key: cord-0851710-6idi5frm authors: Bussalino, Elisabetta; De Maria, Andrea; Russo, Rodolfo; Paoletti, Ernesto title: Immunosuppressive therapy maintenance in a kidney transplant recipient with SARS‐CoV‐2 pneumonia: A case report date: 2020-05-08 journal: Am J Transplant DOI: 10.1111/ajt.15920 sha: df31ed83b1fe967b7fcc353c8819c18fa09386ea doc_id: 851710 cord_uid: 6idi5frm The role of systemic inflammation is proving crucial in determining unfavorable outcome in SARS‐CoV‐2–infected patients. Limited data are available regarding immunosuppression management in kidney transplant recipients (KTRs) with SARS‐CoV‐2 pneumonia. We report a case of a 32‐year‐old KTR who developed SARS‐CoV‐2 infection and fully recovered in 15 days while maintaining standard immunosuppressive therapy. The novel coronavirus outbreak has startled the world due to its widespread diffusion and socioeconomic burden. Kidney transplant recipients (KTRs) are perceived to be at high risk of infection, and immunosuppressive therapy management during this global emergency can be a challenge. Herein, we report the case of a KTR who developed SARS-CoV-2 pneumonia and recovered in 15 days while continuing administration of his usual immunosuppressive treatment. The patient is a 32-year-old man who underwent kidney transplantation in September 2017 from a deceased donor; ESRD etiology was unknown. Prior to admission, February 3, 2020, his most recently measured creatinine level was 1.9 mg/dL (eGFR 46 mL/min/1.73 m 2 ). Immunosuppressive therapy consisted in tacrolimus (trough levels 6-8 ng/mL), mycophenolic acid (360 mg BID), and prednisone (5 mg). Induction therapy included ATG and basiliximab. Previous medical history was irrelevant except for hypertension and pericarditis treated with colchicine in February, 2017. On March 12, 2020, the patient was admitted to our emergency room after a fever lasting 3 days, dyspnea and non-productive cough, unsuccessfully treated with amoxicillin-clavulanate 1 g TID. Physical evaluation was normal: body temperature was 38°C and oxygen saturation was 97% in ambient air, blood pressure was 130/70 mm Hg, and respiratory rate was 25 breaths per minute. Laboratory results demonstrated a low percentage of lymphocytes (17.8%), absolute and relative monocytosis (1000/mmc; 16.7%), C-reactive protein (CRP) elevation (47.9 mg/L), and slightly elevated levels of procalcitonin (PCT) (0.33 µg/L). Renal function impairment was observed (creatinine 2.6 mg/dL, eGFR 31 mL/min/1.73 m 2 ). Pneumococcus and Legionella infections were ruled out by negative urinary antigens. Arterial blood gas analysis was suggestive of respiratory alkalosis. Chest X-ray demonstrated diffuse septal thickening in the absence of areas of consolidation. On March 13, nasopharyngeal swab testing was performed and SARS-COV-2 was identified by rRT-PCR (Day 0). and IL-6 levels were significantly decreased (respectively, 18 mg/L and 6.9 ng/L). Renal function was comparable to what it was at admission (creatinine 2.8 mg/dL, eGFR 29 mL/min/1.73 m 2 ) and proteinuria had significantly increased (Day 0:1 g/L; Day 11:3 g/L). Symptoms, laboratory results, and treatments are described in Table 1 . In December 2019, SARS-CoV-2 was identified in Wuhan, China. In February 2020, the first case was diagnosed in Italy, and within a few weeks, the COVID-19 infection has taken on the characteristics of a "pandemic." Based on this rationale and on laboratory results demonstrating hyperinflammation, 5 immunosuppressive therapy was left unchanged and therefore lopinavir/ritonavir was not administered due to proven drug interaction with calcineurin inhibitors. Even though corticosteroid use in COVID-19 pneumonia remains controversial, 6,7 we increased our patient's prednisone dose to 15 mg for 9 days as an anti-inflammatory agent. Interestingly, we did not observe complete recovery of graft function, and moreover, proteinuria developed. Further investigation into these findings is needed. Since discharge, the patient's clinical condition has been closely monitored via telephone. Immunosuppression in critically ill patients is still a matter of debate. As recently highlighted by Ritchie and Singanayagam in their letter, 8 flammation may be consequential and directly related rather than an excessive response by the immune system. Therefore, the impact of immunosuppressive therapy is crucial in transplant recipients. In conclusion, although our evidence is anecdotal, it may provide some clinical insight into therapeutic management. Maintaining immunosuppression could be beneficial in stopping, or at least mitigating the "cytokine storm" that usually leads to poor outcome in these patients and, only secondarily, in preventing graft rejection. Further studies are warranted to confirm these findings and to evaluate the clinical and laboratory characteristics of the KTRs who might benefit from this therapeutic strategy. The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation. The data that support the findings of this study are available on request from the corresponding author, [EP] and with permission from Policlinico San Martino. The data are not publicly available due to their containing information that could compromise the privacy of research participant. Ernesto Paoletti https://orcid.org/0000-0002-5509-6252 Coronaviruses and immunosuppressed patients. 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