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Journal articles on the topic 'Angiotensin converting enzyme Angiotensin II Proteinuria. Kidneys'

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Published: 4 June 2021

Last updated: 4 February 2022

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1

BENIGNI, ARIELA, SUSANNA TOMASONI, ELENA GAGLIARDINI, et al. "Blocking Angiotensin II Synthesis/Activity Preserves Glomerular Nephrin in Rats with Severe Nephrosis." Journal of the American Society of Nephrology 12, no. 5 (2001): 941–48. http://dx.doi.org/10.1681/asn.v125941.

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Abstract. Angiotensin-converting enzyme inhibitors restore size-selective dysfunction of the glomerular barrier in experimental animals and humans with proteinuric nephropathies, although the structural and molecular determinants of such an effect are not completely understood. This study used an accelerated model of experimental nephrosis to assess nephrin gene and protein expression in the kidney and the possible modulating effect of drugs that block angiotensin II (AII) synthesis/activity. Passive Heymann nephritis (PHN) and control animals were studied at day 7, month 4, and month 8. Addit

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Jung, F. F., T. M. Kennefick, J. R. Ingelfinger, J. P. Vora, and S. Anderson. "Down-regulation of the intrarenal renin-angiotensin system in the aging rat." Journal of the American Society of Nephrology 5, no. 8 (1995): 1573–80. http://dx.doi.org/10.1681/asn.v581573.

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Progressive deterioration of renal function occurs during normal aging. Previous studies on the aging kidney have demonstrated glomerular hemodynamic changes, specifically, glomerular capillary hypertension, as maladaptations that lead to proteinuria and glomerular sclerosis over time. Aging rats treated with angiotensin-converting enzyme inhibition have relatively less proteinuria and sclerosis, suggesting that age-related changes in renal function may be associated with alterations in the intrarenal renin-angiotensin system, which thus may play a major role in the pathogenesis of these malad

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Mata-Greenwood, Eugenia, Arlin B. Blood, LeeAnna D. Sands, Shannon L. Bragg, Daliao Xiao, and Lubo Zhang. "A novel rodent model of pregnancy complications associated with genetically determined angiotensin-converting enzyme (ACE) activity." American Journal of Physiology-Endocrinology and Metabolism 315, no. 1 (2018): E52—E62. http://dx.doi.org/10.1152/ajpendo.00289.2017.

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Brown Norway (BN) and Lewis (LW) inbred rat strains harbor different angiotensin-converting enzyme ( Ace) polymorphisms that result in higher ACE activity in BN than LW rats. Thus we hypothesized that pregnant BN rats would show pregnancy complications linked to angiotensin II (AII) activity. We performed longitudinal and cross-sectional studies in pregnant LW and BN rats. We found that BN rats have significantly higher ACE activity and AII levels at prepregnancy and throughout pregnancy compared with LW rats, except at midgestation. BN placentas and maternal kidneys had significantly higher e

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4

Gupta, Arvind, Upma Narain, and Aditya Sachan. "Comparison of the efficacy of triple blockade, double blockade and single blockade of RAAS in non diabetic chronic kidney disease." International Journal of Advances in Medicine 5, no. 4 (2018): 941. http://dx.doi.org/10.18203/2349-3933.ijam20183124.

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Background: Although dual blockade of the renin-angiotensin-aldosterone system with the combination of an angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker is generally well established as a treatment for nephropathy, this treatment is not fully effective in some patients.Methods: A prospective observational study was done on 600 chronic kidney disease patients during July 2012 to August 2014 to compare the efficacy of triple blockade, double blockade and single blockade of renin-angiotensin-aldosterone system in non diabetic chronic kidney disease.Results: At the end

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Gupta, Arvind, Upma Narain, and Romar Dabu. "Nephro protection property of double blockade versus single blocked of RAAS in delaying the progression of CKD." International Journal of Advances in Medicine 5, no. 3 (2018): 748. http://dx.doi.org/10.18203/2349-3933.ijam20182135.

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Background: Dual renin angiotensin aldosterone system blockade using angiotensin receptor blockers in combination with angiotensin converting enzyme inhibitors is reported to improve proteinuria in non-diabetic patients.Methods: A prospective observational study was done on 810 non-diabetic chronic kidney disease patients during July 2012 to August 2014 to compare the nephro protection property of double blockade and single blocked of renin angiotensin aldosterone system in delaying the progression of chronic kidney disease.Results: At the end of 24 months urinary protein excretion rate of gro

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VAN DIJK, MARJAN A., DORIEN J. M. PETERS, MARTIJN H. BREUNING, and PETER C. CHANG. "The Angiotensin-Converting Enzyme Genotype and Microalbuminuria in Autosomal Dominant Polycystic Kidney Disease." Journal of the American Society of Nephrology 10, no. 9 (1999): 1916–20. http://dx.doi.org/10.1681/asn.v1091916.

