Kidney allograft biopsy findings after COVID‐19

• Published in: American Journal of Transplantation 2021-12, Vol.21 (12), p.4032-4042
• Main Authors: Daniel, Emily, Sekulic, Miroslav, Kudose, Satoru, Kubin, Christine, Ye, Xiaoyi, Shayan, Katayoon, Patel, Ankita, Cohen, David J., Ratner, Lloyd, Santoriello, Dominick, Barry Stokes, M., Markowitz, Glen S., Pereira, Marcus R., D’Agati, Vivette D., Batal, Ibrahim
• Format: Article
• Language: English
• Subjects: Acute Kidney Injury; Allografts; Arteritis; Biopsy; Brief Communication; Brief Communications; clinical research / practice; complication: infectious; COVID-19; Electron microscopy; Female; Graft rejection; Graft Rejection - etiology; Humans; Hybridization; Immunohistochemistry; Immunosuppression; Infarction; infection and infectious agents ‐ viral; Kidney; kidney (allograft) function / dysfunction; Kidney transplantation; kidney transplantation / nephrology; Kidney transplants; Mechanical ventilation; Middle Aged; SARS-CoV-2; Severe acute respiratory syndrome coronavirus 2
• ISSN: 1600-6135; 1600-6143
• DOI: 10.1111/ajt.16804

COVID‐19 has been associated with acute kidney injury and published reports of native kidney biopsies have reported diverse pathologies. Case series directed specifically to kidney allograft biopsy findings in the setting of COVID‐19 are lacking. We evaluated 18 kidney transplant recipients who were infected with SARS‐CoV‐2 and underwent allograft biopsy. Patients had a median age of 55 years, six were female, and five were Black. Fifteen patients developed COVID‐19 pneumonia, of which five required mechanical ventilation. Notably, five of 11 (45%) biopsies obtained within 1 month of positive SARS‐CoV‐2 PCR showed acute rejection (four with arteritis, three of which were not associated with reduced immunosuppression). The remaining six biopsies revealed podocytopathy (n = 2, collapsing glomerulopathy and lupus podocytopathy), acute tubular injury (n = 2), infarction (n = 1), and transplant glomerulopathy (n = 1). Biopsies performed >1 month after positive SARS‐CoV‐2 PCR revealed collapsing glomerulopathy (n = 1), acute tubular injury (n = 1), and nonspecific histologic findings (n = 5). No direct viral infection of the kidney allograft was detected by immunohistochemistry, in situ hybridization, or electron microscopy. On follow‐up, two patients died and most patients showed persistent allograft dysfunction. In conclusion, we demonstrate diverse causes of kidney allograft dysfunction after COVID‐19, the most common being acute rejection with arteritis. Allograft biopsies from kidney transplant recipients with COVID‐19 with acute kidney injury or proteinuria shows a high incidence of acute rejection with arteritis that is not always associated with decreased immunosuppression.