scholarly journals Mesenchymal stem cells and chronic renal artery stenosis

2016 ◽  
Vol 310 (1) ◽  
pp. F6-F9 ◽  
Author(s):  
Elizabeth B. Oliveira-Sales ◽  
Mirian A. Boim
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Artery Stenosis ◽  
Functional Failure ◽  
Ischemic Nephropathy ◽  
Renal Structure

Renal artery stenosis is the main cause of renovascular hypertension and results in ischemic nephropathy characterized by inflammation, oxidative stress, microvascular loss, and fibrosis with consequent functional failure. Considering the limited number of strategies that effectively control renovascular hypertension and restore renal function, we propose that cell therapy may be a promising option based on the regenerative and immunosuppressive properties of stem cells. This review addresses the effects of mesenchymal stem cells (MSC) in an experimental animal model of renovascular hypertension known as 2 kidney-1 clip (2K-1C). Significant benefits of MSC treatment have been observed on blood pressure and renal structure of the stenotic kidney. The mechanisms involved are discussed.

scholarly journals Comparison of the Effects of Mesenchymal Stem Cells with Their Extracellular Vesicles on the Treatment of Kidney Damage Induced by Chronic Renal Artery Stenosis

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Crysthiane Saveriano Rubiao Andre Ishiy ◽  
Milene Subtil Ormanji ◽  
Edgar Maquigussa ◽  
Rosemara Silva Ribeiro ◽  
Antonio da Silva Novaes ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Renal Function ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Chronic Hypoxia ◽  
Progressive Increase ◽  
Artery Stenosis ◽  
Irreversible Damage ◽  
Whole Cells

Background. Chronic renal artery stenosis is considered one of the most common causes of renovascular hypertension (RH). Chronic hypoxia can lead to irreversible damage to renal tissue and to a progressive deterioration of renal function. We have previously shown that bone marrow-derived mesenchymal stem cells (BMSCs) improved renal parenchyma and function in a model of RH (2 kidneys, 1 clip model (2K-1C) in rats. Microvesicles (MVs) and exosomes (EXs) released by MSCs have been shown to induce effects similar to those induced by whole cells but with fewer side effects. In this study, we compared the effects of adipose-derived MSCs (ASCs) with those of the MVs and EXs released by ASCs on tissue inflammation and renal function in 2 K-1C rats. Results. Flow cytometry analysis showed that even after 15 days, ASCs were still detected in both kidneys. The expression of a stem cell homing marker (SDF1-α) was increased in ASC-treated animals in both the stenotic and contralateral kidneys. Interestingly, SDF1-α expression was also increased in MV- and EX-treated animals. A hypoxia marker (HIF1-α) was upregulated in the stenotic kidney, and treatments with ASCs, MVs, and EXs were effective in reducing the expression of this marker. Stenotic animals showed a progressive increase in systolic blood pressure (SBP), while animals treated with ASCs, MVs, and EXs showed a stabilization of SBP, and this stabilization was similar among the different treatments. Stenotic animals developed significant proteinuria, which was reduced by ASCs and MVs but not by EXs. The increased expression of Col I and TGFβ in both kidneys was reduced by all the treatments, and these treatments also effectively increased the expression of the anti-inflammatory cytokine IL-10 in both kidneys; however, only ASCs were able to reduce the overexpression of the proinflammatory cytokine IL-1β in both kidneys of 2K-1C animals. Conclusion. The results of this study demonstrated that the EVs released by ASCs produced beneficial results but with lower efficacy than whole cells. ASCs produced stronger effects in this model of renal chronic hypoxia, and the use of EVs instead of whole cells should be evaluated depending on the parameter to be corrected.

scholarly journals Mesenchymal Stem Cells and Endothelial Progenitor Cells Decrease Renal Injury in Experimental Swine Renal Artery Stenosis Through Different Mechanisms