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Abstract. Autosomal dominant polycystic kidney disease (ADPKD) has a variable clinical course. Clinical parameters associated with a worse prognosis are hypertension and proteinuria or microalbuminuria (MA). Because chronic stimulation of the renin-angiotensin system is likely to be present in ADPKD patients, the effect of the angiotensin-converting enzyme insertion/deletion (ACE I/D) genotype on the variability of these clinical parameters was examined in untreated ADPKD patients. Proteinuria and MA were determined in 24-h urine collections. BP measurements were performed with an ambulatory m

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7

Wu, L. L., A. Cox, C. J. Roe, M. Dziadek, M. E. Cooper, and R. E. Gilbert. "Secreted protein acidic and rich in cysteine expression after subtotal nephrectomy and blockade of the renin-angiotensin system." Journal of the American Society of Nephrology 8, no. 9 (1997): 1373–82. http://dx.doi.org/10.1681/asn.v891373.

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Secreted protein acidic and rich in cysteine (SPARC) is an extracellular matrix-associated protein with antiadhesive, antiproliferative, and matrix remodeling properties. SPARC gene and protein expression were investigated after subtotal nephrectomy (STNx), a model of noninflammatory progressive renal injury. In addition, the effect of blockade of the renin-angiotensin system by the angiotensin-converting enzyme inhibitor ramipril or by the angiotensin II receptor antagonist valsartan was examined. The STNx rats developed hypertension, proteinuria, and renal impairment. These changes were asso

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8

Park, Changhyun, Eun Kyoung Lee, So Mi Kim, et al. "Acute Kidney Injury after Administering Dapagliflozin to a Diabetic Patient with Acute Cerebral Infarction." Korean Journal of Medicine 95, no. 6 (2020): 404–8. http://dx.doi.org/10.3904/kjm.2020.95.6.404.

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Dapagliflozin is a recently developed oral anti-diabetic drug and SGLT2 inhibitor with well-known cardioprotective and renoprotective effects. Although a reduction of the glomerular filtration rate is induced by volume depletion and tubule-glomerular feedback during the early period after administering a SGLT2 inhibitor, the renal prognosis improves more with a decrease of proteinuria. However, the risk of acute kidney injury increases in heart failure and hypovolemia patients, and in those taking certain drugs, such as non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhib

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Binz-Lotter, Julia, Christian Jüngst, Markus M. Rinschen, et al. "Injured Podocytes Are Sensitized to Angiotensin II–Induced Calcium Signaling." Journal of the American Society of Nephrology 31, no. 3 (2020): 532–42. http://dx.doi.org/10.1681/asn.2019020109.

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BackgroundInhibition of angiotensin II (AngII) signaling, a therapeutic mainstay of glomerular kidney diseases, is thought to act primarily through regulating glomerular blood flow and reducing filtration pressure. Although extravascular actions of AngII have been suggested, a direct effect of AngII on podocytes has not been demonstrated in vivo.MethodsTo study the effects of AngII on podocyte calcium levels in vivo, we used intravital microscopy of the kidney in mice expressing the calcium indicator protein GCaMP3.ResultsIn healthy animals, podocytes displayed limited responsiveness to AngII

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Severova-Andreevska, Galina, Ilina Danilovska, Aleksandar Sikole, Zivko Popov, and Ninoslav Ivanovski. "Hypertension after Kidney Transplantation: Clinical Significance and Therapeutical Aspects." Open Access Macedonian Journal of Medical Sciences 7, no. 7 (2019): 1241–45. http://dx.doi.org/10.3889/oamjms.2019.264.

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Most of the kidney transplanted patients develop arterial hypertension after renal transplantation. Together with very well-known and usual risk factors, post-transplant hypertension contributes to the whole cardiovascular morbidity and mortality in the kidney transplant population. The reasons of post-transplant hypertension are factors related to donors and recipients, immunosuppressive therapy like Calcineurin Inhibitors (CNI) and surgery procedures (stenosis and kinking of the renal artery and ureteral obstruction). According to Eighth National Committee (JNC 8) recommendations, blood pres

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11

Liebau, Max C., D. Lang, J. Böhm, et al. "Functional expression of the renin-angiotensin system in human podocytes." American Journal of Physiology-Renal Physiology 290, no. 3 (2006): F710—F719. http://dx.doi.org/10.1152/ajprenal.00475.2004.

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Experimental and clinical studies impressively demonstrate that angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) significantly reduce proteinuria and retard progression of glomerular disease. The underlying intraglomerular mechanisms are not yet fully elucidated. As podocyte injury constitutes a critical step in the pathogenesis of glomerular proteinuria, beneficial effects of ACEI and ARB may partially result from interference with a local renin-angiotensin system (RAS) in podocytes. The knowledge of expression and function of a local RAS in podocytes is

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Grist, Caroline, Cormac Breen, Rachel Kesse-Adu, and Jo Howard. "A Retrospective Study Of The Anti-Proteinuric Effects Of Hydroxyurea and Angiotensin-Converting Enzyme Inhibitors Or Angiotensin II Receptor Blockers In Adults With Sickle Cell Disease." Blood 122, no. 21 (2013): 4678. http://dx.doi.org/10.1182/blood.v122.21.4678.4678.

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Glomerulopathy, associated with initial glomerular hyperfiltration followed by the development of microalbuminuria/proteinuria, is a well recognised complication of Sickle Cell Disease. There is evidence for the efficacy of Angiotensin-Converting Enzyme Inhibitors (ACE-I) or Angiotensin II Receptor Blockers (ARB) in reducing microalbuminuria in this population, and in common with other proteinuric kidney diseases the use of these agents is increasingly commonplace. In children the additional benefit of Hydroxyurea (HU) with microalbuminuria/proteinuria has previously been shown. The effect of

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Amuchastegui, S. C., N. Azzollini, M. Mister, A. Pezzotta, N. Perico, and G. Remuzzi. "Chronic allograft nephropathy in the rat is improved by angiotensin II receptor blockade but not by calcium channel antagonism." Journal of the American Society of Nephrology 9, no. 10 (1998): 1948–55. http://dx.doi.org/10.1681/asn.v9101948.

