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renin angiotensin aldosterone and progression renal function

Elizabeth do Espirito Santo Cestário, Letícia Aparecida Barufi Fernandes, Luiz Tadeu Giollo-Júnior, Jéssica Rodrigues Roma Uyemura, Camila Suemi Sato Matarucco, Manoel Idelfonso Paz Landim, Luciana Neves Cosenso-Martin, Lúcia Helena Bonalume Tácito, Heitor Moreno, José Fernando Vilela-Martin, Juan Carlos Yugar-Toledo
BACKGROUND: Resistant hypertension is characterized when the blood pressure (BP) remains above the recommended goal after taking three antihypertensive drugs with synergistic actions at their maximum recommended tolerated doses, preferably including a diuretic. Identifying the contribution of intravascular volume and serum renin in maintaining BP levels could help tailor more effective hypertension treatment, whether acting on the control of intravascular volume or sodium balance, or acting on the effects of the renin-angiotensin-aldosterone system (RAAS) on the kidney...
February 12, 2018: Trials
Yan Liu, David Goldfarb, Tarek M El-Achkar, John C Lieske, Xue-Ru Wu
Expression of Tamm-Horsfall protein (THP or uromodulin) is highly restricted to the kidneys' thick ascending limb (TAL) of loop of Henle. Despite the unique location and recent association of THP gene mutations with hereditary uromodulin-associated kidney disease and THP single nucleotide polymorphisms with chronic kidney disease and hypertension, the physiological function(s) of THP and its pathological involvement remain incompletely understood. By studying age-dependent changes of THP knockout (KO) mice, we show here that young KO mice had significant salt and water wasting but were partially responsive to furosemide, due to decreased luminal translocation of Na-K-Cl cotransporter 2 (NKCC2) in the TAL...
January 10, 2018: American Journal of Physiology. Renal Physiology
Julie A Lovshin, Geneviève Boulet, Yuliya Lytvyn, Leif E Lovblom, Petter Bjornstad, Mohammed A Farooqi, Vesta Lai, Leslie Cham, Josephine Tse, Andrej Orszag, Daniel Scarr, Alanna Weisman, Hillary A Keenan, Michael H Brent, Narinder Paul, Vera Bril, Bruce A Perkins, David Zi Cherney
BACKGROUND: In type 1 diabetes (T1D), adjuvant treatment with inhibitors of the renin-angiotensin-aldosterone system (RAAS), which dilate the efferent arteriole, is associated with prevention of progressive albuminuria and renal dysfunction. Uncertainty still exists as to why some individuals with long-standing T1D develop diabetic kidney disease (DKD) while others do not (DKD resistors). We hypothesized that those with DKD would be distinguished from DKD resistors by the presence of RAAS activation...
January 11, 2018: JCI Insight
Milton Packer
Diabetes is characterized by increased activity of the sodium-hydrogen exchanger (NHE) in the glomerulus and renal tubules, which contributes importantly to the development of nephropathy. Despite the established role played by the exchanger in experimental studies, it has not been specifically targeted by those seeking to develop novel pharmacological treatments for diabetes. This review demonstrates that many existing drugs that are commonly prescribed to patients with diabetes act on the NHE1 and NHE3 isoforms in the kidney...
April 2018: Diabetes, Obesity & Metabolism
Hajime Kataoka
AIMS: Chloride (Cl) is an established key electrolyte for the activation of the renin-angiotensin-aldosterone system. Recent studies have shown the serum Cl as a key electrolyte for the regulation of body fluid distribution in heart failure (HF) patients. The clinical differences of worsening HF status according to the changes in serum Cl concentration are unclear. METHODS AND RESULTS: Data from 47 chronic HF patients were analysed. Upon worsening HF, each patient exhibited at least two HF-related signs...
November 2017: ESC Heart Failure
Ionut Nistor, Johan De Sutter, Christiane Drechsler, David Goldsmith, Maria Jose Soler, Charles Tomson, Andrzej Wiecek, Mihaela-Dora Donciu, Davide Bolignano, Wim Van Biesen, Adrian Covic
The presumed superiority of renin-angiotensin-aldosterone system (RAAS)-blocking agents over other antihypertensive agents in patients with diabetes to delay development of end-stage kidney disease (ESKD) has recently been challenged. In addition, there is ongoing uncertainty whether RAAS-blocking agents reduce mortality and/or delay ESKD in patients with diabetes and chronic kidney disease (CKD) stages 3-5. In this subgroup, there might be an expedited need for renal replacement therapy (RRT) when RAAS-blocking agents are used...
