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MINERVA UROLOGICA E NEFROLOGICA

A Journal on Nephrology and Urology


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Minerva Urologica e Nefrologica 2002 March;54(1):29-36

language: English

Diagnosis and treatment of atherosclerotic renal artery stenosis (ARAS)

Geddes C. C., Jardine A. G. *

From the Renal Unit and *University Department of Medicine and Therapeutics Western Infirmary, Glasgow, United Kingdom


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Atherosclerotic renal artery stenosis (ARAS) is an increasingly common cause of secondary hypertension and progressive chronic renal failure. Recent studies provide valuable information about the pathophysiology, natural history, diagnosis and treatment of ARAS. The pathophysiology of ARAS is more complex than experimental models using clipped renal arteries because the renal artery narrowing is gradual, may be bilateral, may affect smaller intra-renal arteries and other co-existing nephropathies are often present. Patients with ARAS have high mortality due to associated co-morbidity and progression of renal failure may be less common than previously thought. Magnetic resonance arteriography offers great promise for diagnosing of ARAS as it is non-invasive and can provide data on kidney function. In patients with ARAS, the co-existence of atherosclerotic disease in other vascular beds means that aspirin, blood pressure reduction, advice to stop smoking and lipid lowering therapy are likely to be associated with reduced vascular events. The effect of these approaches on the progression of ARAS is unclear but likely to be beneficial. Re-vascularisation of occluded renal arteries is an attractive option for treatment of ARAS but data from the few randomised controlled studies that have been published do not support its widespread application. Arterial stenting has a higher technical success rate than angioplasty while surgical revascularisation does not appear to improve outcome compared with angioplasty. Recent studies examining functional and histological features of kidneys supplied by atherosclerotic stenosed renal arteries may explain why revascularisation is not always beneficial. The results of on-going studies may identify sub-groups of patients with ARAS who gain a clear benefit from re-vascularisation. In the meantime it seems reasonable to attempt re-vascularisation in the following circumstances: severe hypertension resistant to medical therapy, rapidly progressive renal failure with no obvious cause other than ARAS and recurrent “flash” pulmonary oedema.

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