Department of Nephrology and Hypertension University Medical Center Utrecht Utrecht The Netherlands Email: j.j.beutler{at}azu.nl
Sir,
We thank Main and Wroe for their interest in our paper [1]. They argue that the high prevalence of atherosclerotic renal artery stenosis (ARAS) in patients starting dialysis is no proof of its participation in the cause of terminal renal failure. Of course we agree with them: our study was purely observational. However, you could see this differently. Reversing the reasoning, the (hypothetical) finding of a low prevalence of ARAS in these patients would have ruled out its importance as a cause of terminal renal failure. We showed, for the first time with adequate techniques, that this was not the case. The next step, i.e. to connect this ARAS with the origin of terminal renal failure, is based on indirect arguments, but the step is not that big. First, the percentage of ARAS in patients with a known cause for renal failure was 22% (7/31), whereas it was 72% (13/18) in those in whom the cause was hypertension, renovascular disease or unknown. If ARAS is just some innocent bypassing event, these percentages should have been similar. Secondly, we found previously (as did others) that revascularization procedures such as stenting can retard progression of renal dysfunction [2,3]. This had also occurred in some patients in our report. Of course we agree that unilateral ARAS is by itself insufficient as a cause of terminal renal failure. This does not mean, however, that it cannot contribute to renal failure if there is also some other parenchymal renal problem. Also, we know very well that atherosclerotic disease is not limited to the renal arteries, but is a complex problem that will also involve the renal parenchyma and intrarenal vessels. Perhaps the term atherosclerotic renovascular renal failure is better to cover the problem than renal artery stenosis.
Indeed, we need more evidence about the contribution (and how serious this is) of atherosclerotic renovascular disease to the development of terminal renal failure and, specifically, if it is helpful to attack the extrarenal stenosis (apart from antihypertensive and metabolic treatments). Prospective, controlled trials such as the ASTRAL [4] and STAR [5] studies will hopefully give answers. Meanwhile, there is little reason for negligence. The problem is too serious for that.
Conflict of interest statement. None declared.
References