Renal artery stenosis (RAS) is the narrowing of one or both of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia. This narrowing of the renal artery can impede blood flow to the target kidney, resulting in renovascular hypertension – a secondary type of high blood pressure. Possible complications of renal artery stenosis are chronic kidney disease and coronary artery disease. Most cases of renal artery stenosis are asymptomatic, and the main problem is high blood pressure that cannot be controlled with medication. Decreased kidney function may develop if both kidneys do not receive adequate blood flow, furthermore some people with renal artery stenosis present with episodes of flash pulmonary edema. Renal artery stenosis is most often caused by atherosclerosis which causes the renal arteries to harden and narrow due to the build-up of plaque. This is known as atherosclerotic renovascular disease, which accounts for about 90% of cases. This narrowing of renal arteries due to plaque build-up leads to higher blood pressure within the artery and decreased blood flow to the kidney. This decreased blood flow leads to decreased blood pressure in the kidney, which leads to the activation of the Renin-Angiotensin-Aldosterone (RAA) system. Juxtaglomerular cells secrete renin, which converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II then acts on the adrenal cortex to increase secretion of the hormone aldosterone. Aldosterone causes sodium and water retention, leading to an increase in blood volume and blood pressure. Therefore, people with RAS have chronic high blood pressure because their RAA system is hyperactivated. The pathophysiology of renal artery stenosis leads to changes in the structure of the kidney that are most noticeable in the tubular tissue. If the stenosis is longstanding and severe, the glomerular filtration rate in the affected kidneys never recovers and (prerenal) kidney failure is the result.
Nikolaos Stergiopoulos, Vasiliki Bikia, Patrick Segers
Lydia Aslanidou, Fotios Savvopoulos