RENALMANIFESTATIONS AND COMPLICATIONS OF COVID (original) (raw)
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Journal of the College of Physicians and Surgeons Pakistan, 2020
Acute kidney injury (AKI) is relatively common in critically ill coronavirus disease 2019 (COVID-19) patients and it increases mortality and prolongs hospital stay. This article aimed to investigate the history, virology, epidemiology, clinical manifestations, pathophysiology and management of COVID-19 disease, in general, and the pathogenetic mechanisms of severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV2)-induced kidney damage, in particular. Keywords like SARS-CoV2, COVID-19, renal impairment, sepsis, viremia, etc. were used to find relevant publications from PubMed, Scopus, Google Scholar, and clinical trials registry websites. According to different studies, kidney involvement in COVID-19 typically occurs in patients who develop acute respiratory distress syndrome (ARDS) or multiorgan failure. The kidney damage in COVID-19 has been shown to be multifactorial, involving direct viral infection, indirect injury by sepsis, hemodynamic alterations, cytokine storm, disseminated intravascular coagulation and other unknown mechanisms. The presence in kidney of angiotensin-converting enzyme 2 (ACE2), a receptor for the virus, has been proven, but few cases of direct viral presence in kidney tissue have been published. Therefore, further studies are needed to investigate the exact mechanisms underlying kidney impairment. Since the development of AKI is one of the important risk factors for mortality in COVID-19 patients, optimal management of AKI may improve the outcomes.
Acute kidney injury and COVID-19
The Egyptian Journal of Internal Medicine
Background Coronavirus disease 2019 (COVID-19) is a recent pandemic infectious disease caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2). COVID-19 may lead to acute kidney injury (AKI). Main text SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) and dipeptidyl peptidase 4(DPP4) as entry point receptors in the alveolar type II cell of the lung. However, the expression of ACE2 is 100-fold higher in kidney tissue than the lung, though the potential entry point of SARS-CoV-2 for renal tissue and induction of AKI remains undefined. Therefore, reduction of ACE2 and high circulating angiotensin II in COVID-19 may together participate in the induction of AKI. Thereby, direct ACE2 activator is under investigation to be used as an effective therapy in the management COVID-19-induced AKI. Besides, the direct effect via invasion of SARS-CoV-2 may lead to glomerulopathy and renal proximal tubular necrosis. Conclusion COVID-19 may associate with AKI due to direct effect of...
Cleveland Clinic Journal of Medicine
S evere acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), gains entry into target cells through the angiotensin-converting enzyme 2 (ACE2) receptors. ACE2 receptors are present in the kidneys as well as the lungs, heart, and intestinal cells. 1-8 The renin-angiotensin system plays an important role in human physiology. Angiotensin I is cleaved from angiotensinogen by renin and converted to angiotensin II by ACE. Angioten-REVIEW
Renal Manifestations of Covid-19: Physiology and Pathophysiology
Journal of Clinical Medicine
Corona virus disease 2019 (COVID-19) imposes a serious public health pandemic affecting the whole world, as it is spreading exponentially. Besides its high infectivity, SARS-CoV-2 causes multiple serious derangements, where the most prominent is severe acute respiratory syndrome as well as multiple organ dysfunction including heart and kidney injury. While the deleterious impact of SARS-CoV-2 on pulmonary and cardiac systems have attracted remarkable attention, the adverse effects of this virus on the renal system is still underestimated. Kidney susceptibility to SARS-CoV-2 infection is determined by the presence of angiotensin-converting enzyme 2 (ACE2) receptor which is used as port of the viral entry into targeted cells, tissue tropism, pathogenicity and subsequent viral replication. The SARS-CoV-2 cellular entry receptor, ACE2, is widely expressed in proximal epithelial cells, vascular endothelial and smooth muscle cells and podocytes, where it supports kidney integrity and func...
