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Fibromuscular dysplasia (FMD) is believed to cause hypertension via similar mechanisms as atherosclerotic renal artery stenosis (ARAS), i.e. due to a decrease in renal blood flow which subsequently leads to increased renin secretion. However, given the differences in the blood pressure response to revascularization between patients with ARAS and FMD we questioned whether this is true.

Design and method:

In 58 patients with multifocal renal artery FMD (33 unilateral) and 111 patients with high grade ARAS (64 unilateral) we selectively measured mean renal blood flow (MRBF) in both kidneys using the 133Xenon-washout-method (off medication). Blood samples were taken from the aorta and both renal veins to determine renal vein renin ratio and renin secretion rate (RSR: venous-arterial difference*renal plasma flow).


MRBF was higher in kidneys with FMD as compared to ARAS (p < 0.001 vs. FMD for both kidneys in unilateral and bilateral FMD/ARAS) (Figure 1). Lateralization of renin secretion was found in unilateral ARAS: 20 patients had a renal vein renin ratio above cut-off (<1.5 according to previous literature) and RSR was significantly higher in the affected kidney as compared to the unaffected kidney [median 0.29 (interquartile range 0.09–1.07) vs. 0.17 (0.00–0.42) mU/100 g kidney/min; p < 0.001]. In unilateral FMD, however, no lateralization was found: renal vein renin ratio was below cut-off in all patients and no differences in RSR were found between both kidneys. Systemic renin levels and RSR were significantly higher in ARAS as compared to FMD (p < 0.001) after adjustment for pre-existing differences in age, gender, body mass index, and 24 h urinary sodium excretion using an ANCOVA model. The association between renin levels and blood pressure was inverse in FMD as compared to ARAS (Figure 1, bottom panel).


As compared to ARAS, renal blood flow is more preserved, local renin secretion is not increased, and the association between renin levels and blood pressure is inverse in FMD. These findings all contradict with the generally accepted view that fibromuscular dysplasia induces hypertension via decreased renal blood flow and increased renin secretion and suggest a different pathophysiological mechanism.

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