ABSTRACT
Goldblatt first demonstrated the link between renal artery stenosis (RAS) and persistent hypertension in 1934.1 In this experimental work, he showed that hypertension could be induced by placement of a clip on the renal artery and he subsequently showed that the hypertension would subside after the clip was removed. While the presence of such curable hypertension has been proven in humans, the causeand-effect relationship between renal artery stenosis and hypertension is more complex than originally suspected. Renal artery stenosis does not always result in hypertension; in fact, it is common in the ageing normotensive population and it is far more common than renovascular hypertension (RVH), whose classical definition is based on cure or amelioration of the hypertension after revascularization. Indeed, based on autopsy and arteriographic studies, up to 30-50% of normotensive patients can have moderate or even severe RAS with the prevalence increasing with age.2-4 Moreover, RAS is often present as an incidental or secondary finding in hypertensive patients and does not represent the aetiology of the hypertension.4 Consequently, even though renovascular disease is the most common cause of secondary hypertension,5 it comes as no surprise that revascularization of an atherosclerotic renal artery stenosis (the commonest cause of renovascular disease) does not always result in amelioration or cure of the hypertension. Consequently, the clinical question still remains: Which hypertensive patients have a renal artery stenosis that, if corrected, will lead to cure or amelioration of the hypertension?
