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.

scholarly journals The transcription factor Sox6 controls renin expression during renal artery stenosis

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0002792020
Author(s):  
Mohammad Saleem ◽  
Luz Saavedra-Sánchez ◽  
Pierina Barturen-Larrea ◽  
Jose A. Gomez
Keyword(s):  
Blood Pressure ◽  
Transcription Factor ◽  
Mouse Model ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Transcriptional Regulatory Network ◽  
Colorimetric Assay ◽  
Kidney Injury ◽  
Artery Stenosis

Background: Renal artery stenosis (RAStenosis) or renal artery occlusion is an intractable problem affecting about 6% of people over 65 and up to 40% of the people with coronary or peripheral vascular disease in the Unites States. In RAStenosis, the renal renin angiotensin aldosterone system (RAAS) plays a key role, with renin recognized as the disease driver. Renin is mainly produced in the kidney and in this study, we will determine a new function for the transcription factor Sox6 in the control of renal renin during RAStenosis. Method: We hypothesize that knocking out Sox6 in Ren1d positive cells will protect mice against renovascular hypertension, and kidney injury. To test our hypothesis, we used a new transgenic mouse model the Ren1dcre/Sox6fl/fl (Sox6 KO). In this mouse, Sox6 is knockout in renin expressing cells. We used a modified two kidney one clip (2K1C) Goldblatt mouse model to induce RAStenosis and renovascular hypertension. Blood pressure was measured with tail-cuff method. Renin, prorenin, Sox6, and N-GAL expressions levels were measured with Western blot, in situ hybridization, and immunohistochemistry. Creatinine levels were measured with colorimetric assay. Results: Systolic blood pressure was significantly lower in Sox6 KO two weeks after RAStenosis compared to Sox6 WT (Ren1dcre/Sox6wt/wt). When stenosed kidneys were compared, renin, prorenin, and N-GAL expressions levels in the kidney were lower in Sox6 KO compared to Sox6 WT mice. Furthermore, creatinine clearance was preserved in Sox6 KO compared to Sox6 WT mice. Conclusions: Our data indicate that Sox6 controls renal renin and prorenin expression and as such has a new function in renovascular hypertension induced by RAStenosis. These results point to a novel transcriptional regulatory network controlled by Sox6.

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 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.

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