with an estimated glomerular filtration rate (eGFR) of 58 mL/min/1.73 m2 at baseline. Following brentuximab, his SCr peaked at 1073 µmol/L over a 4-week period. Acute interstitial nephritis (AIN) was diagnosed after other causes of acute kidney injury were ruled out and subsequently confirmed on kidney biopsy. The patient was started on prednisone 50 mg daily. This was continued for 3 weeks, followed by a 5-week taper. The patient's SCr decreased to 156 µmol/L by completion of the prednisone taper. He was not rechallenged with brentuximab. A kidney biopsy confirmed AIN in keeping with injury from an immune checkpoint inhibitor (ICI). However, brentuximab is not an ICI. The AIN from ICIs typically has tubulointerstitial inflammatory infiltrate comprised of T lymphocytes such as the case presented here. Therefore, this represents both a novel histopathologic finding in AIN from a non-ICI medication and a rare complication of brentuximab, previously only presented in abstract form.
Brentuximab vedotin is a combination monoclonal antibody to anti-CD30 conjugated to the anti-tubulin agent monomethyl auristatin E. It is approved for the treatment of mycosis fungoides, Hodgkin's lymphoma, and systemic anaplastic large cell lymphoma. Brentuximab has been associated with a number of potential adverse reactions; however, reports of renal complications are rare. A 73-year-old male with mycosis fungoides was admitted to hospital with acute kidney injury following his third cycle of brentuximab. The patient's serum creatinine (SCr) was 122 µmol/L with an estimated glomerular filtration rate (eGFR) of 58 mL/min/1.73 m2 at baseline. Following brentuximab, his SCr peaked at 1073 µmol/L over a 4-week period. Acute interstitial nephritis (AIN) was diagnosed after other causes of acute kidney injury were ruled out and subsequently confirmed on kidney biopsy. The patient was started on prednisone 50 mg daily. This was continued for 3 weeks, followed by a 5-week taper. The patient's SCr decreased to 156 µmol/L by completion of the prednisone taper. He was not rechallenged with brentuximab. A kidney biopsy confirmed AIN in keeping with injury from an immune checkpoint inhibitor (ICI). However, brentuximab is not an ICI. The AIN from ICIs typically has tubulointerstitial inflammatory infiltrate comprised of T lymphocytes such as the case presented here. Therefore, this represents both a novel histopathologic finding in AIN from a non-ICI medication and a rare complication of brentuximab, previously only presented in abstract form.
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Acute Kidney Injury IV: Diagnostic Studies and Prevention

