Silva Antônio V B DA, Campanati João DE A G, Barcelos Isadora DE S, Santos Alberto C L, Deus Uildson P DE, Soares Telma DE J, Amaral Liliany S DE B
Universidade Federal da Bahia, Instituto Multidisciplinar em Saúde, 45029-094 Vitória da Conquista, BA, Brazil.
An Acad Bras Cienc. 2022 Dec 5;94(suppl 3):e20211501. doi: 10.1590/0001-3765202220211501. eCollection 2022.
COVID-19 is a pandemic disease caused by the SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) responsible for millions of deaths worldwide. Although the respiratory system is the main target of COVID-19, the disease can affect other organs, including the kidneys. Acute Kidney Injury (AKI), commonly seen in patients infected with COVID-19, has a multifactorial cause. Several studies associate this injury with the direct involvement of the virus in renal cells and the indirect damage stimulated by the infection. The direct cytopathic effects of SARS-CoV-2 are due to the entry and replication of the virus in renal cells, changing several regulatory pathways, especially the renin-angiotensin-aldosterone system (RAAS), with repercussions on the kallikrein-kinin system (KKS). Furthermore, the virus can deregulate the immune system, leading to an exaggerated response of inflammatory cells, characterizing the state of hypercytokinemia. The such exaggerated inflammatory response is commonly associated with hemodynamic changes, reduced renal perfusion, tissue hypoxia, generation of reactive oxygen species (ROS), endothelial damage, and coagulopathies, which can result in severe damage to the renal parenchyma. Thereby, understanding the molecular mechanisms and pathophysiology of kidney injuries induced by SARS-COV-2 is of fundamental importance to obtaining new therapeutic insights for the prevention and management of AKI.
新冠病毒病（COVID-19）是一种由严重急性呼吸综合征冠状病毒2（SARS-CoV-2）引起的大流行性疾病，已在全球造成数百万人死亡。虽然呼吸系统是COVID-19的主要靶器官，但该疾病也可影响包括肾脏在内的其他器官。急性肾损伤（AKI）在感染COVID-19的患者中很常见，其病因是多因素的。多项研究将这种损伤与病毒直接侵袭肾细胞以及感染引发的间接损害联系起来。SARS-CoV-2的直接细胞病变效应是由于病毒在肾细胞中的侵入和复制，改变了多种调节途径，尤其是肾素-血管紧张素-醛固酮系统（RAAS），进而对激肽释放酶-激肽系统（KKS）产生影响。此外，该病毒可使免疫系统失调，导致炎症细胞反应过度，呈现出高细胞因子血症状态。这种过度的炎症反应通常与血流动力学变化、肾灌注减少、组织缺氧、活性氧（ROS）生成、内皮损伤和凝血病相关，这些都可能导致肾实质严重受损。因此，了解SARS-CoV-2所致肾损伤的分子机制和病理生理学对于获得预防和管理AKI的新治疗思路至关重要。