Case Reports in Nephrology
The renin-angiotensin system plays a very critical role in hypertension, diabetes, and kidney and heart diseases. The blockade of the renin-angiotensin system results in the prevention of progression of renal and cardiac damage. There have been controversial hypotheses raised regarding the safety of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in COVID-19 (coronavirus disease 2019). We present the case series of four patients (2 men and 2 women; 1 Caucasian and 3 African Americans; two survived and two died) with confirmed COVID-19, presenting with respiratory symptoms and acute kidney injury, who have been on angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Membrane-bound angiotensin-converting enzyme 2 (ACE2) has been implicated as the gateway for viral entry into the human cell in causing the infection. The factors contributing to acute kidney injury are diuretics, iodinated contrast administration, hemodynamic instability a...
Kidney Issues Associated with COVID-19 Disease
Encyclopedia
Infection with SARS-CoV-2 and the resulting COVID-19 can cause both lung and kidney damage. SARS-CoV-2 can directly infect renal cells expressing ACE2 receptors, resulting in kidney damage, and acute kidney injury (AKI) has been reported in COVID-19 hospitalized patients. The pathophysiology of COVID-19-associated AKI is multifactorial. Local and systemic inflammation, immune system dysregulation, blood coagulation disorders, and activation of the renin-angiotensin-aldosterone system (RAAS) are factors that contribute to the development of AKI in COVID 19 disease. COVID-19 patients with kidney involvement have a poor prognosis, and patients with chronic kidney disease (CKD) infected with SARS-CoV-2 have an increased mortality risk. CKD patients with COVID-19 may develop end-stage renal disease (ESRD) requiring dialysis. In particular, patients infected with SARS-CoV-2 and requiring dialysis, as well as patients who have undergone kidney transplantation, have an increased risk of mor...
Acute Kidney Injury in COVID-19: a Brief Review
Indian Journal of Surgery, 2021
The contemporary evolution of the coronavirus disease 2019 (COVID-19) outbreak from the Wuhan, China, with a high rate of transmission will act the global medical emergency with immense morbidity and mortality rate across the world. The cell entry of COVID-19 via angiotensin-converting enzyme 2 receptor (ACE-2 receptor) will damage the respiratory system by the cytopathic effect induced by replication of the virus genome in the host and respond respiratory failure with an elevation of cytokine factorlike interleukin (IL) IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha), etc. However, the lung-kidney cross talk will evidence the activation of molecular mechanisms from pro-inflammatory cytokines and concerned with kidney damage, though the elevated rate of ACE-2 receptor in the kidney will enhance the possibility of mortality with consideration of acute kidney injury. This review provides relevant information which suggests the rate of mortality in COVID-19 patient associated with acute kidney injury (AKI) which lacks critical monitoring of kidney function with a clinical consideration of intervention to avoid kidney damage in the initial stage of the disease.
Current knowledge on mechanisms involved in SARS-CoV-2 infection and kidney diseases
Journal of Advanced Biotechnology and Experimental Therapeutics, 2020
ABSTRACT: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is cause of a global pandemic which is demolishing global health and economy. SARS-CoV-2 infected patients are hospitalized with pneumonia where almost 20-30% of patients are led to kidney failure. The entry of SARS-CoV-2 into the systemic circulation leads to acute kidney injury (AKI) which may develop chronic kidney disease (CKD). In addition, patients who are diagnosed with AKI or CKD are at major risk of SARS-CoV-2 infection. Although a significant number of compounds have been proposed and the existing drugs have also been tested for repurposing, no specific therapy has been approved yet. SARS-CoV-2 invades human cells binding to the receptor of angiotensin-converting enzyme 2 (ACE2) via the receptor-binding domain. Cells that express ACE2 are susceptible to SARS-CoV-2 infection and the proportion of ACE2-positive cells in kidney proximal tubule is approximately 4%, indicating that SARS-CoV-2 might damage the kidney tubules leading to fatal kidney injury. Therefore, a better understanding of the potential mechanisms involved in SARS-CoV-2 infection-mediated kidney disease may unveil a novel therapeutic strategy against kidney diseases during COVID-19.