1D.11

Abstract

Objective: Although fibromuscular dysplasia (FMD) is the second commonest cause of renovascular hypertension, knowledge on renal microvasculature and renin-angiotensin-system-activity in kidneys with FMD are scarce. Given the fairly good results of revascularization, we hypothesized that renal microvasculature is intact in kidneys with FMD. Design and method: In 58 patients with multifocal renal artery FMD (off medication) we selectively measured mean renal blood flow (MRBF) in both kidneys using the 133Xenon-washout-method. Blood samples were taken from the aorta and both renal veins to determine renin secretion rate (RSR) and creatinine-extraction (a proxy for glomerular filtration) for each kidney (both calculated as venous-arterial difference*renal plasma flow). Hypertensive patients without renovascular abnormalities (essential hypertension, EH), matched for age, gender, and dietary sodium intake (using 24 h urinary sodium excretion as a proxy) served as controls in a 1:2 ratio. Results: MRBF was comparable between FMD and EH (Figure). In EH but not in FMD, MRBF was significantly lower in the left kidney as compared to the right (*p < 0.001). Although a wide variation was observed, we found that systemic renin levels were somewhat higher in FMD as compared to EH [median 19.6 (interquartile range 12.0–35.2) vs. 12.1 (8.4–19.9); p < 0.001)], but without differences in RSR per kidney (Figure). Creatinine-extraction was also comparable between FMD and EH. In unilateral FMD, no differences were found between the affected and non-affected kidney with regard to MRBF, RSR, or creatinine-extraction (left column). MRBF was associated with 24 h urinary sodium excretion in FMD (Beta 0.357;p = 0.015), but not in EH.Conclusions: MRBF and creatinine-extraction in kidneys with FMD is comparable to EH and to the unaffected kidney in patients with unilateral FMD, indicating that renal microvascular function is preserved in kidneys with FMD. The association between MRBF and sodium intake supports this hypothesis. Our findings that MRBF is preserved and RSR is not increased in kidneys with FMD contradict with the commonly held hypothesis on renovascular hypertension that states that hypertension is induced by increased renin secretion in response to decreased blood flow. Therefore, other pathophysiological mechanisms probably (also) play a role.