Prasad Narayan, Agrawal Sanjay K
Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India.
Department of Nephrology, All India Institute of Medical Sciences, New Delhi, India.
Indian J Nephrol. 2020 May-Jun;30(3):161-165. doi: 10.4103/ijn.IJN_120_20. Epub 2020 May 13.
Coronavirus disease 19 (COVID-19) is caused by severe acute respiratory syndrome-corona virus (SARS-CoV-2), a beta coronavirus, mainly involves the respiratory tract, and the clinical features simulate to a severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) of the past. The genome of the SARS-CoV-2, isolated from a cluster-patient with a typical pneumonia after visiting Wuhan, had 89% nucleotide identitical with bat SARS-like-CoVZXC21 and 82% with that of human SARS-CoV. It enters the respiratory tract through angiotensin converting enzyme-2 (ACE2) receptors on alveoli. It may induce lung injury through direct cytopathic effect, involving effector T cells or causing sepsis and inducing cytokine storm. With a similar mechanism, it can cause acute kidney injury (AKI). The overall incidence of AKI is 5.1%, and AKI is an independent risk factor for mortality. The hazard ratio of death increases with the increasing severity of AKI. Management of COVID-19 with AKI is primarily supportive care, and at present, there are no evidence based effective antivirals for the treatment.
新型冠状病毒肺炎(COVID-19)由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起,这是一种β冠状病毒,主要累及呼吸道,其临床特征类似于过去的严重急性呼吸综合征(SARS)和中东呼吸综合征(MERS)。从一名去过武汉后出现典型肺炎的聚集性病例中分离出的SARS-CoV-2基因组,与蝙蝠SARS样冠状病毒ZXC21的核苷酸同源性为89%,与人类SARS-CoV的核苷酸同源性为82%。它通过肺泡上的血管紧张素转换酶2(ACE2)受体进入呼吸道。它可能通过直接细胞病变效应诱导肺损伤,涉及效应T细胞或导致脓毒症并引发细胞因子风暴。通过类似机制,它可导致急性肾损伤(AKI)。AKI的总体发生率为5.1%,且AKI是死亡的独立危险因素。死亡风险比随AKI严重程度的增加而升高。伴有AKI的COVID-19的治疗主要是支持性治疗,目前尚无循证有效的抗病毒药物用于治疗。