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The clinical course and outcomes of immunocompromised patients, such as transplant recipients, with COVID‐19 remain unclear. It has been postulated that a substantial portion of the disease burden seems to be mediated by the host immune activation to the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). Herein, we present a simultaneous heart‐kidney transplant (SHKT) recipient who was hospitalized for the management of respiratory failure from volume overload complicated by failure to thrive, multiple opportunistic infections, and open non‐healing wounds in the setting of worsening renal dysfunction weeks prior to the first case of SARS‐CoV‐2 being detected in the state of Connecticut. After his third endotracheal intubation, routine nucleic acid testing (NAT) for SARS‐CoV‐2, in anticipation of a planned tracheostomy, was positive. His hemodynamics, respiratory status, and ventilator requirements remained stable without any worsening for 4 weeks until he had a negative NAT test. It is possible that the immunocompromised status of our patient may have prevented significant immune activation leading up to clinically significant cytokine storm that could have resulted in acute respiratory distress syndrome and multisystem organ failure. [ABSTRACT FROM AUTHOR]

The widespread transmission of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) continues to propagate the coronavirus disease 2019 (COVID‐19) pandemic with solid organ transplant (SOT) recipients being an exceptionally vulnerable population for poor outcomes. Treatments for COVID‐19 are limited; however, monoclonal antibodies are emerging as a potential therapeutic option to change the trajectory of high‐risk patients. This retrospective single center cohort study evaluated the outcomes of SOT recipients with mild to moderate COVID‐19 who received bamlanivimab monotherapy. Eighteen SOT recipients (15 kidney, 2 liver, and 1 heart) received the medication between November 9, 2020 and February 10, 2021 with no reported infusion reactions. One patient experienced headache and fatigue following the infusion that resolved within 3 days. Fourteen patients continued their recovery as an outpatient with no further escalation in care. Three patients required hospitalization: two for suspected bacterial pneumonia 9 and 32 days postinfusion, respectively, and one for acute kidney injury 7 days postinfusion. One patient had an emergency room visit for gastrointestinal symptoms 24 days postinfusion. In this small cohort of SOT recipients, bamlanivimab monotherapy appeared to be a well‐tolerated option for treatment of mild to moderate COVID‐19, but it was not completely effective in preventing hospitalization. One month following the end of this cohort, COVID‐19 treatment guidance changed due to the rising prevalence of resistant variants. For this reason, bamlanivimab is now recommended to be used only in combination with etesevimab. Further studies are needed to fully elucidate the role of this therapy in SOT recipients. [ABSTRACT FROM AUTHOR]

Utilization of Hepatitis B virus (HBV)‐infected kidney allografts represents an opportunity to bridge the gap between organ supply and demand. Highly efficacious vaccines and antiviral therapies allow these allografts to be transplanted with negligible risk to the recipient. The purpose of this study was to describe the prophylactic strategies and related clinical outcomes of kidney transplant recipients who received a kidney from an HBV viremic donor. Eight patients received an allograft from an HBV viremic deceased kidney donor between January 1, 2017 and December 4, 2020. All recipients were immune to hepatitis B with a surface antibody titer greater than or equal to 10 mIU/ml (range: 12 ‐ > 1000 mIU/ml). After transplant, 62.5% demonstrated HBV core antibody seroconversion at an average of 47.4 ± 28.5 days post‐transplant. Anti‐viral prophylaxis was initiated in 87.5% of patients; 62.5% preemptively during the transplant admission (range 1–3 days post‐transplant) and 25% following HBcAb seroconversion (range 45–304 days post‐transplant). Of the four patients who were started on entecavir preemptively, two subsequently core converted. These two patients had an HBV surface antibody less than 100 mIU/ml at the time of transplant. None of the recipients converted to HBV surface antigen positivity. The average estimated glomerular filtration rate was 41 ± 19 ml/min/1.73m2, and there were no significant elevations in liver enzymes through one year post‐transplant. The use of HBV viremic kidney allografts may represent an additional source of transplant organs; however, more studies are needed to better elucidate the optimal protective strategies for these recipients. [ABSTRACT FROM AUTHOR]

