Kidney disease is associated with in-hospital death of patients with COVID-19

Cheng, Yuansheng; Luo, Ran; Wang, Kun; Zhang, Meng; Wang, Zhixiang; Dong, Lei; Li, Junhua; Yao, Ying; Ge, Shuwang; Xu, Gang

doi:10.1016/j.kint.2020.03.005

Cited by 2,484 publications

(3,282 citation statements)

References 24 publications

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“…Within a hospitalized population, rates of ICU admission range between 26-32% across most studies (35,48,(51)(52)(53)57). Several studies have identified older age and baseline burden of comorbidity, such as diabetes, hypertension, prior coronary disease and prior lung disease, as predictors of more significant disease progression with higher rates of ARDS, AKI, cardiac injury, ICU admission and death (51)(52)(53)58,59). Increases in markers of inflammation, coagulation, and cardiac injury also correlate with disease severity and rise throughout the course of the disease (53,54,56).…”

Section: Disease Progressionmentioning

confidence: 99%

“…Estimates vary as to the incidence of acute kidney injury in COVID-19, ranging between 0.5-15% (35,48,52,53,56,59). Among hospitalized patients the rates of proteinuria (43.9%) and hematuria (26.7%) appear to be even higher (59). Acute kidney injury occurs in the first few days after admission in patients with baseline chronic kidney disease, and after 7-10 days in patients with normal baseline renal function (59).…”

Section: Renal Injurymentioning

confidence: 99%

“…Acute kidney injury occurs in the first few days after admission in patients with baseline chronic kidney disease, and after 7-10 days in patients with normal baseline renal function (59). Mechanisms of renal injury have been hypothesized to include both acute tubular necrosis (ATN), direct cytotoxic effects of the virus itself, and immune-mediated damage (59).…”

Section: Renal Injurymentioning

confidence: 99%

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COVID-19 for the Cardiologist

Atri

Siddiqi

Lang

et al. 2020

JACC: Basic to Translational Science

268

137

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Highlights-Severe acute respiratory virus-2 (SARS-CoV2), the infection responsible for coronavirus disease-2019 (COVID-19), has spread globally leading to a devastating loss of life. In a few short months, the clinical and scientific communities have rallied to rapidly evolve our understanding of the mechanism(s) of disease and potential therapeutics. -This review discusses the current understanding of the basis virology of SARS-CoV2 and the epidemiology, clinical manifestations, including cardiovascular, and mortality of COVID-19. A detailed review of the viral life cycle and putative mechanism(s) of injury frames the discussion of possible preventative and therapeutic strategies. -The ongoing, unprecedented collective effort will, without a doubt, advance our ability to prevent the spread and optimally care for patients suffering from COVID-19. SummaryThe coronavirus disease-2019 (COVID-19), a contagious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV2), has reached pandemic status. As it spreads across the world, it has overwhelmed healthcare systems, strangled the global economy and led to a devastating loss of life. Widespread efforts from regulators, clinicians and scientists are driving a rapid expansion of knowledge of the SARS-CoV2 virus and the COVID-19 disease.We review the most current data with a focus on our basic understanding of the mechanism(s) of disease and translation to the clinical syndrome and potential therapeutics. We discuss the basic virology, epidemiology, clinical manifestation, multi-organ consequences, and outcomes. With a focus on cardiovascular complications, we propose several mechanisms of injury. The virology and potential mechanism of injury form the basis for a discussion of potential disease-modifying therapies.

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Section: Disease Progressionmentioning

confidence: 99%

Section: Renal Injurymentioning

confidence: 99%

Section: Renal Injurymentioning

confidence: 99%

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COVID-19 for the Cardiologist

Atri

Siddiqi

Lang

et al. 2020

JACC: Basic to Translational Science

268

137

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“…The dialysis patients are usually older with comorbid disease and are the high mortality risk group of COVID-19 infection. 10 Since the droplet spreading and the contact infection are preventable, we suggest all patients and the medical staffs have their face masks during the dialysis therapy. A good indoor air ventilation, stringent environment cleaning and disinfect are mandatory.…”

Section: Received 25 March 2020; Accepted 26 March 2020mentioning

confidence: 99%

Take proactive measures for the pandemic COVID-19 infection in the dialysis facilities

Lee¹,

Lin²,

Chiu³

et al. 2020

Journal of the Formosan Medical Association

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“…In the kidney, abundant ACE2 and TMPRSS2 coexpression in proximal tubular and progenitor cells also makes them potential targets of virus infection. Acute kidney injury (AKI) has been noted in a small but significant proportion of patients with COVID-19 disease and is an independent risk factor for in-hospital mortality 16 . Histopathology of kidney tissue obtained at autopsy in patients with SARS-CoV-2 infection showed severe acute tubular necrosis with lymphocytic infiltration and the presence of viral nucleocapsid proteins 17 .…”

mentioning

confidence: 99%

Cell-Type-Specific Expression of Renin-Angiotensin-System Components in the Human Body and Its Relevance to SARS-CoV-2 Infection

Suryawanshi

Morozov

Muthukumar

et al. 2020

Preprint

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We have analyzed the cell-type-specific expression of the renin-angiotensin system (RAS) components across 141 cell types or subtypes as defined by single-cell RNA-seq (scRNAseq) analysis. ACE2, one of the components of RAS, also facilitates SARS-CoV-2 entry into cells in cooperation with its associated protease TMPRSS2. Therefore, our analysis also contributes to the understanding of SARS-CoV-2 infection, spreading of the virus throughout the body, and potential viral interference with RAS in COVID-19 patients.The COVID-19 pandemic caused by SARS coronavirus 2 (SARS-CoV-2) has created a global health emergency with more than a million confirmed cases as of April 4, 2020 1 . For cellular entry, SARS-CoV-2 relies on the interaction of its glycosylated viral spike (S) protein with the host membrane-bound aminopeptidase angiotensin-converting enzyme 2 (ACE2). Subsequently, transmembrane protease serine 2 (TMPRSS2) cleaves S and/or ACE2 protein, which facilitates the fusion of viral and cellular membranes 2 . ACE2 is also a crucial component of RAS, which regulates several key physiological processes such as blood pressure and electrolyte balance and viral infection of ACE2-expressing cells may impair RAS function 3 .The secreted and systemically distributed protease renin (REN) activates RAS by proteolytically cleaving plasma angiotensinogen (AGT) to produce the 10-amino-acid (aa) hormonal peptide, angiotensin I (Ang I). Subsequently, Ang I is processed to the 8-aa Ang II by the metallopeptidase angiotensin-converting enzyme (ACE) present on the surface of pulmonary and kidney endothelial cells. Ang II is the active peptide in RAS triggering vasoconstriction, sodium retention, and fibrosis and signals by binding to its receptor AGTR1 or AT1R. ACE2, a metallopeptidase paralogous to ACE, counters the activity of ACE by digesting Ang II to the 7 aa Ang-(1-7) form, thereby attenuating the effects of Ang II 3 . Ang-(1-7) signals through binding to the G-protein coupled receptor MAS1 as well as the receptor AGTR2 or AT2R. Activation of MAS1 protein is coupled with several downstream pathways including activation of phospholipase A2 was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission.

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Kidney disease is associated with in-hospital death of patients with COVID-19

Cited by 2,484 publications

References 24 publications

COVID-19 for the Cardiologist

COVID-19 for the Cardiologist

Take proactive measures for the pandemic COVID-19 infection in the dialysis facilities

Cell-Type-Specific Expression of Renin-Angiotensin-System Components in the Human Body and Its Relevance to SARS-CoV-2 Infection

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