key: cord-0708257-yae7ip3j authors: Mohamed, Maha; Smith, Jeannina; Parajuli, Sandesh; Garg, Neetika; Aziz, Fahad; Mandelbrot, Didier; Djamali, Arjang; Zhong, Weixiong title: Successful management of T‐cell mediated rejection in a recent kidney transplant recipient with COVID‐19 associated severe acute respiratory syndrome date: 2021-04-08 journal: Transpl Infect Dis DOI: 10.1111/tid.13598 sha: f86b21dc98ad7354796330c557cd03c3ee085026 doc_id: 708257 cord_uid: yae7ip3j COVID‐19‐associated vasculitis has been reported as a defining feature of systemic disease including acute kidney injury. However, the understanding of COVID‐19 kidney transplant‐related injuries is still evolving. We report a case of AKI with isolated vasculitis (v2 lesion) in a new kidney transplant recipient with COVID‐19 pneumonia. glomeruli were normal and focal few atrophic tubules with minimal interstitial fibrosis were identified, as shown in Figure 1 . Intravascular fibrin thrombi were not seen. Electron microscopy from two glomeruli recovered from the paraffin block was examined ( Figure 4) . The glomeruli showed normo-cellularity, no basement membrane alterations, and no electron-dense deposits ( Figure 4A and 4B ). There was minimal foot process effacement. We report a case of AKI and predominantly v2 lesion involving small arteries and arterioles in a kidney transplant recipient with COVID-19 pneumonia within 1 month after transplantation. At the time of biopsy, we were unable to clearly determine whether this pathological finding was related to TCMR or COVID-19 infection. However, as the patient responded to high dose IV steroids, the diagnosis of TCMR became more plausible. Isolated intimal arteritis may be seen in rejection and typically involves medium-sized arteries, commonly in grade II TCMR and occasionally in ABMR. The biopsy in our case showed unusual pathological changes with predominantly endothelial cell hyperplasia involving multiple small arteries and arterioles which coexisted with inflammation in the i-IFTA area. 5 Covid-19 infection has been reported to cause vasculitis and vasculopathy directly through tissue tropism, indirect innate immunity related inflammatory response, and leukocyte debris. 6 Therefore, differential diagnosis in our patient includes acute TCMR and Covid-19-associated vasculitis. Tubular injury is most likely secondary to vascular changes. However, the clinical course and progression timeline which included immunosuppression minimization, response to pulse steroids with gradual maximization of the immunosuppressive regimen, and absence of viral inclusion bodies on the biopsy support that the AKI was more likely secondary to TCMR. Banff i-IFTA2 or 3 score is an essential component of chronic active TCMR. However, it is not sufficient to make a diagnosis of chronic active TCMR as it also requires at least ti2 and t2 lesions involving cortical tubules other than severely atrophic tubules. 5, 7 i-IFTA itself is not a specific lesion and is seen in the context of tissue injury because of many causes other than TCMR, including BK virus nephropathy and ABMR. 7 infection (20 -28% vs 1 -5%). 12 Accordingly, the balance between timing, effective and safe utilization of induction therapy and maintenance immunosuppression and the intensity of the regimen plays a pivotal role in the management of these patients so as to achieve allograft survival without compromising the recipient survival. 11, 13 Our case highlights the possibility of TCMR in recently transplanted patients whose immunosuppression is reduced in the context of severe COVID pneumonia. We further report that TCMR may be safely managed with pulse steroids in patients with early post-transplant COVID-19 pneumonia. The authors of this case report certify that they have no conflict of interest to disclose as described by the Transplant Infectious Disease Journal. 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The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.