Cytomegalovirus (CMV) is a significant cause of morbidity in kidney transplant recipients (KTR). Historically at our institution, KTR with low and intermediate CMV risk received 6 months of valganciclovir if they received lymphocyte depleting induction therapy. This study evaluates choice and duration of CMV prophylaxis based on donor (D) and recipient (R) CMV serostatus and the incidence of post‐transplant CMV viremia in low (D‐/R‐) and intermediate (R+) risk KTR receiving lymphocyte‐depleting induction therapy. A protocol utilizing valacyclovir for 3 months for D‐/R‐ and valganciclovir for 3 months for R+ was evaluated. Adult D‐/R‐ and R+ KTR receiving anti‐thymocyte globulin, rabbit or alemtuzumab induction from 8/20/2016 to 9/30/2018 were evaluated through 1 year post‐transplant. Patients were excluded if their CMV serostatus was D+/R‐, received a multi‐organ transplant, or received basiliximab. Seventy‐seven subjects met the inclusion criteria: 25 D‐/R‐ (4 historic group, 21 experimental group) and 52 R+ (31 historic, 21 experimental). No D‐/R‐ patients experienced CMV viremia. Among the R+ historic and experimental groups, there was no significant difference in viremia incidence (35.5% vs 52.4%; P =.573). Of these cases, the peak viral load was similar between the groups (median [IQR], 67 [<200‐444] vs <50 [<50‐217]; P =.711), and there was no difference in the incidence of CMV syndrome (16.1% vs 14.3%; P = 1.000) or CMV related hospitalization (12.9% vs 14.3%; P = 1.000). No patient experienced tissue invasive disease. These results suggest limiting valganciclovir exposure may be possible in low and intermediate risk KTR receiving lymphocyte‐depleting induction therapy with no apparent impact on CMV‐related outcomes. [ABSTRACT FROM AUTHOR]

Noncirrhotic hyperammonemia (NCH) is a rare but often fatal complication of solid organ transplantation. We present a case wherein an infectious cause of NCH was suspected following kidney transplantation (KT) and the patient was promptly started on empirical antibiotic treatment which proved to be lifesaving. A 56‐year‐old Chinese woman with a past medical history of end‐stage renal disease secondary to ischemic nephropathy and cerebrovascular accident received a kidney from a 52‐year‐old brain‐dead donor with a Kidney Donor Profile Index score of 70%. She experienced immediate graft function and was discharged on post‐operative day (POD) 4. On POD 10, she presented with a fever, acute onset of confusion, and abdominal pain. Her mental status deteriorated and required emergent intubation. Empiric broad‐spectrum antibiotics were initiated. On hospital day 3, a serum ammonia was 889 μmol/L (normal <53 μmol/L). A urine sample was sent for Ureaplasma polymerase chain reaction (PCR) testing, and moxifloxacin and doxycycline were empirically started. Her ammonia rapidly normalized, and her mental status improved 48 hours after antibiotic initiation. She was extubated 5 days into treatment and was discharged after an 11‐day hospitalization. Following discharge, her urine test resulted positive for Ureaplasma parvum or Ureaplasma urealyticum DNA detection with the 16S rRNA gene amplification probe. Mental status changes and hyperammonemia in the first 30 days post‐KT should raise suspicion for NCH, and prompt empiric treatment with antimicrobials covering Ureaplasma and Mycoplasma should be considered. [ABSTRACT FROM AUTHOR]

Post‐transplant lymphoproliferative disorder (PTLD) is an uncommon, but well‐described complication after liver transplantation. Most recently, Hepatitis C virus (HCV) has been implicated in the development of PTLD. A HCV‐negative 62‐year‐old man with autoimmune hepatitis received a HCV nucleic acid amplification test‐positive liver graft from a 73‐year‐old brain‐dead donor (D+/R−). After his recovery from the operation, the patient was treated for HCV and achieved an undetectable viral load. He was readmitted 6 months after transplant with a spontaneous perisplenic hematoma, weight loss, failure to thrive, low‐grade fevers, and abnormal liver function tests. He had a rapid clinical deterioration and expired shortly after admission. His liver biopsy demonstrated EBV‐negative monomorphic B‐cell PTLD. Our case is the first to report an aggressive early‐onset EBV‐negative monomorphic B‐cell PTLD in a HCV D+/R− liver transplant. This case illustrates the paucity of knowledge on HCV seroconversion and its involvement in EBV‐negative monomorphic B‐cell PTLD development. [ABSTRACT FROM AUTHOR]