January 1, 2018: Nephrology, Dialysis, Transplantation
Sheila Bermejo, Carles Oriol García, Eva Rodríguez, Clara Barrios, Sol Otero, Sergi Mojal, Julio Pascual, María José Soler
BACKGROUND AND OBJECTIVES: Diabetic kidney disease is the leading cause of end-stage chronic kidney disease. The renin-angiotensin-aldosterone system (RAAS) blockade has been shown to slow the progression of diabetic kidney disease. Our objectives were: to study the percentage of patients with diabetic kidney disease treated with RAAS blockade, to determine its renal function, safety profile and assess whether its administration is associated with increased progression of CKD after 3 years of follow-up...
October 25, 2017: Nefrología: Publicación Oficial de la Sociedad Española Nefrologia
Tarak Srivastava, Hongying Dai, Daniel P Heruth, Uri S Alon, Robert E Garola, Jianping Zhou, R Scott Duncan, Ashraf El-Meanawy, Ellen T McCarthy, Ram Sharma, Mark L Johnson, Virginia J Savin, Mukut Sharma
Recently we and others have found that hyperfiltration-associated increase in biomechanical forces, namely tensile stress and fluid flow shear stress (FFSS) can directly and distinctly alter podocyte structure and function. The ultrafiltrate flow over the major processes and cell body generates FFSS to podocyte. Our previous work suggests that COX2-PGE2-EP2 axis plays an important role in mechanoperception of FFSS in podocyte (Srivastava et al. Am J Physiol Renal Physiol 307: F1323-F1333, 2014). To address mechanotransduction of the perceived mechanical stimulus through EP2 receptor, cultured podocytes were exposed to FFSS (2 dynes/cm2) for 2hrs...
September 6, 2017: American Journal of Physiology. Renal Physiology
Mariadelina Simeoni, Annarita Armeni, Chiara Summaria, Annamaria Cerantonio, Giorgio Fuiano
RATIONAL: The inhibition of renin-angiotensin-aldosterone system (RAAS) is a major strategy for slowing the progression of chronic kidney disease (CKD). The utility of anti-RAAS agents in patients with congenital or acquired solitary kidney is still controversial. OBJECTIVE: A systematic literature review was conducted. MAIN FINDINGS: The conclusions of the few available studies on the topic are homogeneously in agreement with a long-term reno-protective activity of anti-RAAS drugs in patients with solitary kidney, especially if patients are hypertensive or proteinuric...
November 2017: Renal Failure
Fan Zhang, Hong Liu, Di Liu, Yexin Liu, Huiqiong Li, Xia Tan, Fuyou Liu, Youming Peng, Hongqing Zhang
Proteinuria and decline of renal function are associated with progression of kidney disease. The Renin Angiotensin Aldosterone System (RAAS) plays an important role in blood pressure regulation, fluid volume, and sodium balance. Overactivity of RAAS contributes to the pathogenesis of a variety of clinical conditions including progress of chronic kidney disease (CKD). This review summarizes the use of RAAS inhibitors as dual therapy or monotherapy in different stages of kidney disease. Experimental and clinical studies have demonstrated RAAS inhibitors prevent proteinuria, kidney fibrosis and slow decline of renal function and thus play a protective role in both early and end stages of kidney disease...
August 8, 2017: Current Hypertension Reports
Tajda Keber, Martin Tretjak, Andreja Cokan Vujkovac, Marija Mravljak, Katja Ravber, Bojan Vujkovac
BACKGROUND Fabry disease is a rare and progressive X-linked inherited disorder of glycosphingolipid metabolism that is due to deficient or absent lysosomal a-galactosidase A activity. Among its other associated signs and symptoms, patients present with renal failure and proteinuria, which are markers of disease progression. Renin-angiotensin-aldosterone system (RAAS) blockers can slow the progression of chronic renal failure and proteinuria. In fact, some studies have shown the beneficial effects of paricalcitol on proteinuria...
June 9, 2017: American Journal of Case Reports
Rafaelle Lira, Mariana Oliveira, Marcela Martins, Caroline Silva, Simone Carvalho, Ana Carolina Stumbo, Erika Cortez, Karine Verdoorn, Marcelo Einicker-Lamas, Alessandra Thole, Laís de Carvalho
Renovascular hypertension (RVH) is a progressive disease, leading to chronic kidney disease when untreated and no specific treatment is available. Therefore, development of new therapeutic modalities is imperative. RVH is triggered by renal artery stenosis and subsequent renin-angiotensin-aldosterone system activation; it can be experimentally induced by the 2 Kidneys-1 Clip (2K1C) model. This study investigates the therapeutic potential of renal subcapsular mesenchymal stem cell (MSC) infusion in 2K1C rats...
April 3, 2017: Cell and Tissue Research
Tarak Srivastava, Ganesh Thiagarajan, Uri S Alon, Ram Sharma, Ashraf El-Meanawy, Ellen T McCarthy, Virginia J Savin, Mukut Sharma
Congenital anomalies of the kidney and urinary tract (CAKUT) including solitary kidney constitute the main cause of progressive chronic kidney disease (CKD) in children. Children born with CAKUT develop signs of CKD only during adolescence and do not respond to renin-angiotensin-aldosterone system blockers. Early cellular changes underlying CKD progression to end-stage renal disease by early adulthood are not well understood. The mechanism of maladaptive hyperfiltration that occurs from loss of functional nephrons, including solitary kidney, is not clear...
