Part Ⅰ：COVID-19 Infection in Kidney Transplant Recipients
Mar 04, 2022
Contact: emily.li@wecistanche.com
By 21 March 2020 infections related to the novel coronavirus SARS-CoV-2 had affected people from 177 countries and caused 11,252 reported deaths worldwide. Little is known about the risk, presentation, and outcomes of SARS-CoV-2 (COVID-19) infection in kidney transplantation recipients, who may be at high risk due to long-term immunosuppression, comorbidity, and residual chronic kidney disease. Whilst COVD-19 is predominantly a respiratory disease, in severe cases, it can cause kidney and multi-organ failure. It is unknown if immunocompromised hosts are at higher risk of more severe systemic disease. Therefore, we report on seven cases of COVID-19 in kidney transplant recipients (median age 54 (range 45-69), three females, from a cohort of 2082 managed transplant follow-up patients) over a six-week period in three south London hospitals. Two of seven patients presented within three months of transplantation. Overall, two were managed on an out-patient basis, but the remaining five required hospital admission, four in intensive care units. All patients displayed respiratory symptoms and fever. Other common clinical features included hypoxia, chest crepitation, lymphopenia, and high C-reactive protein. Very high D dimer, ferritin, and troponin levels occurred in severe cases and are likely prognostic. Immunosuppression was modified in six of seven patients. Three patients with severe disease were diabetic. During a three-week follow up one patient recovered, and one patient died. Thus, our findings suggest COVD-19 infection in kidney transplant patients may be severe, requiring intensive care admission. The symptoms are predominantly respiratory and associated with fever. Most patients had their immunosuppression reduced and were treated with supportive therapy.
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The novel coronavirus 2019 (or coronavi-rus disease 2019 [COVID-19]) infection. which originated in the city of Wuhan, in Hubei province, China, in December 2019 shares close similarities in its genomic structure with the severe acute respiratory syndrome coronavirus (SARS-CoV)that caused the SARS global pandemic in 2003 and the Middle East respiratory syndrome(MERS) epidemic in 2012(MERS-CoV), and even closer similarities to bat SARS-like betacoronavirus (bat-SL-CoVZC45 betacoronavirus and bat-SL-CoVZXC21):2. Between December 31, 2019, and March 27, 2020.532692COVID-19cases and24.077 deaths worldwide have been identified as being caused by a newly identified enveloped RNA virus named SARS-CoV-2.In the United Kingdom, between January 31, 2020, and March20,2020,3983 cases were identified with 177(4% of tested patients)deaths."Due to its widespread nature, COVID-19 was declared a pandemic by World Health Organization on March 11, 2020, and 176 countries are affected as of March 27, 2020.
The SARS pandemic was reported to affect both pediatric and adult kidney transplant recipients in Hong Kong, with less severe dis-ease in the pediatric population. One liver transplant patient died from the SARS-CoV infection in 2003. The MERS coronavirus infection had a variable impact on kidney transplant recipients. In 1 report of 2 kidney transplant patients, one died of progressive respiratory disease and acute kidney injury while the other survived. To the best of our knowledge, only 1 patient with kidney transplantation has been reported in the literature who suffered from COVID-19 infection in Wuhan, China, and improved 13 days after hospital admission." The 63-year-old kidney transplant recipient presented with fever, chest pain, cough, low lymphocyte, high serum C-reactive protein(CRP), and an abnormal chest computed tomography scan on February 2, 2020. Tacrolimus and mycophenolate administration was discontinued. He was treated with oxygen, methylprednisolone, umifenovir, moxifloxacin, biapenem, iv. Ig, inhaled inter-feron-U,and pantoprazole. He made a successful recovery and was discharged on day 13.
Table 1| Clinical characteristics and outcome of 7 kidney transplant patients with COVD-19 infection
We report here the first 7 cases of COVID. 19 in kidney transplant recipients in south London hospitals.
Cases
We have seen 7 cases of kidney transplant recipients with proven COVID-19 infection in south London in March 2020. These patients are described herein, and their main characteristics are summarized in Tables 1 and 2.
Table 2 | Blood parameters during COVID-19 infection
Patient 1. An A48-year-old man with a deceased donor kidney transplant in 1989 with a failing transplant kidney (estimated glomerular filtration rate [eGFRl: 15-18 ml/min per 1.73 m))called the National Health Service (111) help-line in the first week of March 2020 with cough, fever, and mild shortness of breath. He tested positive for COVID-19 by nose and throat swabs taken on March 2. As he was clinically well, he was asked to stay at home and self-isolate. His immunosuppression was azathioprine 75 mg once daily (OD) and prednisolone 5 mg OD, which was not changed, He was not on an angiotensin-converting enzyme inhibitor and/or angiotensin receptor blocker at the time of presentation. He has made a full recovery. The transplant kidney function remained stable.