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Functional and structural changes of chronic renal allograft failure share similarities with other chronic nephropathies with low nephron number. In models of reduced nephron number, angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers prevented proteinuria and retarded renal lesions. This study investigates whether blockade of angiotensin II activity prevented chronic allograft injury in the Fisher 344 --> Lewis rat kidney transplant model, and compares its effect with that of calcium channel blockers, the main antihypertensive agents used in transplant patients to

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14

Corman, B., S. Chami-Khazraji, J. Schaeverbeke, and J. B. Michel. "Effect of feeding on glomerular filtration rate and proteinuria in conscious aging rats." American Journal of Physiology-Renal Physiology 255, no. 2 (1988): F250—F256. http://dx.doi.org/10.1152/ajprenal.1988.255.2.f250.

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Food intake increases glomerular filtration and proteinuria in adult rats. That this postprandial hyperfiltration could be age dependent was investigated in 3-, 10-, 20-, and 30-mo-old rats. Glomerular filtration rate and protein excretion were measured in fed or 24 h fasted conscious animals. In the 3-mo-old rats food ingestion increased renal filtration by 45% from 1.17 +/- 0.08 to 1.73 +/- 0.11 ml.min-1.g kidney wt-1 (n = 6). As the animals became older, the differences between fed and fasted periods became smaller: in 30-mo-old rats glomerular filtration rate was 0.85 +/- 0.03 and 1.01 +/-

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Thompson, Michele M., Terry T. Oyama, Francis J. Kelly, Thomas M. Kennefick, and Sharon Anderson. "Activity and responsiveness of the renin-angiotensin system in the aging rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 5 (2000): R1787—R1794. http://dx.doi.org/10.1152/ajpregu.2000.279.5.r1787.

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The systemic renin-angiotensin system (RAS) is suppressed in normal aging, but the activity of the tissue RAS is not well defined. We examined the systemic and intrarenal RAS status of aging normal rats and responses to suppression and stimulation of the production of endogenous ANG II. Studies were performed in young (3 mo) and early aging (15 mo) male Sprague-Dawley rats. Angiotensin-converting enzyme inhibitors modestly decreased mean arterial pressure (MAP) in young (3 mo) and early aging (15 mo) rats and limited proteinuria in the older rats. There were no significant age-related effects

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REMUZZI, GIUSEPPE, CARLA ZOJA, ELENA GAGLIARDINI, DANIELA CORNA, MAURO ABBATE, and ARIELA BENIGNI. "Combining an Antiproteinuric Approach with Mycophenolate Mofetil Fully Suppresses Progressive Nephropathy of Experimental Animals." Journal of the American Society of Nephrology 10, no. 7 (1999): 1542–49. http://dx.doi.org/10.1681/asn.v1071542.

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Abstract. Chronic renal diseases progress to organ insufficiency, which may require replacement therapy within one to three decades even independently of the type of initial insults. In the majority of cases, the degrees of proteinuria and interstitial leukocyte infiltration and scarring are strictly correlated with the rate of disease progression. This study tests the hypothesis that excess intrarenal protein traffic may cause lymphocyte-dependent interstitial injury that, while not fully controlled by antiproteinuric therapy, can be further inhibited by concomitant immunosuppression. A prima

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Peces, Ramón, Jorge Martínez-Ara, Carlos Peces, et al. "Nephrotic Syndrome and Idiopathic Membranous Nephropathy Associated with Autosomal-Dominant Polycystic Kidney Disease." Scientific World JOURNAL 11 (2011): 1041–47. http://dx.doi.org/10.1100/tsw.2011.94.

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We report the case of a 38-year-old male with autosomal-dominant polycystic kidney disease (ADPKD) and concomitant nephrotic syndrome secondary to membranous nephropathy (MN). A 3-month course of prednisone 60 mg daily and losartan 100 mg daily resulted in resistance. Treatment with chlorambucil 0.2 mg/kg daily, low-dose prednisone, plus an angiotensin-converting enzyme inhibitor (ACEI) and an angiotensin II receptor blocker (ARB) for 6 weeks resulted in partial remission of his nephrotic syndrome for a duration of 10 months. After relapse of the nephrotic syndrome, a 13-month course of mycoph

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Watts, Nelson B. "Albuminuria and Diabetic Nephropathy: an Evolving Story." Clinical Chemistry 37, no. 12 (1991): 2027–28. http://dx.doi.org/10.1093/clinchem/37.12.2027.

