Relationship Between Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and the Etiology of Acute Kidney Injury (AKI)

Abstract

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Since it was first recognized in December 2019, it has resulted in the ongoing worldwide pandemic. Although acute hypoxic respiratory failure (AHRF) and acute respiratory distress syndrome (ARDS) are the main features of the disease, the involvement of other organs needs to be explored. There has been a growing concern regarding the association between acute kidney injury (AKI) and poor outcomes in SARS-CoV-2 patients. Based on current observational data, AKI is the 2 nd most common cause of morbidity and mortality behind ARDS in SARS-CoV-2 patients. Angiotensin-converting enzyme 2 (ACE2) receptor has been shown to be the cornerstone of SARS-CoV-2 infection and possibly plays a significant role in the occurrence of renal injury. The pathogenesis of AKI is likely multifactorial that involves not only direct viral invasion but also dysregulated immune response in the form of cytokine storm, ischemia to kidneys, hypercoagulable state, and rhabdomyolysis, among others. We performed a literature search of the Pubmed and Google Scholar database from 1996 to 2020 using the following keywords: severe acute respiratory syndrome coronavirus 2, coronavirus disease 2019, angiotensin-converting enzyme 2 receptor, and acute kidney injury to find the most pertinent and highest-quality of evidence. Any cited references were reviewed to identify relevant literature. The purpose of this review is to discuss, explore, and summarize the relationship between AKI in SARS-CoV-2 patients, with a focus on its epidemiology, association with ACE2 receptors, and pathogenesis of AKI.

The incidence of pleural effusion in COVID-19 pneumonia: State-of-the-art review

“…6 , 17 , 22 , 29 , 56 , 57 , 61 At least 15% and more of COVID-19 patients developed either acute heart failure or kidney failure during their clinical course, increasing to more than 50% in critically ill patients. 62 , 63 The clinical state of fluid overload has been described as a potential etiology in SARS-related pleural effusions. 64 However, no study has been performed to determine the pre-existing comorbidities of congestive heart failure, hypoalbuminemia, chronic liver disease, and chronic renal failure with the risk of pleural effusions development in COVID-19 patients.…”

Pathophysiology and Clinical Manifestations of COVID-19-Related Acute Kidney Injury—The Current State of Knowledge and Future Perspectives

“…The kidney picture presents with diffuse proximal tubule injury with loss of the brush border and frank necrosis accompanied by vacuolar degeneration and tubulointerstitial fibrosis. Electron microscopy imaging shows SARS-CoV-2 viruses in the tubular epithelium (predominantly in the proximal tubule and podocytes) [3,40]. In the interstitial compartment, inflammatory cell forms infiltrate, and edema can be seen.…”

“…On the vascular level, the picture of AKI demonstrates vasoconstriction of intrarenal vessels, increased vascular permeability, and microthrombi formation [3]. Vascular endothelium damage occurs, which can be observed as swelling of endothelial cells.…”

“…It was hypothesized that ACE2 gene polymorphisms may predispose to kidney injury induced by SARS-CoV-2 infection [48][49][50]. Interestingly, SARS-CoV-2 infection both prevents ACE2 from attaching to the receptor and alternates ACE2 expression within the proximal tubular cells, especially in the areas of acute tubular injury [3,51]. Accumulation of the AGII protein, not converted to AG1-7, promotes inflammation by increasing cytokine release and allowing easier immune cell infiltration of the tissues [52,53].…”

“…Patients diagnosed with COVID-19 present a wide range of various impairments and organ dysfunctions, while the course of the disease depends on the individual, ranging from asymptomatic infection to severe symptoms and even fatal incidents [2,3]. The most common clinical manifestations include interstitial and alveolar pneumonia, with around 5-20% progressing to acute respiratory distress syndrome (ARDS), septic shock, or multiple organ failure [3][4][5][6]. Despite the most prevalently diagnosed respiratory manifestations, gastrointestinal, neurological, olfactory, and cardiac symptoms are also very common in patients of various ages.…”