What common clinical finding in fibromuscular dysplasia patients contributes to hypertension?

In fibromuscular dysplasia, a condition that often affects the renal arteries, one of the hallmark findings is the increased secretion of renin. This occurs because the altered renal blood flow, typically due to stenosis or narrowing of the renal arteries caused by fibromuscular dysplasia, is perceived by the kidneys as low blood volume or low perfusion pressure. In response, the juxtaglomerular cells in the kidneys secrete renin, leading to activation of the renin-angiotensin-aldosterone system (RAAS).

The increased renin secretion results in higher levels of angiotensin II, a potent vasoconstrictor, which leads to increased blood pressure. Additionally, angiotensin II stimulates the secretion of aldosterone, which promotes sodium and water retention, further elevating blood volume and, consequently, blood pressure. Therefore, in patients with fibromuscular dysplasia, the excess renin contributes significantly to their hypertension, making this finding a critical aspect of the pathophysiology of the condition.