Stem Cells ◽  
2012 ◽  
Vol 31 (1) ◽  
pp. 117-125 ◽  
Author(s):  
Xiang-Yang Zhu ◽  
Victor Urbieta-Caceres ◽  
James D. Krier ◽  
Stephen C. Textor ◽  
Amir Lerman ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Renal Artery ◽  
Progenitor Cells ◽  
Renal Artery Stenosis ◽  
Endothelial Progenitor Cells ◽  
Renal Injury ◽  
Artery Stenosis ◽  
Endothelial Progenitor

Renovascular Hypertension and Stenosis

2018 ◽  
Author(s):  
J. Gregory Modrall
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Radiographic Finding ◽  
Artery Stenosis ◽  
Clinical Predictors ◽  
Ischemic Nephropathy ◽  
Renal Artery Stenting

Renal artery stenosis (RAS) may present clinically as an incidental radiographic finding in an asymptomatic patient, or it may be the etiology of renovascular hypertension or ischemic nephropathy. Incidental RAS should be treated medically. The available clinical trial data suggest that medical management is the primary treatment for presumed renovascular hypertension. Renal artery stenting should be reserved for patients who fail medical therapy. When renal artery stenting is contemplated for presumed renovascular hypertension or ischemic nephropathy, clinical studies suggest that there are clinical predictors of outcomes that may be useful in identifying patients with a higher probability of a favorable clinical response to stenting. Clinical predictors of a favorable blood pressure response to renal artery stenting include (1) a requirement of four or more antihypertensive medications, (2) preoperative diastolic blood pressure greater than 90 mm Hg, and (3) preoperative clonidine use. The only clinical predictor of improved renal function with stenting is the rate of decline of estimated glomerular filtration rate (eGFR) in the weeks prior to stenting. Patients with a more rapid decline in eGFR have a higher probability of improved renal function after stenting compared with those with relatively stable eGFR prior to stenting. Finally, surgical renal artery revascularization remains a viable option but is usually reserved for younger, fit patients with unfavorable anatomy for stenting. Pediatric renovascular disease responds poorly to endovascular therapy and requires a surgical plan to address both renal artery stenoses and concomitant abdominal aortic coarctation if present. Renal artery stenosis in pediatric patients is best treated with reimplantation of the renal artery or interposition grafting using the autogenous internal iliac artery as a conduit. This review contains 39 references, 15 figures, and 3 tables. Key Words: chronic kidney disease, hypertension, renal artery stenosis, renovascular, stenting

scholarly journals An Outline of Renal Artery Stenosis Pathophysiology—A Narrative Review

Life ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 208
Author(s):  
Lukasz Dobrek
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Kidney Tissue ◽  
Clinical Manifestations ◽  
Kidney Injury ◽  
Artery Stenosis ◽  
Tissue Remodelling ◽  
Ischemic Nephropathy ◽  
Sympathetic Nervous Systems

Renal artery stenosis (RAS) is conditioned mainly by two disturbances: fibromuscular dysplasia or atherosclerosis of the renal artery. RAS is an example of renovascular disease, with complex pathophysiology and consequences. There are multiple pathophysiological mechanisms triggered in response to significant renal artery stenosis, including disturbances within endothelin, kinin–kallikrein and sympathetic nervous systems, with angiotensin II and the renin–angiotensin-aldosterone system (RAAS) playing a central and key role in the pathogenesis of RAS. The increased oxidative stress and the release of pro-inflammatory mediators contributing to pathological tissue remodelling and renal fibrosis are also important pathogenetic elements of RAS. This review briefly summarises these pathophysiological issues, focusing on renovascular hypertension and ischemic nephropathy as major clinical manifestations of RAS. The activation of RAAS and its haemodynamic consequences is the primary and key element in the pathophysiological cascade triggered in response to renal artery stenosis. However, the pathomechanism of RAS is more complex and also includes other disturbances that ultimately contribute to the development of the diseases mentioned above. To sum up, RAS is characterised by different clinical pictures, including asymptomatic disorders diagnosed in kidney imaging, renovascular hypertension, usually characterised by severe course, and chronic ischemic nephropathy, described by pathological remodelling of kidney tissue, ultimately leading to kidney injury and chronic kidney disease.

Sign in / Sign up

Export Citation Format

Share Document