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Abstract The lifetime risk of diabetic nephropathy is ˜45% for patients with Type I (insulin-dependent) diabetes (1) and at least 30-35% for patients with Type II (non-insulin-dependent) diabetes (2, 3). In Type I diabetes, the incidence of readily detectable nephropathy rises steeply 10 years after the onset of diabetes (1). The progression from the appearance of “clinical proteinuria” (a positive test for protein upon routine urinalysis) to end-stage renal failure requiring dialysis or kidney transplantation occurs over about five years. This progression is usually relentless (4), but the ra

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Agarwal, Rajiv. "Proinflammatory effects of oxidative stress in chronic kidney disease: role of additional angiotensin II blockade." American Journal of Physiology-Renal Physiology 284, no. 4 (2003): F863—F869. http://dx.doi.org/10.1152/ajprenal.00385.2002.

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Oxidative stress plays an important role in causing progressive chronic kidney disease (CKD). We examined the influence of add-on ANG II receptor blockade administered as losartan (50 mg/day for 1 mo) on oxidative stress and proinflammatory state of the kidney in patients with CKD. All subjects were taking an angiotensin-converting enzyme inhibitor plus other antihypertensive agents. Oxidative stress to lipids and proteins was measured by an HPLC assay for malondialdehyde (MDA) and carbonyl concentration, respectively. Urinary inflammation was measured by monocyte chemotactic protein-1 (MCP-1)

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CORDONNIER, DANIEL J., NICOLE PINEL, CLAIRE BARRO, et al. "Expansion of Cortical Interstitium Is Limited by Converting Enzyme Inhibition in Type 2 Diabetic Patients with Glomerulosclerosis." Journal of the American Society of Nephrology 10, no. 6 (1999): 1253–63. http://dx.doi.org/10.1681/asn.v1061253.

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Abstract. Renal interstitial expansion is now considered a useful marker of progression of several nephropathies. This study describes a multicenter, prospective, double-blind, placebo-controlled, randomized trial of the effects of Perindopril (4 mg/d) on kidney structure and function over 2 yr in 26 type 2 diabetic patients with proteinuria ranging from 70 to 4210 mg/d and relatively preserved GFR (creatinine clearance >60 ml/min). All patients underwent baseline renal biopsy, but four (15%) were not randomized because of the presence of nondiabetic nephropathy. The remaining 22 were rando

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Griffin, Karen A., Maria M. Picken, George Bakris, and Anil K. Bidani. "Relative antihypertensive and glomeruloprotective efficacies of enalapril and candesartan cilexetil in the remnant kidney model." Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (2001): S191—S195. http://dx.doi.org/10.1177/14703203010020013301.

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The present studies were performed to investigate whether the differences described between the two modalities for interruption of the renin-angiotensin-aldosterone system (RAAS), angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin AT 1receptor antagonists (AIIA) result in differences in renoprotective efficacy in the rat remnant kidney model. Male Sprague-Dawley rats with an initial body weight of 225—300 g, underwent 5/6 renal ablation and had radiotransmitters installed for radiotelemetric blood pressure (BP) measurements, owing to the known limitations of periodic tail-cuff BP

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Viering, Daan H. H. M., Anneke P. Bech, Jeroen H. F. de Baaij, et al. "Functional tests to guide management in an adult with loss of function of type-1 angiotensin II receptor." Pediatric Nephrology 36, no. 9 (2021): 2731–37. http://dx.doi.org/10.1007/s00467-021-05018-7.

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Abstract Background Genetic loss of function of AGT (angiotensinogen), REN (renin), ACE (angiotensin-converting enzyme), or AGTR1 (type-1 angiotensin II receptor) leads to renal tubular dysgenesis (RTD). This syndrome is almost invariably lethal. Most surviving patients reach stage 5 chronic kidney disease at a young age. Methods Here, we report a 28-year-old male with a homozygous truncating mutation in AGTR1 (p.Arg216*), who survived the perinatal period with a mildly impaired kidney function. In contrast to classic RTD, kidney biopsy showed proximal tubules that were mostly normal. During t

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Ruiz-Ortega, M., D. Gómez-Garre, X. H. Liu, J. Blanco, R. Largo, and J. Egido. "Quinapril decreases renal endothelin-1 expression and synthesis in a normotensive model of immune-complex nephritis." Journal of the American Society of Nephrology 8, no. 5 (1997): 756–68. http://dx.doi.org/10.1681/asn.v85756.

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Angiotensin-converting enzyme (ACE) inhibitors diminish proteinuria and the progression to renal failure in several experimental models of renal injury. Endothelin-1 (ET-1) possesses potent biological actions on renal vessels and has been considered as a potential mediator of renal damage. Because angiotensin II (Ang II) induces ET-1 synthesis in endothelial and mesangial cells, we hypothesized that some of the beneficial effects of the ACE inhibitors could result from the blockade of ET-1 synthesis. In a normotensive model of immune-complex nephritis, in which there exists an increase in rena

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Ahmed, Sheikh Salahuddin, Md Aminul Haque Khan, and Tarafdar Runa Laila. "Treatment and Prevention of Common Complications of Chronic Kidney Disease." Journal of Enam Medical College 4, no. 1 (2014): 45–55. http://dx.doi.org/10.3329/jemc.v4i1.18069.