Patient 2. A 67-year-old woman with insulin-dependent type 2 diabetes and end-stage kidney disease on hemodialysis therapy for 4 years received a deceased donor kidney transplant in March 2019. Her eGFR was 45 to 55 ml/min per 1.73 m*. She was maintained on tacrolimus with levels between 5 and 8 ng/ml, mycophenolate mofetil (MMF)250 mg twice a day(BD), and prednisolone 5 mg OD. Her other medications included ramipril, aspirin, alfacalcidol, and amiloride. She presented on March 5 with a cough. fever, and shortness of breath. Chest X-ray revealed bilateral patchy consolidation (Figure la). SARS-CoV-2 RNA polymerase chain reaction tests from nose and throat viral swabs were positive. Bronchial washing for pneumocystis polymerase chain reaction was negative, as was blood polymerase chain reaction for cytomegalovirus DNA. There was no other positive microbiological diagnosis. She was hypoxic with peripheral oxygen saturation of 86% and a respiratory rate of 26 breaths/min, so she was transferred to the intensive therapy unit(TU) and commenced noninvasive ventilation (continuous positive airway pressure for type 1 respiratory failure)and subsequent intubation and ventilation as her clinical condition deteriorated. Serum CRP on admission was 83 mg/l.hemoglobin 110 g/. with normal total white cell count, and mild lymphopenia (lymphocyte count 0.8 ×10°/). She was treated with broad-spectrum antibiotics. No specific antiviral drugs were given. MMF was ceased. Low-dose tacrolimus was initially continued but stopped 1 day before death. On day 3 post-admission, she developed acute kidney injury (AKI, with a serum creatinine increase to 225 umol/l.She remained stable on the ventilator with reducing oxygen requirements and improvement in lung infiltrates on chest X-ray(Figure 1b)but deteriorated markedly on March 16 with high serum lactate and lactate dehydrogenase levels and an acute rise of CRP to 190. She developed severe metabolic acidosis resistant to correction on continuous venovenous hemodiafiltration, probably owing to an intra-abdominal event (bowel infarction and/or intra-abdominal sepsis), She deteriorated rapidly and died on March 17.
Figure 1 | Case 2: Chest X-ray (a) on admission showing bilateral patchy consolidation and (b) 8 days later showing improvement in lung infiltrates.
Patient 3. A 54-year-old woman with a history of adult polycystic kidney disease, end-stage kidney disease in 2012, was on hemodialysis for 7 years and received a deceased donor kidney transplant in December 2019. Soon thereafter, she experienced an episode of cytomegalovirus infection and developed post-transplant diabetes mellitus. Her medications included BD doses of tacrolimus 11 mg and MMF 500 mg and OD doses of prednisolone 5 mg, amlodipine 5 mg, aspirin 75 mg, bisoprolol 2.5 mg, co-trimoxazole 480 mg, doxazosin 2 mg, isoniazid 300 mg, omeprazole 20 mg, pyridoxine 25 mg, and gliclazide 120 mg and 80 mg (morning and evening). Three months after the deceased donor's kidney transplantation, on March 10, she presented with shortness of breath to the emergency department. On initial assessment, her oxygen saturations were 60%with a heart rate of 105 beats/min and blood pressure of 190/99 mm Hg. She was started immediately on continuous positive airway pressure and her oxygen saturations improved to 87%. Auscultation of the chest revealed widespread crepitations and her chest X-ray showed bilateral pulmonary infiltrates (Supplementary Figure S1A). She was found to be positive for SARS-CoV-2 RNA. Her cytomegalovirus, adenovirus, and another respiratory viral screen along with atypical pneumonia serologies were negative. There was no other positive microbiological diagnosis. She developed features of acute respiratory distress syndrome and AKI （creatinine 242 μmol/l， baseline 132 μumol/l).
Her respiratory status rapidly deteriorated in the emergency department and she required intubation 8 hours later and continues to be ventilated currently. MMF was stopped on March 10 and tacrolimus on March 16. Broad-spectrum antibiotics and antiviral, oseltamivir was administered. She was also empirically treated for pneumocystis with high dose co-trimoxazole. Serum CRP decreased from 329 mg/ on day of admission to 169 mg/l 7 days later. She became anuric and started continuous venovenous hemofiltration, which continues. Her latest chest X-ray showed some resolution of the pulmonary infiltrates.
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