Renal artery stenosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The pathophysiology of Renal artery stenosis (RAS) involves narrowing off the renal artery due to atherosclerosis or fibromuscular dysplasia as two major etiological factors responsible. This narrowing of the renal artery causes a reduction of the blood flow to the kidneys. This, in turn, activates the renin-angiotensin system causing, an increase in levels of angiotensin II. The angiotensin II further leads to an increase in aldosterone from the adrenal cortex that acts on the distal convoluted tubule, increasing reabsorption of sodium and excretion of potassium resulting in hypernatremia and hypokalemia. These changes in electrolyte concentration lead to rising in blood pressure. These features are reversible with the correction of stenosis. In some cases, the renal artery stenosis remains underdiagnosed and presents later as a complex disorder ranging from secondary hypertension to End-stage renal disease. | The pathophysiology of Renal artery stenosis (RAS) involves narrowing off the renal artery due to atherosclerosis or fibromuscular dysplasia as two major etiological factors responsible. This narrowing of the renal artery causes a reduction of the blood flow to the kidneys. This, in turn, activates the renin-angiotensin system causing, an increase in levels of angiotensin II. The angiotensin II further leads to an increase in aldosterone from the [[adrenal cortex]] that acts on the distal convoluted tubule, increasing reabsorption of sodium and excretion of potassium resulting in [[hypernatremia]] and [[hypokalemia]]. These changes in electrolyte concentration lead to rising in [[blood pressure]]. These features are reversible with the correction of [[stenosis]]. In some cases, the [[renal artery stenosis]] remains underdiagnosed and presents later as a complex disorder ranging from secondary hypertension to End-stage renal disease. | ||
[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]] | [[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]] | ||
Revision as of 19:39, 20 November 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]
Overview
The reduction in renal blood flow secondary to renal artery stenosis stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system. Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling.[1]
Pathophysiology
The pathophysiology of Renal artery stenosis (RAS) involves narrowing off the renal artery due to atherosclerosis or fibromuscular dysplasia as two major etiological factors responsible. This narrowing of the renal artery causes a reduction of the blood flow to the kidneys. This, in turn, activates the renin-angiotensin system causing, an increase in levels of angiotensin II. The angiotensin II further leads to an increase in aldosterone from the adrenal cortex that acts on the distal convoluted tubule, increasing reabsorption of sodium and excretion of potassium resulting in hypernatremia and hypokalemia. These changes in electrolyte concentration lead to rising in blood pressure. These features are reversible with the correction of stenosis. In some cases, the renal artery stenosis remains underdiagnosed and presents later as a complex disorder ranging from secondary hypertension to End-stage renal disease.