May 1, 2017: Nephrology, Dialysis, Transplantation
Yuxuan Wang, Chengcheng Wang, Xiuli Zhang, Harvest F Gu, Liang Wu
Diabetic nephropathy is characterized by hypertension, progressive albuminuria, glomerulosclerosis and declines in glomerular filtration rate leading to end stage renal disease. Although the pathogenesis of diabetic nephropathy is not fully understood, current treatment of the patients with diabetic nephropathy is mainly based upon the control of hyperglycaemia and management of blood pressures. Several drugs, which are originally developed for hypertension therapy, have been adopted for stabilization of renal function in diabetic nephropathy...
February 14, 2017: Current Diabetes Reviews
Norishi Ueda
Sphingolipids (SLs) regulate apoptosis, proliferation, and stress response. SLs, including ceramide, glycosphingolipids (glucosylceramide, lactosylceramide, and gangliosides) and sphingosine-1-phosphate (S1P), play a role in the pathogenesis and progression of genetic (lysosomal storage disease, congenital nephrotic syndrome and polycystic kidney disease) and non-genetic forms of chronic kidney diseases (CKDs). SLs metabolism defects promote complications (cardiovascular events, etc.) via oxidant stress in CKDs...
2017: Current Medicinal Chemistry
Xin Zhang, Lilach O Lerman
The metabolic syndrome (MetS) is a cluster of cardiovascular risk factors including insulin resistance (IR), dyslipidemia, and hypertension, which may also foster development of chronic kidney disease. The mechanisms of MetS-induced kidney disease are not fully understood. The purpose of this review is to summarize recent discoveries regarding the impact of MetS on the kidney, particularly on the renal microvasculature and cellular mitochondria. Fundamental manifestations of MetS include IR and adipose tissue expansion, the latter promoting chronic inflammation and oxidative stress that exacerbate IR...
May 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
Jianyong Zhong, Hai-Chun Yang, Agnes B Fogo
Chronic kidney disease (CKD) will progress to end stage without treatment, but the decline of renal function may not be linear. Compared with glomerular filtration rate and proteinuria, new surrogate markers, such as kidney injury molecule-1, neutrophil gelatinase-associated protein, apolipoprotein A-IV, and soluble urokinase receptor, may allow potential intervention and treatment in the earlier stages of CKD, which could be useful for clinical trials. New omic-based technologies reveal potential new genomic and epigenomic mechanisms that appear different from those causing the initial disease...
March 1, 2017: American Journal of Physiology. Renal Physiology
Yasuhiko Tomino
Chronic kidney disease (CKD) is a worldwide public health problem that affects millions of people from all racial and ethnic groups. Although CKD is not one specific disease, it is a comprehensive syndrome that includes IgA nephropathy. As reported by the Japanese Society of Nephrology, 13.0 million people have CKD. In Japan, major causes of end-stage kidney disease are type 2 diabetic nephropathy, chronic glomerulonephritis, especially IgA nephropathy, hypertensive nephrosclerosis, and polycystic kidney disease...
December 2016: Kidney Research and Clinical Practice
Thomas Vanhove, Roel Goldschmeding, Dirk Kuypers
All causes of renal allograft injury, when severe and/or sustained, can result in chronic histological damage of which interstitial fibrosis and tubular atrophy are dominant features. Unless a specific disease process can be identified, what drives interstitial fibrosis and tubular atrophy progression in individual patients is often unclear. In general, clinicopathological factors known to predict and drive allograft fibrosis include graft quality, inflammation (whether "nonspecific" or related to a specific diagnosis), infections, such as polyomavirus-associated nephropathy, calcineurin inhibitors (CNI), and genetic factors...
April 2017: Transplantation
Nao Uchida, Naonori Kumagai, Kandai Nozu, Xue Jun Fu, Kazumoto Iijima, Yoshiaki Kondo, Shigeo Kure
Alport syndrome is a progressive renal disease caused by mutations in COL4A3, COL4A4, and COL4A5 genes that encode collagen type IV alpha 3, alpha 4, and alpha 5 chains, respectively. Because of abnormal collagen chain, glomerular basement membrane becomes fragile and most of the patients progress to end-stage renal disease in early adulthood. COL4A5 mutation causes X-linked form of Alport syndrome, and two mutations in either COL4A3 or COL4A4 causes an autosomal recessive Alport syndrome. Recently, renin-angiotensin-aldosterone system (RAAS) blockade has been shown to attenuate effectively disease progression in Alport syndrome...
November 2016: Tohoku Journal of Experimental Medicine
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