I read with great interest the paper by Asgharpour et al., about kidney findings in coronavirus disease 2019 (COVID-19) cases. As they reported, acute kidney injury (AKI) is a common complication of COVID-19 that worsens the overall prognosis.1 I thank them for presenting the representative and crucial data that needs clarification from specialists. Although several reports indicated the relationship between COVID-19, inflammatory response and accompanying systemic problems, this paper is one of the most comprehensive and systematic presentations in the literature.
Asgharpour et al., reviewed the kidney findings in patients with COVID-19, in addition to describing pathologies of other organ systems.1 This paper reported that acute tubular necrosis (ATN) and glomerular involvement were detected in renal tissue analysis in patients with COVID-19. However, they declared that there is no evidence of viral particles on ultrastructural examination by electron microscopy; and researchers never detected severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA successfully from renal tissue of infected patients.1 In a recent report by Braun et al., SARS-CoV-2 was isolated from one post-mortem sample of kidney in autopsy series from 63 patients that produced a 1000-times increase in viral RNA after 48 hours of cell infection in vitro; and they added that this finding showed that the virus maintains infective potential, even under post-mortem conditions.2 Moreover, they found that this human-derived SARS-CoV-2 shows replication in cultured kidney tubular epithelial cells of a non-human primate. In view of these findings, they suggested that renal cells can be targeted by SARS-CoV-2 and renal tropism can be associated with disease severity.2 In another study by Vijayan et al. that refers to the previous report, the authors present possible renal implications, and clinical outcomes of SARS-CoV-2 infection of kidneys.3 These reports declared that SARS-CoV-2 mRNA, which may cause collapsing glomerulopathy as well as acute tubular injury, was detected in renal tissue.2,3
Previous reports focused on the importance of assessing renal functions in SARS-CoV-2, and they indicated that chronic renal failure is the strongest mortality reason for SARS-CoV-2 infected patients. This was even more serious compared with other risk factors such as chronic heart or lung disease. Vijayan et al. speculated that these findings might be a reflection of kidney tropism by SARS-CoV-2.3 According to the above reports, kidneys are important and risky targets of SARS-CoV-2; and this point should be kept in mind in addition to other organ systems’ findings during the management of the disease.
The definition of viral pathogenic factors may play a key role in clarifying pathogenicity and treatment strategies. Variable cellular responses against virus and affected organs should be identified for describing symptoms and associated findings. So, I congratulate Braun et al.2 for illuminating the possible kidney tropism of SARS-CoV-2 and, I thank Asgharpour et al.1 for the presentation of a comprehensive updated paper for patients with COVID-19-related kidney disease. I believe that the systemic reflections of the disease will be better understood by clarifying micro implications.