Saudi Journal of Kidney Diseases and Transplantation

LETTER TO THE EDITOR
Year
: 2020  |  Volume : 31  |  Issue : 6  |  Page : 1448--1450

The specificity of the novel coronavirus infection in transplantation recipients


Driss Elkabbaj, Abdelali Bahadi 
 Department of Nephrology-Dialysis and Kidney Transplantation, Military Hospital of Instruction Mohamed 5, Rabat, Morocco

Correspondence Address:
Driss Elkabbaj
Department of Nephrology-Dialysis and Kidney Transplantation, Military Hospital of Instruction Mohamed 5, Rabat
Morocco




How to cite this article:
Elkabbaj D, Bahadi A. The specificity of the novel coronavirus infection in transplantation recipients.Saudi J Kidney Dis Transpl 2020;31:1448-1450


How to cite this URL:
Elkabbaj D, Bahadi A. The specificity of the novel coronavirus infection in transplantation recipients. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2021 Aug 1 ];31:1448-1450
Available from: https://www.sjkdt.org/text.asp?2020/31/6/1448/308371


Full Text



To the Editor,

A novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causing a SARS with its disease designated as coronavirus disease-2019 (COVID-19), emerged from its epicenter in Wuhan, China in December 2019 and is now a global pandemic. COVID-19 involves 292,142 confirmed cases and 12,784 deaths in the last update on March 21, 2020.[1] The majority of COVID-19 cases (87%) occur between 30 and 79 years of age and most (81%) are mild (no or mild pneumonia). The remaining 14% present with severe symptoms (e.g., with dyspnea, hypoxia, or >50% lung involvement on imaging within 24–48 h) while 5% require care in an intensive care unit (e.g., with respiratory failure, shock, or multiorgan dysfunction).[2] The case-fatality rate has been touted to be 2.3% overall, no deaths were reported among non-critical cases. However, death rates climb in those aged ≥80 years (15%) and in nearly half of those requiring critical care.[2] Most of the fatal cases have occurred in patients with advanced age or underlying medical comorbidities(including cardiovascular disease, diabetes mellitus, chronic lung disease, hypertension, and cancer).[2],[3] This article will discuss the specificity of COVID-19 in transplanted patients.

Person-to-person spread of SARS-CoV-2 is thought to occur mainly via respiratory droplets, resembling the spread of influenza. The viral shedding may occur stealthily for days or weeks in asymptomatic carriers, especially children,[1],[2],[3] and fecal shedding has been noted in patients without diarrhea.[3] Significant environmental contamination has been noted, including a sink, toilet bowl, and the surfaces of the air outlet ventilators in hospitalized patients.[4] It is, therefore, prudent to advise transplant recipients to rigorously practice social distancing strategies, disinfection, hand hygiene, and avoidance of areas known to harbor potentially infected individuals.

Solid organ transplant recipients are under chronic immunosuppression, and respiratory infections may present atypically. Unlike other viruses (adenovirus, rhinovirus, norovirus, influenza, and respiratory syncytial virus),[5],[6] COVID-19 does not give particularly more severe symptoms in transplant recipients than in the rest of the population.[7],[8] The clinical manifestations may not be different from other patients, with mild (fever, fatigue, dry cough, anorexia, and body aches) and severe symptoms (dyspnea, acute respiratory distress syndrome). In patients with COVID-19, the white blood cell count can vary. Leukopenia, leukocytosis, and lymphopenia have been reported, although lymphopenia appears most common.[7],[8] In the transplant recipients, the lymphopenia is similar to non-transplant patients. The chest computed tomography (CT) in patients with COVID-19 most commonly demonstrates ground-glass opacification with or without consolidative abnormalities, consistent with viral pneumonia.[9],[10] Case series have suggested that chest CT scan abnormalities are more likely to be bilateral, have a peripheral distribution, and involve the lower lobes. Less common findings include pleural thickening, pleural effusion, and lymphadeno-pathy. The CT images can be superimposed on non-transplanted patients.[11] For laboratory testing, the SARS-CoV-2 RNA is detected by reverse-transcription polymerase chain reaction, in the collection of a nasopharyngeal swab specimen, the positive viral RNA tests reported is 32%, the highest rates of positive viral RNA tests were reported from bronchoalveolar lavage (95%) and sputum (72%).[12] Other, less common symptoms have included headache, sore throat, and rhinorrhea. In addition to respiratory symptoms, gastrointestinal symptoms (e.g., nausea and diarrhea) have also been reported.[8] One case of kidney transplant was manifested by digestive signs (vomiting) with fever without cough, pulmonary signs appeared after.[13]

If the patient has initially mild symptoms, he/she should be isolated with close monitoring of progress-to-severe form, it may progress over the course of a week. The dyspnea had developed in one study of 138 patients, not transplanted, hospitalized in Wuhan for pneumonia due to SARS-CoV-2, after a median of five days since the onset of symptoms, and hospital admission occurred after a median of seven days of symptoms.[7] In another study, the median time to dyspnea was eight days.[8] If the transplanted patient developed severe disease, it is a major complication, Other complications have included arrhythmia, acute cardiac involvement or shock,[7] the immunosuppressive treatment should be discontinued, the rest of the treatment should be the same as a patient not taking immunosuppressive therapy. The therapy for manifest disease is gravely lacking at this time although promise is on the horizon. While several molecules are under investigation, remdesivir (an adenosine analog that incorporates into viral RNA chains and results in premature termination) and chloroquine (an anti-malarial drug that prevents viral cell fusion, and interferes with glycosylation of cellular receptors of SARS-CoV appear to have early in-vitro evidence in support of their potential activity against SARS-CoV-2.[14],[15] Due to the interaction of Ritonavir with calci-neurin inhibitors, tacrolimus must be withdrawn. We must limit the intake of gluco-corticoids, The World Health Organization recommends that glucocorticoids not be used in patients with COVID-19 pneumonia,[16] unless urgently indicated (e.g., outbreak of severe kidney disease, organ rejection).

In conclusion, the SARS-CoV-2 case reports in transplant recipients indicate that the clinical features, diagnosis, management, and prevention of COVID-19 are not very different compared with non-transplanted patients although some specifics are noted. They can have atypical symptoms, if the patient has severe disease, the immunosuppressive treatment should be discontinued and one should be careful of the interaction of ritonavir with calcineurin inhibitors and reduce the dose if the reduction of glomerular filtration is present.

Conflict of interest: None declared.

References

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