scholarly journals Renin angiotensin aldosterone system (RAAS) inhibitors in the prevention of early renal disease in diabetes

10.3410/m2-18 ◽  
2010 ◽  
Vol 2 ◽  
Author(s):  
Luigi Gnudi ◽  
David Goldsmith
Keyword(s):  
Renal Disease ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Inhibitors

scholarly journals Renin Angiotensin Aldosterone System Antagonism in 2019 Novel Coronavirus Acute Lung Injury

2021 ◽  
Author(s):  
Davide Ventura ◽  
Amy L Carr ◽  
R Duane Davis ◽  
Scott Silvestry ◽  
Linda Bogar ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Ii Receptor ◽  
Pulmonary Tissue ◽  
Renin Angiotensin Aldosterone System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Receptor Blockers ◽  
Membrane Bound ◽  
Raas Inhibitors ◽  
Novel Coronavirus

Abstract It has been established SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2), a membrane-bound regulatory peptide, for host cell entry. Renin-angiotensin-aldosterone system (RAAS) inhibitors have been reported to increase ACE2 in type 2 pneumocytes pulmonary tissue. Controversy exists for the continuation of ACE inhibitors, angiotensin II receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) in the current pandemic. ACE2 serves as regulatory enzyme in maintaining homeostasis between proinflammatory Angiotensin II and anti-inflammatory Angiotensin 1,7 peptides. Derangements in these peptides are associated with cardiovascular disease and are implicated in the progression of acute respiratory distress syndrome (ARDS). Augmentation of the ACE2/Ang1,7 axis represent a critical target in the supportive management of COVID-19 associated lung disease. Observational data describing the use of RAAS inhibitors in the setting of SARS-CoV-2 have not borne signals of harm to date. However, equipoise persists requiring an analysis of novel agents including recombinant human-ACE2 and existing RAAS inhibitors while balancing ongoing controversies associated with increased coronavirus infectivity and virulence.

scholarly journals Renin-angiotensin-aldosterone system inhibitors – a realm of confusion in COVID-19

2021 ◽  
Vol 4 (Special2) ◽  
pp. 389-394
Author(s):  
Angela Madalina Lazar
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Current Knowledge ◽  
Angiotensin Receptor Blockers ◽  
Protective Effects ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Inhibitors

Currently, there is a persisting dispute regarding the renin-angiotensin-aldosterone-system (RAAS) inhibitors' safety of use in COVID-19 pandemics. On one side, RAAS inhibitors appear to determine an overexpression of ACE2, the receptor of SARS-CoV-2. Therefore, they could increase the risk of SARS-CoV-2 infection and its degree of severity. On the other side, the discontinuation of RAAS leads to cardiovascular decompensation and has been discouraged by the major medical societies. Also, large-cohort studies report beneficial or at least neutral effects for the RAAS inhibitors in COVID-19 patients. Worldwide, millions of patients receive RAAS inhibitors for the treatment of hypertension and other important comorbidities. In this context, knowledge of the exact effect of these medications becomes of crucial significance. This paper aims to fill in a gap in the current knowledge and presents a putative mechanism by which RAAS inhibitor administration's beneficial results can be explained better. RAAS inhibitors can be beneficial, as they counteract the excessive detrimental activation of the classical angiotensin-converting enzyme (ACE) axis, decreasing the angiotensin II levels. The angiotensin receptor blockers (ARBs) increase the angiotensin II levels, while the angiotensin-converting enzyme inhibitors (ACEI) increase the angiotensin I levels; these substrates will compete with the SARS-CoV-2 for the ACE2 binding, decreasing the viral infectivity. In addition, following the RAAS inhibitors treatment, the up-regulated ACE2 will cleave these substrates (angiotensin I and II), particularly to angiotensin 1-7 that possesses vasodilator, protective effects.

Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Nephron ◽  
1975 ◽  
Vol 15 (1) ◽  
pp. 35-49 ◽  
Author(s):  
P. Weidmann ◽  
M.H. Maxwell ◽  
P. Rowe ◽  
R. Winer ◽  
S.G. Massry
Keyword(s):  
Renal Disease ◽  
Chronic Renal Disease ◽  
Plasma Potassium ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

scholarly journals Advances in the Renin-Angiotensin-Aldosterone System: Relevance to Diabetic Nephropathy

2008 ◽  
Vol 8 ◽  
pp. 434-445 ◽  
Author(s):  
Audrey Koitka ◽  
Christos Tikellis
Keyword(s):  
Diabetic Nephropathy ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Renal Disease ◽  
Converting Enzyme ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Angiotensin Type 2 Receptor

