Coronavirus disease 2019 (COVID-19) has become a pandemic since first being described in January 2020. Clinical manifestations in non-transplant patients range from asymptomatic infection to severe pneumonia with acute respiratory distress syndrome, multiorgan system failure, and death. Limited reports in kidney transplant recipients suggest similar characteristics in that population. We report here the first case series of COVID-19 infection occurring in pancreas transplant recipients.

The optimal management in transplant recipients with coronavirus disease 2019 (COVID-19) remains uncertain. The main concern is the ability of immunosuppressed patients to generate sufficient immunity for antiviral protection. Here, we report on immune monitoring facilitating a successful outcome of severe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-associated pneumonia, meningoencephalitis, gastroenteritis, and acute kidney and pancreas graft failure in a pancreas-kidney transplant recipient. Despite the very low numbers of circulating B, NK, and T cells identified in follow-up, a strong SARS-CoV-2 reactive T cell response was observed. Importantly, we detected T cells reactive to Spike, Membrane, and Nucleocapsid proteins of SARS-CoV-2 with majority of T cells showing polyfunctional proinflammatory Th1 phenotype at all analyzed time points. Antibodies against Spike protein were also detected with increasing titers in follow-up. Neutralization tests confirmed their antiviral protection. A correlation between cellular and humoral immunity was observed underscoring the specificity of demonstrated data. We conclude that analyzing the kinetics of nonspecific and SARS-CoV-2-reactive cellular and humoral immunity can facilitate the clinical decision on immunosuppression adjustment and allow successful outcome as demonstrated in the current clinical case. Although the antiviral protection of the detected SARS-CoV-2-reactive T cells requires further evaluation, our data prove an ability mounting a strong SARS-CoV-2-reactive T cell response with functional capacity in immunosuppressed patients.

Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) preferentially affects epithelia of the upper and lower respiratory tract. Thus, impairment of kidney function has been primarily attributed until now to secondary effects such as cytokine release or fluid balance disturbances. We provide evidence that SARS-CoV-2 can directly infiltrate a kidney allograft. A 69-year-old male, who underwent pancreas-kidney transplantation 13 years previously, presented to our hospital with coronavirus disease 2019 (COVID-19) pneumonia and impaired pancreas and kidney allograft function. Kidney biopsy was performed showing tubular damage and an interstitial mononuclear cell infiltrate. Reverse transcriptase polymerase chain reaction from the biopsy specimen was positive for SARS-CoV-2. In-situ hybridization revealed SARS-CoV-2 RNA in tubular cells and the interstitium. Subsequently, he had 2 convulsive seizures. Magnetic resonance tomography suggested meningoencephalitis, which was confirmed by SARS-CoV-2 RNA transcripts in the cerebrospinal fluid. The patient had COVID-19 pneumonia, meningoencephalitis, and nephritis. SARS-CoV-2 binds to its target cells through angiotensin-converting enzyme 2, which is expressed in a broad variety of tissues including the lung, brain, and kidney. SARS-CoV-2 thereby shares features with other human coronaviruses including SARS-CoV that were identified as pathogens beyond the respiratory tract as well. The present case should provide awareness that extrapulmonary symptoms in COVID-19 may be attributable to viral infiltration of diverse organs.

The novel coronavirus disease 2019 (COVID-19) is associated with increased risk of thromboembolic events, but the extent and duration of this hypercoagulable state remain unknown. We describe the first case report of renal allograft infarction in a 46-year-old kidney-pancreas transplant recipient with no prior history of thromboembolism, who presented 26 days after diagnosis of COVID-19. At the time of renal infarct, he was COVID-19 symptom free and repeat test for SARS-CoV-2 was negative. This case report suggests that a hypercoagulable state may persist even after resolution of COVID-19. Further studies are required to determine thromboprophylaxis indications and duration in solid organ transplant recipients with COVID-19.

https://doi.org/10.1016/j.kint.2020.09.004

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly contagious pathogen causing the novel coronavirus disease 2019 (COVID-19), the ongoing unprecedented pandemic in 2020 SARS-CoV-2 primarily targets the respiratory systems, so acute respiratory distress syndrome is the major cause of death Clinical courses of COVID-19 are variable and unpredictable, while some epidemiologic and clinical factors have been found to have a negative impact on the disease prognosis Despite a growing report on clinical characteristics and prognosis of patients with COVID-19, the data in the special population, including transplant recipients, is still limited Herein we report on the clinical features and fatal outcome of COVID-19 in a dual pancreas-kidney transplant recipient (with failure of the pancreas graft) Our case illustrates the similarities and differences of the COVID-19 disease course between transplant recipients and the general population We proposed that the preexisting T-cell dysfunction from the long-term use of immunosuppressive agents in organ transplant recipients adversely affects COVID-19 prognosis and worsens COVID-19 mortality