scholarly journals Effect of Dual Blockade of Renin-Angiotensin System on Proteinuria

2013 ◽  
Vol 1 (1) ◽  
pp. 18-20
Author(s):  
Eqerem Hasani ◽  
Alma Idrizi ◽  
Myftar Barbullushi
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Receptor Blocker ◽  
Enzyme Inhibitor ◽  
Combined Therapy ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Dual Blockade

Aim: Aim of the study was the evaluation of the effect of dual blockade of the renin-angiotensin system (RAS) on proteinuria. Material and Methods: Sixty patients, included in the study, were treated with angiotensin-converting enzyme inhibitor and angiotensin receptor blocker for a period of 3 months. Results: The dual blockade of RAS resulted with decrease of proteinuria, a slight increase of serum creatinine and was not associated with a lowering of blood pressure.Conclusion: Combined therapy with ACE-I and ARB results in a more complete blockade of the RAS than monotherapy. In proteinuric nephropathies it reduces significantly baseline proteinuria.

scholarly journals The Uterine Placental Bed Renin-Angiotensin System in Normal and Preeclamptic Pregnancy

Endocrinology ◽  
2009 ◽  
Vol 150 (9) ◽  
pp. 4316-4325 ◽  
Author(s):  
Lauren Anton ◽  
David C. Merrill ◽  
Liomar A. A. Neves ◽  
Debra I. Diz ◽  
Jenny Corthorn ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Mrna Expression ◽  
Receptor Binding ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Angiotensin System ◽  
Chorionic Villi ◽  
Renin Angiotensin

Abstract Previously, we demonstrated activation of the renin-angiotensin system in the fetal placental chorionic villi, but it is unknown whether the immediately adjacent area of the maternal uterine placental bed is regulated similarly. This study measured angiotensin peptides, renin-angiotensin system component mRNAs, and receptor binding in the fundus from nonpregnant subjects (n = 19) and in the uterine placental bed from normal (n = 20) and preeclamptic (n = 14) subjects. In the uterine placental bed from normal pregnant women, angiotensin II peptide levels and angiotensinogen, angiotensin-converting enzyme, angiotensin receptor type 1 (AT1), AT2, and Mas mRNA expression were lower as compared with the nonpregnant subjects. In preeclamptic uterine placental bed, angiotensin II peptide levels and renin and angiotensin-converting enzyme mRNA expression were significantly higher than normal pregnant subjects. The AT2 receptor was the predominant receptor subtype in the nonpregnant fundus, whereas all angiotensin receptor binding was undetectable in normal and preeclamptic pregnant uterine placental bed compared with nonpregnant fundus. These findings suggest that the maternal uterine placental bed may play an endocrine role by producing angiotensin II, which acts in the adjacent placenta to vasoconstrict fetal chorionic villi vessels where we have shown previously that AT1 receptors predominate. This would lead to decreased maternal-fetal oxygen exchange and fetal nutrition, a known characteristic of preeclampsia.

scholarly journals Effects of Renin-Angiotensin Inhibition on ACE2 and TMPRSS2 Expression: Insights into COVID-19

2020 ◽  
Author(s):  
Congqing Wu ◽  
Dien Ye ◽  
Adam E. Mullick ◽  
Zhenyu Li ◽  
A.H. Jan Danser ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Viral Entry ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Mrna Abundance ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Increase Risk

AbstractAngiotensin-converting enzyme 2 (ACE2), a component of the renin-angiotensin system, is a receptor for SARS-CoV-2, the virus that causes COVID-19. To determine whether the renin-angiotensin inhibition regulates ACE2 expression, either enalapril (an angiotensin-converting enzyme inhibitor) or losartan (an AT1 receptor blocker) was infused subcutaneously to male C57BL/6J mice for two weeks. Neither enalapril nor losartan changed abundance of ACE2 mRNA in lung, ileum, kidney, and heart. Viral entry also depends on transmembrane protease serine 2 (TMPRSS2) to prime the S protein. TMPRSS2 mRNA was abundant in lungs and ileum, modest in kidney, but barely detectable in heart. TMPRSS2 mRNA abundance was not altered by either enalapril or losartan in any of the 4 tissues. Next, we determined whether depletion of angiotensinogen (AGT), the unique substrate of the renin-angiotensin system, changes ACE2 and TMPRSS2 mRNA abundance. AGT antisense oligonucleotides (ASO) were injected subcutaneously to male C57BL/6J mice for 3 weeks. Abundance of ACE2 mRNA was unchanged in any of the 4 tissues, but TMPRSS2 mRNA was significantly decreased in lungs. Our data support that the renin-angiotensin inhibition does not regulate ACE2 and hence are not likely to increase risk for COVID-19.

scholarly journals Acute Kidney Injury in a Case Series of Patients with Confirmed COVID-19 (Coronavirus Disease 2019): Role of Angiotensin-Converting Enzyme 2 and Renin-Angiotensin System Blockade

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Avantika Chenna ◽  
Venu Madhav Konala ◽  
Subhasish Bose ◽  
Sasmit Roy ◽  
Bhaskar Reddy Madhira ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Angiotensin Converting Enzyme ◽  
Angiotensin Receptor Blockers ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Receptor Blockers

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 apart from ACE inhibitors, and angiotensin receptor blockers. The ACE inhibitors and ARBs were stopped in these patients due to acute kidney injury. We also discussed the role of ACE2 and the renin-angiotensin system (RAS) blockade in patients with COVID-19 infection along with pathogenesis.