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Chronic kidney disease (CKD) is a worldwide public health problem with an increasing incidence and prevalence. Outcomes of CKD include not only complications of decreased kidney function and cardiovascular disease but also kidney failure causing increased morbidity and mortality. Unfortunately, CKD is often undetected and undertreated because of its insidious onset, variable progression, and length of time to overt kidney failure. Diabetes is now the leading cause of CKD requiring renal replacement therapy in many parts of the world, and its prevalence is increasing disproportionately in the d

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Velkoska, Elena, Rachael G. Dean, Luke Burchill, Vicki Levidiotis, and Louise M. Burrell. "Reduction in renal ACE2 expression in subtotal nephrectomy in rats is ameliorated with ACE inhibition." Clinical Science 118, no. 4 (2009): 269–79. http://dx.doi.org/10.1042/cs20090318.

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Alterations within the RAS (renin–angiotensin system) are pivotal for the development of renal disease. ACE2 (angiotensin-converting enzyme 2) is expressed in the kidney and converts the vasoconstrictor AngII (angiotensin II) into Ang-(1–7), a peptide with vasodilatory and anti-fibrotic actions. Although the expression of ACE2 in the diabetic kidney has been well studied, little is known about its expression in non-diabetic renal disease. In the present study, we assessed ACE2 in rats with acute kidney injury induced by STNx (subtotal nephrectomy). STNx and Control rats received vehicle or ram

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de Goeij, Moniek C. M., Madieke Liem, Dinanda J. de Jager, et al. "Proteinuria as a Risk Marker for the Progression of Chronic Kidney Disease in Patients on Predialysis Care and the Role of Angiotensin-Converting Enzyme Inhibitor/Angiotensin II Receptor Blocker Treatment." Nephron Clinical Practice 121, no. 1-2 (2012): c73—c82. http://dx.doi.org/10.1159/000342392.

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Rosselli, Jennifer L., Stacey M. Thacker, Julie P. Karpinski, and Katherine A. Petkewicz. "Treatment of IgA Nephropathy: An Update." Annals of Pharmacotherapy 45, no. 10 (2011): 1284–96. http://dx.doi.org/10.1345/aph.1q122.

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Objective: To review current literature regarding treatment options for immunoglobulin A nephropathy (IgAN). Data Sources: A MEDLINE search was performed using the terms IgA nephropathy, Berger's disease, immunoglobulin A nephropathy, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, fish oil, omega-3 fatty acids, statins. hydroxymethylglutaryl-CoA reductase Inhibitors, immunosuppressive therapy, corticosteroids, mycophenolate mofetil, cyclophosphamide, cyclosporine, azathioprine, leflunomide, antiplatelets, anticoagulants, vitamin E, infliximab, calcitriol, and intra

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Yamaleyeva, Liliya M., Shea Gilliam-Davis, Igor Almeida, K. Bridget Brosnihan, Sarah H. Lindsey, and Mark C. Chappell. "Differential regulation of circulating and renal ACE2 and ACE in hypertensive mRen2.Lewis rats with early-onset diabetes." American Journal of Physiology-Renal Physiology 302, no. 11 (2012): F1374—F1384. http://dx.doi.org/10.1152/ajprenal.00656.2011.

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We examined the impact of early diabetes on the circulating and kidney renin-angiotensin system (RAS) in male and female mRen2.Lewis (mRen2) hypertensive rats. Diabetes (DB) was induced by streptozotocin (STZ; 65 mg/kg) at 11 wk of age for 4 wk without insulin replacement. Systolic blood pressures were not increased in DB males or females compared with controls (CON). Circulating angiotensin-converting enzyme 2 (ACE2) increased ninefold ( P < 0.05) in DB females and threefold ( P < 0.05) in DB males, but circulating ACE and ANG II were higher in the DB groups. Serum C-reactive protein wa

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Palm, Fredrik, and Lina Nordquist. "Renal oxidative stress, oxygenation, and hypertension." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (2011): R1229—R1241. http://dx.doi.org/10.1152/ajpregu.00720.2010.

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Hypertension is closely associated with progressive kidney dysfunction, manifested as glomerulosclerosis, interstitial fibrosis, proteinuria, and eventually declining glomerular filtration. The postulated mechanism for development of glomerulosclerosis is barotrauma caused by increased capillary pressure, but the reason for development of interstitial fibrosis and the subsequently reduced kidney function is less clear. However, it has been hypothesized that tissue hypoxia induces fibrogenesis and progressive renal failure. This is very interesting, since recent reports highlight several differ

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ABBATE, MAURO, CARLA ZOJA, DANIELA ROTTOLI, et al. "Antiproteinuric Therapy while Preventing the Abnormal Protein Traffic in Proximal Tubule Abrogates Protein- and Complement-Dependent Interstitial Inflammation in Experimental Renal Disease." Journal of the American Society of Nephrology 10, no. 4 (1999): 804–13. http://dx.doi.org/10.1681/asn.v104804.

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Abstract. In proteinuric glomerulopathies, the excess traffic of proteins into the renal tubule is a candidate trigger of interstitial inflammatory and immune events leading to progressive injury, and a key target for the renoprotective action of antiproteinuric drugs. Among proteins trafficked to the proximal tubule, the third component of complement (C3) can be activated locally and contribute to inflammation at sites of protein reabsorption. Experiments were performed in rats with renal mass reduction (RMR, 5/6 nephrectomy) with the following aims: (1) to study Ig (IgG) and complement depos

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Vásconez, Cesar Igor, Alejandro Xavier Campoverde, and Victoria Trejo Martínez. "MANEJO Y SEGUIMIENTO CLÍNICO DE PACIENTE CON SINDROME DE ALPORT FASE IV." Revista Medica Vozandes 32, no. 1 (2021): s1—s2. http://dx.doi.org/10.48018/rmv.v32.i1.s1.

