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

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.

Abstract 379: Insulin Attenuated Albuminuria by Upregulating Angiotensin Converting Enzyme 2 (ACE2) in Type 1 Diabetic Akita Mice

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Esam Salem ◽  
Hari K Somineni ◽  
Harshita Chodavarapu ◽  
Mariana Morris ◽  
Khalid M Elased
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Urinary Albumin Excretion ◽  
Renin Angiotensin System ◽  
Urinary Albumin ◽  
Converting Enzyme ◽  
Diabetic Kidney ◽  
Angiotensin Converting Enzyme 2 ◽  
Albumin Excretion ◽  
Akita Mice

Diabetic nephropathy (DN) is a microvascular complication of diabetes that is clinically diagnosed by a progressive increase in albuminuria. Alterations within renin angiotensin system balance contribute to the pathogenesis of diabetic kidney disease. Angiotensin converting enzyme 2 (ACE2), a metallocarboxypetidase, has a renoprotective role due to its ability to form Angiotensin (1-7) [Ang-(1-7)] by degrading Angiotensin II (Ang II). Accumulating evidence shows that strict glycemic control attenuates diabetic kidney damage. Therefore, the aim of this study is to test the hypothesis that normalizing hyperglycemia with insulin will reduce albuminuria by increasing ACE2 in Akita diabetic mice. Type 1 diabetic Akita mice (C57BL/6-Ins2Akita/J) and their wild type (WT) littermates were used. Metabolic parameters were monitored weekly. Urine was collected over 24 hours to measure the urinary albumin, total protein and ACE2 activity. Akita mice developed significant hyperglycemia (Akita: 452±6; WT: 118±2 mg/dL), hypoinsulinemia (Akita: 0.5; WT: 1.5 ng/mL) and hypoadiponectinemia (Akita: 3.0; WT: 6.0 μg/mL) compared to WT mice. There was a significant increase in urinary albumin excretion (Akita: 2.1±0.2; WT: 0.2±0.06 mg/day) in Akita mice compared to WT mice. In addition, Akita mice demonstrated a significant decrease in renal (Akita: 3±0.3; WT: 4.1±0.1 pmol/hr/μg protein) and urinary (Akita: 0.2±0.03; WT: 0.7±0.1 pmol/hr/μg protein) ACE2 activity compared to WT mice (P<0.05). Western blot & immunohistochemistry revealed downregulation of renal ACE2 & nephrin protein expression in Akita mice compared to WT mice. Treatment with insulin implants (LinβitR) for 10 weeks significantly decreased hyperglycemia in Akita mice (treated: 135±21; untreated: 452±6 mg/dL). Insulin treatment significantly decreased urinary albumin excretion (treated: 0.18±0.2; untreated: 2.1±0.2 mg/day) and increased urinary ACE2 activity (treated: 1.3±0.3; untreated: 0.2±0.03 pmol/hr/μg protein) in Akita mice. In conclusion, normalizing hyperglycemia in Akita mice with insulin increased ACE2 activity and attenuated albuminuria.

scholarly journals Murine recombinant angiotensin-converting enzyme 2 attenuates kidney injury in experimental Alport syndrome

2017 ◽  
Vol 91 (6) ◽  
pp. 1347-1361 ◽  
Author(s):  
Eun Hui Bae ◽  
Fei Fang ◽  
Vanessa R. Williams ◽  
Ana Konvalinka ◽  
Xiaohua Zhou ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Alport Syndrome ◽  
Kidney Injury ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 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 Angiotensin-(3–4) modulates angiotensin converting enzyme 2 (ACE2) downregulation in proximal tubule cells due to overweight and undernutrition: implications regarding the severity of renal lesions in Covid-19 infection

2020 ◽  
Author(s):  
Rafael Luzes ◽  
Humberto Muzi-Filho ◽  
Amaury Pereira-Acácio ◽  
Thuany Crisóstomo ◽  
Adalberto Vieyra
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Kidney Injury ◽  
Converting Enzyme ◽  
Present Communication ◽  
Proximal Tubule Cells ◽  
Angiotensin Converting Enzyme 2 ◽  
Renal Lesions ◽  
Nutritional Conditions ◽  
Angiotensin Converting Enzymes

AbstractThe renal lesions – including severe acute kidney injury – are severe outcomes in SARS-CoV-2 infections. There are no reports regarding the influence of the nutritional status on the severity and progress of these lesions. Ageing is also an important risk factor. In the present communication we compare the influence of overweight and undernutrition in the levels of renal angiotensin converting enzymes 1 and 2. Since the renin-angiotensin-aldosterone system (RAAS) has been implicated in the progress of kidney failure during Covid-19, we also investigated the influence of Angiotensin-(3–4) (Ang-(3–4)) the shortest angiotensin-derived peptide, which is considered the physiological antagonist of several angiotensin II effects. We found that both overweight and undernutrition downregulate the levels of angiotensin converting enzyme 2 (ACE2) without influence on the levels of ACE1 in kidney rats. Administration of Ang-(3–4) recovers the control levels of ACE2 in overweight but not in undernourished rats. We conclude that chronic and opposite nutritional conditions play a central role in the pathophysiology of renal Covid-19 lesions, and that the role of RAAS is also different in overweight and undernutrition.

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