COVID-19, Angiotensin-Converting Enzyme 2 and Renin-Angiotensin System Inhibition: Implications for Practice

2021 ◽  
Vol 17 ◽  
Author(s):  
Vasiliki Katsi ◽  
George Pavlidis ◽  
George Charalambous ◽  
Dimitrios Tousoulis ◽  
Konstantinos Toutouzas
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Viral Entry ◽  
Enzyme Inhibitor ◽  
Experimental Studies ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Increased Risk ◽  
Ras Inhibitors

Background : Recent studies suggested that patients with coronavirus disease 2019 (COVID-19) who use renin-angiotensin system (RAS) inhibitors have an increased risk of respiratory failure and death. The hypothesis was that angiotensin-converting enzyme inhibitor (ACEIs) or angiotensin receptor blocker (ARBs) may up-regulate ACE2 expression that is used as receptor for viral entry into cells. Objective: The purpose of this review is to discuss the existing evidence on the interaction between COVID-19 infection, ACE2 and ACEIs or ARBs and to examine the main implications for clinical practice. In addition, novel therapeutic strategies for blocking ACE2-mediated COVID-19 infection will be displayed. Methods : We performed a comprehensive review of the literature to identify data from clinical and experimental studies for the association between COVID-19 infection, ACE2 and RAS inhibition. Results: The current clinical and experimental evidence for ACEIs or ARBs to facilitate severe acute respiratory distress syndrome-coronavirus-2 (SARS-CoV-2) is insufficient to suggest discontinuing these drugs. Several observational studies arrive at the conclusion that the continued use of RAS inhibitors is unlike to be harmful in COVID-19-positive patients. Conclusions: Further randomized trials are needed to answer definitely the question of whether RAS inhibitors are harmful or beneficial to patients with COVID-19.

scholarly journals Studi Penggunaan Obat Untuk Menangani Gangguan Natrium dan Kalium Pasien Penyakit Ginjal Terminal di RS Muhammadiyah Bandung

2019 ◽  
Vol 5 (3) ◽  
pp. 233
Author(s):  
Yunisa Friscia Yusri ◽  
Lia Amalia ◽  
Ida Lisni
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Converting Enzyme Inhibitor ◽  
Angiotensin Receptor Blocker ◽  
Enzyme Inhibitor ◽  
Receptor Blocker ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Cross Sectional ◽  
Renin Angiotensin ◽  
Converting Enzyme Inhibitor

Penyakit ginjal terminal dapat menyebabkan terganggunya pengaturan keseimbangan Natrium (Na) dan Kalium (K). Gangguan tersebut dapat disebabkan oleh fungsi ginjal yang menurun dan pengaruh antihipertensi golongan penghambat SRAA (Sistem Renin Angiotensin Aldosteron) seperti ACEI (Angiotensin-Converting Enzyme Inhibitor) dan ARB (Angiotensin Receptor Blocker). Gangguan ini dapat menyebabkan aritmia, edema otak, henti jantung hingga kematian. Penelitian ini bertujuan untuk mengetahui penggunaan obat serta pengaruh penggunaan antihipertensi ACEI dan ARB terhadap gangguan Na dan K pada kondisi pasien pradialisis. Penelitian ini merupakan penelitian deskriptif-potong lintang (cross-sectional) pada kondisi pasien pradialisis di Rumah Sakit Muhammadiyah Bandung. Dari penelitian diperoleh 22 pasien yang memenuhi kriteria inklusi, yaitu pasien yang memiliki hasil pengukuran kadar Na dan K pada kondisi pradialisis. Dari 22 pasien tersebut sebanyak 59,09% mengalami hiponatremia, 45,45% mengalami hiperkalemia, dan 4,55% mengalami hipokalemia. Untuk mengatasi kondisi hiponatremia digunakan infus NaCl 3%. Sedangkan untuk mengatasi kondisi hiperkalemia digunakan furosemid, kalsium glukonat, dan kalsium polistiren sulfonat baik tunggal maupun kombinasi. Gangguan Na dan K harus segera diatasi untuk mencegah terjadinya kerusakan sel. Penggunaan antihipertensi ACEI, ARB maupun kombinasi keduanya secara statistik tidak bermakna yang berarti tidak terdapat pengaruh penggunaan obat tersebut terhadap munculnya kondisi hiponatremia maupun hiperkalemia pada pasien.Kata kunci: Hiponatremia, Hiperkalemia, ACEI, ARB

An Experimental Model of Encapsulating Peritoneal Sclerosis

2009 ◽  
Vol 29 (2_suppl) ◽  
pp. 49-50 ◽  
Author(s):  
Tokihiko Sawada ◽  
Yasuo Ishii ◽  
Ichiro Nakajima ◽  
Shohei Fuchinoue ◽  
Keiichi Kubota ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Converting Enzyme Inhibitor ◽  
Transforming Growth Factor ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Dependent Manner ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Converting Enzyme Inhibitor

In Japan, only about 3% of all patients with end-stage renal disease are maintained by continuous ambulatory peritoneal dialysis (CAPD). Although the reasons for the low proportion of patients receiving CAPD are multifactorial, encapsulating peritoneal sclerosis (EPS), a fatal complication of CAPD, is a major factor. In 1995 we developed a rat model of EPS, and in 2001 also developed an EPS model in mice. These rodent EPS models are reliable, reproducible, and inexpensive and have been used by other investigators. The renin–angiotensin system negatively regulates the transforming growth factor-beta signaling pathway, which plays a major role in tissue fibrosis. To investigate the anti-EPS effect of renin–angiotensin system inhibition, an angiotensin-converting enzyme inhibitor, quinapril, was administered to an EPS model in mice. Quinapril was found to inhibit EPS, both macro- and microscopically, in a dose-dependent manner. We report our experience of developing the experimental in vivo EPS model, and the inhibitory effect of this angiotensin-converting enzyme inhibitor on EPS.

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