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Introduction Alport syndrome (AS) is a hereditary disease of the basement membranes caused by mutations in type IV collagen. This disease is characterized by the presence of progressive hereditary nephropathy associated with sensory deafness, as well as ocular lesions. AS has an incidence of 1 in every 50,000 live births, constituting 1 to 2% of the cause of chronic kidney disease (CKD) in Europe and 3% of CKD in the American pediatric population; it is considered to be the cause of terminal uremia in 0.6 to 4.6% of terminal patients in the United States and Europe. At the moment there is no c

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Bozkurt, Devrim, Pinar Cetin, Savas Sipahi, et al. "The Effects of Renin–angiotensin System Inhibition on Regression of Encapsulating Peritoneal Sclerosis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 28, no. 5_suppl (2008): 38–42. http://dx.doi.org/10.1177/089686080802805s08.

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Background Encapsulating peritoneal sclerosis (EPS) is a clinical syndrome associated with symptoms of ileus and irreversible sclerosis of both visceral and parietal peritoneum. Peritoneal dialysis (PD) patients rarely develop EPS, a severe life-threatening condition of unknown pathogenesis. Angiotensin II is known to promote fibrosis and inflammation in various tissues. Renin–angiotensin system (RAS) blockade provides advantages in the course of diseases such as hypertension, chronic kidney disease, and proteinuria. We have also previously shown that RAS blockade has beneficial effects on hyp

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Murkamilov, I. T., I. S. Sabirov, V. V. Fomin, and Zh A. Murkamilova. "Focal segmental glomerulosclerosis: current status of the problem." Russian Archives of Internal Medicine 10, no. 1 (2020): 38–46. http://dx.doi.org/10.20514/2226-6704-2020-10-1-38-46.

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One of the most prognostically unfavorable variants of glomerulopathy is focal segmental glomerulosclerosis (FSHC), which is detected by nephrobiopsy in 5-20% of patients with nephrotic syndrome (NS) and in 15% of adult patients with chronic glomerulonephritis. FSGS recurs in a transplanted kidney in 30-50% of patients. Among adult patients with FSH, men predominate. A poor prognosis of FSHC is explained by the heterogeneity of the disease and is exacerbated by a poor response to treatment. According to current data, FSGS is characterized by sclerosis of the mesangial matrix, hyalinosis, damag

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DePatis, Keri Lillian, and Catherine Harrington. "The Impact of Pharmacist-delivered Motivational Interviewing on Chronic Kidney Disease Identification and Management in Patients with Diabetes Mellitus and Low Socioeconomic Status." INNOVATIONS in pharmacy 10, no. 4 (2019): 8. http://dx.doi.org/10.24926/iip.v10i4.2109.

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Purpose: Chronic kidney disease (CKD) is a common complication among patients with diabetes mellitus; however, noncompliance with the recommended annual screening is common. Increased screening among high-risk patients is important to identify the early stages CKD, potentially resulting in earlier treatment, slower progression, fewer complications, and decreased healthcare expenditures. Motivational interviewing (MI) has previously been shown to be effective for various behaviors, such as smoking cessation and cholesterol level control. The objective of this study is to evaluate the effectiven

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Semin, Sergey G., O. B. Kolbe, A. B. Moiseev, A. I. Turchinskaya, and E. E. Vartapetova. "VITAMIN D NEPHROPROTECTIVE STRATEGY OF CHILDREN WITH CHRONIC RENAL DISEASE." Medical Journal of the Russian Federation 25, no. 1 (2019): 59–64. http://dx.doi.org/10.18821/0869-2106-2019-25-1-59-64.

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According to current conception, the process of forming of nephrosclerosis despite the origins is detected by the force of the same cellular and molecular mechanisms. Hence primary triggers cause elevated production of range of cellular response mediators, cytokines and growth factors such as transforming plateled-derived growth factor, fibroblast growth factor, interferon gamma, nuclear factor and others, by means of sequential processes, is followed by the replacement of kidney tissue. One of the most studied aspects of the process of nephrosclerosis is the influence of anginotensin II. Ther

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Steele, T. H., and L. Challoner-Hue. "Intrarenal angiotensin II inhibition influences the actions of atrial natriuretic peptide." Clinical Science 78, no. 5 (1990): 475–80. http://dx.doi.org/10.1042/cs0780475.

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1. We previously found that kidneys isolated from salt-restricted rats were refractory to atrial natriuretic peptide compared with kidneys from salt-loaded rats. Because the intrarenal tissue renin-angiotensin system may modulate renal responses to atrial natriuretic peptide, we examined the effect of dietary NaCl loading on the responses of isolated perfused kidneys from normal rats to atrial natriuretic peptide, before and after the addition of angiotensin II receptor antagonists or angiotensin I converting enzyme inhibitors to the perfusate. 2. Atrial natriuretic peptide increased the glome

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37

Moriyama, T., H. Kitamura, S. Ochi, et al. "Association of angiotensin I-converting enzyme gene polymorphism with susceptibility to antiproteinuric effect of angiotensin I-converting enzyme inhibitors in patients with proteinuria." Journal of the American Society of Nephrology 6, no. 6 (1995): 1676–78. http://dx.doi.org/10.1681/asn.v661676.