Hypertension is now recognized as a key contributory factor to the development and progression of kidney disease in both type 1 and type 2 diabetes. The renin angiotensin system (RAS) and its effector molecule angiotensin II, in particular, have a range of hemodynamic and nonhemodynamic effects that contribute not only to the development of hypertension, but also to renal disease. As a result, therapeutic inhibition of the RAS with angiotensin-converting enzyme inhibitors and/or selective angiotensin II type 1 receptor blockers has been proposed as a key strategy for reducing kidney damage beyond the expected effects one would observe with blood pressure reduction per se. Although the relationship between the RAS and the progression of diabetic renal disease has been known for many decades, recent advances have revealed a more complex paradigm with the discovery of a number of new components. Thus, further understanding of these new components of the renin angiotensin aldosterone system (RAAS), such as the angiotensin type 2 receptor subtype, angiotensin converting enzyme 2, and the recently cloned renin receptor, is likely to have therapeutic implications for disorders such as diabetic nephropathy, where interruption of the RAAS is widely used.

scholarly journals Renin Angiotensin Aldosterone System Blockade and Renal Disease in Patients With Type 2 Diabetes: An Asian perspective from the RENAAL study

Diabetes Care ◽  
2004 ◽  
Vol 27 (4) ◽  
pp. 874-879 ◽  
Author(s):  
J. C.N. Chan ◽  
N. M.S. Wat ◽  
W.-Y. So ◽  
K. S.L. Lam ◽  
C.-T. Chua ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Renal Disease ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

scholarly journals Renin-Angiotensin-Aldosterone System peptide profiles in patients with COVID-19

2021 ◽  
Author(s):  
Alexander Kutz ◽  
Anna Conen ◽  
Claudia Gregoriano ◽  
Sebastian Haubitz ◽  
Daniel Koch ◽  
...  
Keyword(s):  
Respiratory Infections ◽  
Tertiary Care ◽  
Plasma Renin ◽  
Adverse Outcomes ◽  
Care Hospital ◽  
Renin Angiotensin Aldosterone System ◽  
Peptide Profile ◽  
Renin Angiotensin ◽  
Subgroup Analyses ◽  
Raas Inhibitors

Objective While evidence on the interface between severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection and the renin-angiotensin-aldosterone-system (RAAS) is accumulating, clinical data on RAAS peptide alteration among coronavirus disease-19 (COVID-19) patients is missing. Design and Methods In this exploratory study, we prospectively included adult patients (aged ≥18 years) admitted between February 26 and April 30, 2020 to a tertiary care hospital in Switzerland. We assessed the association of an underlying SARS-CoV-2 infection and equilibrium serum levels of RAAS peptides in hospitalized COVID-19 patients 1:1 propensity-score matched with patients suffering from SARS-CoV-2-negative respiratory infections. Subgroup analyses involved stratification for taking RAAS inhibitors. Results COVID-19 patients had about 50% lower equilibrium serum RAAS peptide levels as compared with matched controls (angiotensin I: 31.6 vs. 66.8pmol/l, -52.7% [95%CI -68.5% to -36.9%]; angiotensin II: 37.7 vs. 92.5pmol/l, -59.2% [95%CI -72.1% to -46.3%]; angiotensin (1-5): 3.3 vs. 6.6pmol/l, -49.7% [95%CI -59.2% to -40.2%]; angiotensin (1-7): 4.8 vs. 7.6pmol/l, -64.9% [95%CI -84.5% to -45.3%]). While the plasma renin activity (PRA-S) was lower in COVID-19 patients (88.6 vs. 207.9pmol/l, -58.5% [95%CI -71.4% to -45.6%]), there was no difference of angiotensin-converting enzyme (ACE) and ACE2 plasma activity between the groups. Subgroup analyses revealed a pronounced RAAS peptide profile depression in COVID-19 patients among those not on RAAS inhibitors. Conclusions As compared with SARS-CoV-2-negative patients, we found a downregulated RAAS in presence of a SARS-CoV-2 infection. Whether the lower levels of the protective angiotensin (1-5) and (1-7) are linked to adverse outcomes in COVID-19 warrants further investigation.

scholarly journals Effect of Renin-Angiotensin-Aldosterone System Inhibitors on Short-Term Mortality After Sepsis

