Solid organ transplant (SOT) recipients are at high risk for severe coronavirus disease 2019 (COVID‐19). Studies suggest that early intervention with monoclonal antibody (MAB) treatment directed against the SARS‐CoV‐2 spike protein may reduce the risk of emergency department visits or hospitalization for COVID‐19, especially in high‐risk patients. Herein we describe our single‐center experience of 93 SOT (50 kidney, 17 liver, 11 lung, 9 heart and 6 dual‐organ) recipients with mild to moderate COVID‐19 who were treated with bamlanivimab or casirivimab‐imdevimab per Emergency Use Authorization guidelines. Median age of recipients was 55 (IQR 44–63) years and 41% were diabetic. Median time from transplant to MAB was 64 (IQR 24–122) months and median time from onset of COVID‐19 symptoms to the infusion was 6 (IQR 4–7) days. All patients had a minimum 30 days of study follow up. The 30‐day hospitalization rate for COVID‐19 directed therapy was 8.7%. Infusion‐related adverse events were rare and generally mild. Biopsy‐proven organ rejection occurred in 2 patients and there were no graft losses or deaths. A comparator group of 72 SOT recipients diagnosed with COVID‐19 who were eligible but did not receive MAB treatment had a higher 30‐day hospitalization rate for COVID‐19 directed therapy (15.3%), although this difference was not statistically significant, after adjustment for age [OR 0.49 (95% CI 0.18‐1.32), p = 0.16]. Our experience suggests that MAB treatment, with respect to the available MAB formulations and circulating viral variants present during our study period, may provide favorable outcomes for mild to moderate COVID‐19 in SOT recipients. This article is protected by copyright. All rights reserved

Background. Transplantation of hepatitis C viremic (HCV+) deceased donor kidney transplants (DDKT) into aviremic (HCV-) recipients is a strategy to increase organ utilization. However, there are concerns around inferior recipient outcomes due to delayed initiation of direct-acting antiviral (DAA) therapy and sustained HCV replication when implemented outside of a research setting. Methods. This was a retrospective single-center matched cohort study of DDKT recipients of HCV+ donors (cases) who were matched 1:1 to recipients of HCV-donors (comparators) by age, gender, race, presence of diabetes, kidney donor profile index, and calculated panel-reactive antibody. Data were analyzed using summary statistics, t-tests, and chi-square tests for between-group comparisons, and linear mixed-effects models for longitudinal data. Results. Each group consisted of 50 recipients with no significant differences in baseline characteristics. The 6-mo longitudinal trajectory of serum creatinine and estimated glomerular filtration rate did not differ between groups. All recipients had similar rates of acute rejection and readmissions (all P > 0.05). One case lost the allograft 151 d posttransplant because of acute rejection, and 1 comparator died on postoperative day 7 from cardiac arrest. HCV+ recipients initiated DAA on average 29 ± 11 d posttransplant. Ninety-eight percent achieved sustained virologic response at 4 and 12 wks with the first course of therapy; 1 patient had persistent HCV infection and was cured with a second course of DAA. Conclusions. Aviremic recipients of HCV+ DDKT with delayed DAA initiation posttransplant had similar short-term outcomes compared with matched recipient comparators of HCV-donors.

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A 35-year-old Caucasian male with end-stage kidney disease due to glomerulonephritis and a failed living-related kidney transplant received a subsequent deceased donor kidney transplant. He was induced with alemtuzumab and solumedrol and maintained on tacrolimus, mycophenolate, and prednisone. Approximately 3 years later, he presented with one month of intermittent fevers, myalgias, malaise, and weight loss. He denied cough, night sweats, joint pain, nausea, vomiting, or diarrhea. He had been caring for an ill cat, but denied other infectious or environmental exposures. He appeared chronically ill but physical exam was otherwise unremarkable including no fever, lymphadenopathy, rash, or murmurs. Workup showed lymphopenia with a white blood cell count of 4400/mcL and an absolute lymphocyte count of 390/mcL (baseline 2380/mcL pre-transplant and 200-250/mcL posttransplant), CD4 count 130, creatinine 2.88 mg/dl (baseline 1.9 mg/dl), AST 50u/L, CRP 71.8 mg/L, and ferritin 9,784 ng/mL. Urinalysis revealed 1 WBC, 1 RBC, and no proteinuria. CT imaging revealed moderate splenomegaly (15.0 cm) and subtle bilateral ground glass opacities within the lungs. Infectious workup returned negative for Human Immunodeficiency Virus,