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The antiproteinuric effect of angiotensin I-converting enzyme (ACE) inhibitors in patients with renal diseases of various origins has been well recognized. However, individual responses regarding the degree of decrease in urinary protein excretion appear to vary considerably. The mechanism underlying this variable response to ACE inhibitors has not been clarified yet. A possible role of ACE gene insertion/deletion (I/D) polymorphism in the responsiveness to antiproteinuric effect of ACE inhibitors is examined. Thirty-six patients with proteinuria (23 men and 13 woman; mean age, 47 +/- 13 yr) w

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WAPSTRA, FRITS H., GERJAN NAVIS, PAUL E. DE JONG, and DICK DE ZEEUW. "Chronic Angiotensin II Infusion But Not Bradykinin Blockade Abolishes the Antiproteinuric Response to Angiotensin-Converting Enzyme Inhibition in Established Adriamycin Nephrosis." Journal of the American Society of Nephrology 11, no. 3 (2000): 490–96. http://dx.doi.org/10.1681/asn.v113490.

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Abstract. Angiotensin-convernting enzyme (ACE) inhibition reduces proteinuria in established adriamycin nephrosis. To investigate whether the reduction in proteinuria is due to decreased generation of angiotensin II (AngII) or to decreased degradation of bradykinin, four series of experiments in established adriamycin nephrosis were performed. In the first series, 2 mg/kg lisinopril reduced BP from 117 ± 4 to 67 ± 2 mmHg and proteinuria from 335 ± 66 to 57 ± 10 mg/24 h after 2 wk of treatment. Subsequent continuous intraperitoneal infusion of AngII (250 ng/kg per min) for 2 wk partially restor

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Ferrario, Carlos M., and Jasmina Varagic. "The ANG-(1–7)/ACE2/mas axis in the regulation of nephron function." American Journal of Physiology-Renal Physiology 298, no. 6 (2010): F1297—F1305. http://dx.doi.org/10.1152/ajprenal.00110.2010.

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The study of experimental hypertension and the development of drugs with selective inhibitory effects on the enzymes and receptors constituting the components of the circulating and tissue renin-angiotensin systems have led to newer concepts of how this system participates in both physiology and pathology. Over the last decade, a renewed emphasis on understanding the role of angiotensin-(1–7) and angiotensin-converting enzyme 2 in the regulation of blood pressure and renal function has shed new light on the complexity of the mechanisms by which these components of the renin angiotensin system

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40

Wilkes, B. M., I. Pion, S. Sollott, S. Michaels, and G. Kiesel. "Intrarenal renin-angiotensin system modulates glomerular angiotensin receptors in the rat." American Journal of Physiology-Renal Physiology 254, no. 3 (1988): F345—F350. http://dx.doi.org/10.1152/ajprenal.1988.254.3.f345.

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The aim of this study was to test the hypothesis that the intrarenal renin-angiotensin system (RAS) modulates glomerular angiotensin II (ANG II) receptors. In one protocol ANG II receptors were measured 7 days after unilateral denervation of the left kidney in rats. There were 50% more receptors in the glomeruli from denervated compared with innervated kidneys (right, 1,037 +/- 108 vs. left, 1,556 +/- 143 fmol/mg; P less than 0.01), which was associated with a 63% reduction (P less than 0.01) in left renal vein renin. The differences in ANG II receptors between the left and right kidneys were

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Hsu, Feng-Yi, Fang-Ju Lin, Huang-Tz Ou, Shih-Hui Huang, and Chi-Chuan Wang. "Renoprotective Effect of Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers in Diabetic Patients with Proteinuria." Kidney and Blood Pressure Research 42, no. 2 (2017): 358–68. http://dx.doi.org/10.1159/000477946.

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42

Stornello, Michele, Enrico V. Valvo, and Luigi Scapellato. "Angiotensin converting enzyme inhibition in normotensive type II diabetics with persistent mild proteinuria." Journal of Hypertension 7 (1989): S314–315. http://dx.doi.org/10.1097/00004872-198900076-00153.

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Bernardi, Stella, Wendy C. Burns, Barbara Toffoli, et al. "Angiotensin-converting enzyme 2 regulates renal atrial natriuretic peptide through angiotensin-(1–7)." Clinical Science 123, no. 1 (2012): 29–37. http://dx.doi.org/10.1042/cs20110403.

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Deficiency of ACE2 (angiotensin-converting enzyme 2), which degrades Ang (angiotensin) II, promotes the development of glomerular lesions. However, the mechanisms explaining why the reduction in ACE2 is associated with the development of glomerular lesions have still to be fully clarified. We hypothesized that ACE2 may regulate the renoprotective actions of ANP (atrial natriuretic peptide). The aim of the present study was to investigate the effect of ACE2 deficiency on the renal production of ANP. We evaluated molecular and structural abnormalities, as well as the expression of ANP in the kid

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Lubrano, R., F. Soscia, M. Elli, et al. "Renal and Cardiovascular Effects of Angiotensin-Converting Enzyme Inhibitor Plus Angiotensin II Receptor Antagonist Therapy in Children With Proteinuria." PEDIATRICS 118, no. 3 (2006): e833-e838. http://dx.doi.org/10.1542/peds.2005-2053.

