scholarly journals Acute kidney injury in the rat causes cardiac remodelling and increases angiotensin-converting enzyme 2 expression

2008 ◽  
Vol 93 (5) ◽  
pp. 622-630 ◽  
Author(s):  
L. Burchill ◽  
E. Velkoska ◽  
R. G. Dean ◽  
R. A. Lew ◽  
A. I. Smith ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Angiotensin Converting Enzyme ◽  
Kidney Injury ◽  
Cardiac Remodelling ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2

scholarly journals Reduced urinary levels of angiotensin-converting enzyme 2 activity predict acute kidney injury in critically ill patients

2020 ◽  
Vol 22 (4) ◽  
pp. 344-354
Author(s):  
Laurent Bitker ◽  
◽  
Sheila K Patel ◽  
Intissar Bittar ◽  
Glenn M Eastwood ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Acute Kidney Injury ◽  
Angiotensin Converting Enzyme ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Urine Collection ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Urine Creatinine

Objective: Angiotensin-converting enzyme 2 activity reflects non-classical renin–angiotensin system upregulation. We assessed the association of urinary angiotensin-converting enzyme 2 (uACE2) activity with acute kidney injury (AKI). Design, setting and participants: A prospective observational study in which we measured uACE2 activity in 105 critically ill patients at risk of AKI. We report AKI stage 2 or 3 at 12 hours of urine collection (AKI12h) and AKI stage 2 or 3 at any time during intensive care unit stay in patients free from any stage of AKI at inclusion (AKIICU). AKI prediction was assessed using area under the receiver-operating characteristics curve (AUROC) and net reclassification indices (NRIs). Main outcome measure: AKI stage 2 or 3 at 12 hours of urine collection. Results: Within 12 hours of inclusion, 32 of 105 patients (30%) had developed AKI12h. Corrected uACE2 activity was significantly higher in patients without AKI12h compared with those with AKI12h (median [interquartile range], 13 [6–24] v 7 [4–10] pmol/min/mL per mmol/L of urine creatinine; P < 0.01). A 10-unit increase in uACE2 was associated with a 28% decrease in AKI12h risk (odds ratio [95% CI], 0.72 [0.46–0.97]). During intensive care unit admission, 39 of 76 patients (51%) developed AKIICU. uACE2 had an AUROC for the prediction of AKI12h of 0.68 (95% CI, 0.57–0.79), and correctly reclassified 28% of patients (positive NRI) to AKI12h. Patients with uACE2 > 8.7 pmol/min/mL per mmol/L of urine creatinine had a significantly lower risk of AKIICU on log-rank analysis (52% v 84%; P < 0.01). Conclusions: Higher uACE2 activity was associated with a decreased risk of AKI stage 2 or 3. Our findings support future evaluations of the role of the non-classical renin–angiotensin system during AKI.

scholarly journals Novel Evidence of Acute Kidney Injury in COVID-19

2020 ◽  
Vol 9 (11) ◽  
pp. 3547
Author(s):  
Ti-I Chueh ◽  
Cai-Mei Zheng ◽  
Yi-Chou Hou ◽  
Kuo-Cheng Lu
Keyword(s):  
Acute Kidney Injury ◽  
Angiotensin Converting Enzyme ◽  
Kidney Injury ◽  
Host Cells ◽  
Current Evidence ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

The coronavirus 2019 (COVID-19) pandemic has caused a huge impact on health and economic issues. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes cellular damage by entry mediated by the angiotensin-converting enzyme 2 of the host cells and its conjugation with spike proteins of SARS-CoV-2. Beyond airway infection and acute respiratory distress syndrome, acute kidney injury is common in SARS-CoV-2-associated infection, and acute kidney injury (AKI) is predictive to multiorgan dysfunction in SARS-CoV-2 infection. Beyond the cytokine storm and hemodynamic instability, SARS-CoV-2 might directly induce kidney injury and cause histopathologic characteristics, including acute tubular necrosis, podocytopathy and microangiopathy. The expression of apparatus mediating SARS-CoV-2 entry, including angiotensin-converting enzyme 2, transmembrane protease serine 2 (TMPRSS2) and a disintegrin and metalloprotease 17 (ADAM17), within the renal tubular cells is highly associated with acute kidney injury mediated by SARS-CoV-2. Both entry from the luminal and basolateral sides of the renal tubular cells are the possible routes for COVID-19, and the microthrombi associated with severe sepsis and the dysregulated renin–angiotensin–aldosterone system worsen further renal injury in SARS-CoV-2-associated AKI. In the podocytes of the glomerulus, injured podocyte expressed CD147, which mediated the entry of SARS-CoV-2 and worsen further foot process effacement, which would worsen proteinuria, and the chronic hazard induced by SARS-CoV-2-mediated kidney injury is still unknown. Therefore, the aim of the review is to summarize current evidence on SARS-CoV-2-associated AKI and the possible pathogenesis directly by SARS-CoV-2.

scholarly journals Renal complications in coronavirus disease 2019: a systematic review

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Taichiro Minami ◽  
Yasunori Iwata ◽  
Takashi Wada
Keyword(s):  
Systematic Review ◽  
Acute Kidney Injury ◽  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Kidney Injury ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
The World ◽  
Life Threatening ◽  
Life Threatening Complication

AbstractThe world today is facing a pandemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which mainly causes a respiratory disease known as coronavirus disease 2019 (COVID-19). Therefore, its pathogenesis and complications should be identified and understood. SARS-CoV-2 infects the host using the angiotensin-converting enzyme 2 (ACE2) as its receptor, which is expressed in several organs including the lungs, heart, kidneys, and intestines. Kidney complications are relatively common, and acute kidney injury (AKI) is a life-threatening complication in patients with COVID-19. In this review, the renal histological patterns of COVID-19 are described in detail, and its potential mechanisms associated with AKI are discussed.

scholarly journals Loss of Angiotensin-Converting Enzyme-2 (Ace2) Accelerates Diabetic Kidney Injury

2007 ◽  
Vol 171 (2) ◽  
pp. 438-451 ◽  
Author(s):  
Denise W. Wong ◽  
Gavin Y. Oudit ◽  
Heather Reich ◽  
Zamaneh Kassiri ◽  
Joyce Zhou ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Kidney Injury ◽  
Converting Enzyme ◽  
Diabetic Kidney ◽  
Angiotensin Converting Enzyme 2
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