Renal Unit, South Cleveland Hospital, Middlesbrough, UK
Sir,
Although Farmer et al. [1] point out that the relationship between renal function and atheromatous renal artery stenosis (ARAS) has hitherto been unclear, their study results are very clear. They have shown that whatever does cause progressive renal failure in hypertensive patients with vascular disease with renal artery stenosis, it is usually not the stenosed renal artery. These results fit nicely with clinical experienceit is not uncommon to do renal angiography in patients with vascular disease with significant renal impairment (i.e. renal function well below half normal) and find ARAS on one side but a good artery on the other. Something else must be causing renal damage in these patients and it is presumably a combination of hypertension and athero-embolic disease. The importance of these results is greatthey invalidate the conclusions of previous studies and the way many of us currently think about renal failure and ARAS, help us to define more accurately the situations in which renal revascularization might be worthwhile, and highlight the difficulties in assessing clinical outcomes.
It is no longer possible to maintain that ARAS is a potentially reversible cause of end-stage renal failure (ESRF) in up to a quarter of patients over 60 going onto dialysis [2,3]. In those studies the co-existence of ARAS and ESRF was assumed to be cause and effect. Only in the much smaller number of patients with bilateral occlusions is ARAS now a believable culprit.
Nephrologists have probably been looking for the wrong type of patient. It is likely that angiography is considered in patients with vascular disease with steadily progressing renal failurebut it now seems that steadily progressing renal failure will be due to hypertensive/athero-embolic disease. Although ARAS is often found in such a setting, intervention is doomed to failure because it is treating the wrong disease (and in theory at least could allow worsening of hypertensive damage). The natural history of renal impairment due to ARAS is probably two sudden jumps at the times of renal artery occlusion. The first jump is often not clinically evident with serum creatinine remaining normal or only slightly raised. The ideal patient for renal revascularization will have a useless kidney beyond an occluded artery and a well-preserved kidney beyond a tight stenosis. Unless such a patient is coincidentally prescribed an ACE inhibitor or angiotensin II receptor antagonist, they will have a near-normal serum creatinine and there may be no clinical clues that they are at high risk of ESRF due to bilateral renal artery occlusion.
When the rationale for intervention is prevention of occlusion, monitoring of clinical outcome becomes difficultone cannot expect any improvement in renal function. A clinically successful intervention is one which delays renal artery occlusionsomething which simply cannot be assessed in individuals.
There is no doubt that renal revascularization by whatever means has a rolein patients with hypertension and fibro-muscular dysplasia, bilateral tight ARAS and pulmonary oedema, tight ARAS to a solitary functioning kidney to either prevent occlusion or allow ACE inhibitor use, and recently occluded arteries to viable kidneys. Probably all these categories combined are outnumbered by patients with hypertension, generalised vascular disease, chronic renal failure and coincidental ARAS. Farmer et al. have given us the explanation why intervention is doomed to failure in most of these patients, in whom we need to concentrate on blood pressure control, smoking cessation and lipid lowering.
References