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Lores, Enrique, Jan Wysocki, and Daniel Batlle. "ACE2, the kidney and the emergence of COVID-19 two decades after ACE2 discovery." Clinical Science 134, no. 21 (2020): 2791–805. http://dx.doi.org/10.1042/cs20200484.

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Abstract Angiotensin-converting enzyme II (ACE2) is a homologue of angiotensin-converting enzyme discovered in 2000. From the initial discovery, it was recognized that the kidneys were organs very rich on ACE2. Subsequent studies demonstrated the precise localization of ACE2 within the kidney and the importance of this enzyme in the metabolism of Angiotensin II and the formation of Angiotensin 1–7. With the recognition early in 2020 of ACE2 being the main receptor of severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2), the interest in this protein has dramatically increased. In this r

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Broekroelofs, J., C. A. Stegeman, G. Navis, A. M. Tegzess, D. De Zeeuw, and P. E. De Jong. "Risk factors for long-term renal survival after renal transplantation: a role for angiotensin-converting enzyme (insertion/deletion) polymorphism?" Journal of the American Society of Nephrology 9, no. 11 (1998): 2075–81. http://dx.doi.org/10.1681/asn.v9112075.

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Chronic progressive renal function loss is a main cause of long-term graft loss after initially successful renal transplantation. Transplanted kidneys share some risk factors for renal function loss, such as hypertension or proteinuria, with diseased native kidneys. Recently, it has been shown that renal function loss is influenced by the angiotensin-converting enzyme (ACE) (insertion/deletion [I/D]) genotype in renal disease in diseased native kidneys. This study examines whether donor or recipient ACE (I/D) genotype is a risk factor for graft loss after renal transplantation. To avoid bias b

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Imig, John D., Gabriel L. Navar, Li-Xian Zou, et al. "Renal endosomes contain angiotensin peptides, converting enzyme, and AT1A receptors." American Journal of Physiology-Renal Physiology 277, no. 2 (1999): F303—F311. http://dx.doi.org/10.1152/ajprenal.1999.277.2.f303.

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Kidney cortex and proximal tubular angiotensin II (ANG II) levels are greater than can be explained on the basis of circulating ANG II, suggesting intrarenal compartmentalization of these peptides. One possible site of intracellular accumulation is the endosomes. In the present study, we tested for endosomal ANG I, ANG II, angiotensin type 1A receptor (AT1A), and angiotensin converting enzyme (ACE) activity and determined whether these levels are regulated by salt intake. Male Sprague-Dawley rats were fed chow containing either high or low dietary sodium for 10–14 days. Blood and kidneys were

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Sharma, Ravindra K., Jing Li, Suraj Krishnan, Elaine M. Richards, Mohan K. Raizada, and Rajesh Mohandas. "Angiotensin-converting enzyme 2 and COVID-19 in cardiorenal diseases." Clinical Science 135, no. 1 (2021): 1–17. http://dx.doi.org/10.1042/cs20200482.

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Abstract The rapid spread of the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has brought into focus the key role of angiotensin-converting enzyme 2 (ACE2), which serves as a cell surface receptor required for the virus to enter cells. SARS-CoV-2 can decrease cell surface ACE2 directly by internalization of ACE2 bound to the virus and indirectly by increased ADAM17 (a disintegrin and metalloproteinase 17)-mediated shedding of ACE2. ACE2 is widely expressed in the heart, lungs, vasculature, kidney and the gastrointestinal (GI) tract, where it counteracts the

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Wysocki, Jan, Arndt Schulze, and Daniel Batlle. "Novel Variants of Angiotensin Converting Enzyme-2 of Shorter Molecular Size to Target the Kidney Renin Angiotensin System." Biomolecules 9, no. 12 (2019): 886. http://dx.doi.org/10.3390/biom9120886.

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ACE2 is a monocarboxypeptidase which generates Angiotensin (1–7) from Angiotensin II (1–8). Attempts to target the kidney Renin Angiotensin System using native ACE2 to treat kidney disease are hampered by its large molecular size, 100 kDa, which precludes its glomerular filtration and subsequent tubular uptake. Here, we show that both urine and kidney lysates are capable of digesting native ACE2 into shorter proteins of ~60–75 kDa and then demonstrate that they are enzymatically very active. We then truncated the native ACE2 by design from the C-terminus to generate two short recombinant (r)AC

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Chaudhari, Vishal Madanlal, Dnyanoba Kishanrao Bhaskar, and Medha Ajit Oak. "Pleiotropic benefits and utility of angiotensin converting enzyme inhibitors in current practice." International Journal of Research in Medical Sciences 9, no. 8 (2021): 2544. http://dx.doi.org/10.18203/2320-6012.ijrms20213114.

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The renin-angiotensin-aldosterone system (RAAS) is responsible for maintaining hemodynamic stability and thereby impacts multiple organ systems, such as the central nervous system, heart, and kidneys. Angiotensin II (ang II) is the main effector of the RAAS. However, overactivity of the RAAS can give rise to cardiovascular disorders, stroke, and nephrosclerosis. Unfavorable effects on cardiovascular system are attributed to ang II. RAAS activation also results in release and increased activity of several hormonal and inflammatory mediators, trigger formation of a number of secondary messengers

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