Hypertension ◽  
2020 ◽  
Vol 75 (2) ◽  
pp. 483-491 ◽  
Author(s):  
Wan-Ting Hsu ◽  
Brandon Patrick Galm ◽  
Gregory Schrank ◽  
Tzu-Chun Hsu ◽  
Shih-Hao Lee ◽  
...  
Keyword(s):  
Propensity Score ◽  
Meta Analysis ◽  
Hazard Ratio ◽  
Short Term ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Mortality Hazard ◽  
Short Term Mortality ◽  
Raas Inhibitors ◽  
Mortality Hazard Ratio

Antagonists of the renin-angiotensin-aldosterone system (RAAS), including ACEIs (angiotensin-converting enzyme inhibitors) and ARBs (angiotensin II receptor blockers), may prevent organ failure. We, therefore, investigated whether specific RAAS inhibitors are associated with reduced mortality in patients with sepsis.We conducted a population-based retrospective cohort study using multivariable propensity score–based regression to control for differences among patients using different RAAS inhibitors. A multivariable-adjusted Cox proportional-hazards regression model was used to determine the association between RAAS inhibitors and sepsis outcomes. To directly compare ACEI users, ARB users, and nonusers, a 3-way propensity score matching approach was performed. Results were pooled with previous evidence via a random-effects meta-analysis. A total of 52 727 patients were hospitalized with sepsis, of whom 7642 were prescribed an ACEI and 4237 were prescribed an ARB. Using propensity score–matched analyses, prior ACEI use was associated with decreased 30-day mortality (hazard ratio, 0.84 [95% CI, 0.75–0.94]) and 90-day mortality (hazard ratio, 0.83 [95% CI, 0.75–0.92]) compared with nonuse. Prior ARB use was associated with an improved 90-day survival (hazard ratio, 0.88 [95% CI, 0.83–0.94]). These results persisted in sensitivity analyses focusing on patients without cancer and patients with hypertension. By contrast, no beneficial effect was found for antecedent β-blockers exposure (hazard ratio, 0.99 [95% CI, 0.94–1.05]). The pooled estimates obtained from the meta-analysis was 0.71 (95% CI, 0.58–0.87) for prior use of ACEI/ARB.The short-term mortality after sepsis was substantially lower among those who were already established on RAAS inhibitor treatment when sepsis occurred.

scholarly journals Clinical Features of COVID-19 in Patients With Essential Hypertension and the Impacts of Renin-angiotensin-aldosterone System Inhibitors on the Prognosis of COVID-19 Patients

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 732-741 ◽  
Author(s):  
Wei Pan ◽  
Jishou Zhang ◽  
Menglong Wang ◽  
Jing Ye ◽  
Yao Xu ◽  
...  
Keyword(s):  
Cox Regression ◽  
Medication History ◽  
Renin Angiotensin Aldosterone System ◽  
Cox Regression Analysis ◽  
Renin Angiotensin ◽  
Reactive Protein ◽  
All Cause Mortality ◽  
History Of ◽  
Raas Inhibitors ◽  
The Impact

Hypertension is one of the most common comorbidities in patients with coronavirus disease 2019 (COVID-19). This study aimed to clarify the impact of hypertension on COVID-19 and investigate whether the prior use of renin-angiotensin-aldosterone system (RAAS) inhibitors affects the prognosis of COVID-19. A total of 996 patients with COVID-19 were enrolled, including 282 patients with hypertension and 714 patients without hypertension. Propensity score-matched analysis (1:1 matching) was used to adjust the imbalanced baseline variables between the 2 groups. Patients with hypertension were further divided into the RAAS inhibitor group (n=41) and non-RAAS inhibitor group (n=241) according to their medication history. The results showed that COVID-19 patients with hypertension had more severe secondary infections, cardiac and renal dysfunction, and depletion of CD8 + cells on admission. Patients with hypertension were more likely to have comorbidities and complications and were more likely to be classified as critically ill than those without hypertension. Cox regression analysis revealed that hypertension (hazard ratio, 95% CI, unmatched cohort [1.80, 1.20–2.70]; matched cohort [2.24, 1.36–3.70]) was independently associated with all-cause mortality in patients with COVID-19. In addition, hypertensive patients with a history of RAAS inhibitor treatment had lower levels of C-reactive protein and higher levels of CD4 + cells. The mortality of patients in the RAAS inhibitor group (9.8% versus 26.1%) was significantly lower than that of patients in the non-RAAS inhibitor group. In conclusion, hypertension may be an independent risk factor for all-cause mortality in patients with COVID-19. Patients who previously used RAAS inhibitors may have a better prognosis.

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