Renal artery stenosis and renovascular disease
Renal artery stenosis (RAS) may cause an ischaemic nephropathy, potentially leading to acute or chronic renal failure, or secondary hypertension. Stenosis of over 70% may have haemodynamically significant effects. Hypertension is a usual consequence of RAS, unless cardiac disease prevents it from developing. A classic but rare presentation is with recurrent episodes of sudden (â€˜flashâ€™) pulmonary oedema associated with hypertension and with reasonably good cardiac function and good or only moderately impaired renal function.
If there is bilateral renal artery stenosis (or stenosis of the artery to a single functioning kidney), worsened renal function (>20% rise in creatinine) after starting an ACE inhibitor is characteristic. However this is not reliable as a diagnostic test (neither sensitive nor specific).
In over-50s it is usually caused by atheroma at the orifice of the renal artery, and is almost always accompanied by disease of other branches of the aorta, particularly peripheral vascular disease. Up to 15% of cases lead to complete occlusion with loss of renal function. If progression is gradual, collaterals may form, restoring some function.
RAS occurs rarely in the young (<30 years), where it is more likely to be caused by fibromuscular dysplasia, which causes an irregular beading pattern on arteriography.
Chronic RAS is difficult to diagnose clinically as there are no specific signs. Hypertension is usual. Urinary dipstick testing is normal or mildly abnormal. Hypokalaemia may occur because of secondary hyperaldosteronism. Non-invasive tests have been greatly improved by gadolinium-enhanced magnetic resonance angiography and CT angiography. Ultrasound: if a small kidney is due to RAS, it is too late to save substantial renal function. Doppler signals are an insensitive guide to RAS.
Young patients with fibromuscular dysplasia in the proximal renal artery often respond to balloon dilatation.
Atheromatous lesions are typically close to the aorta and respond less well to angioplasty, but stenting can improve patency. However this treatment is risky and may not offer substantial benefits except after an acute occlusion. Randomised controlled trials (ASTRAL) have not shown any benefit from stenting in chronic or slowly progressive RAS. This should maybe not be such a surprise, because
- In atherosclerotic RAS there is a poor correlation between the severity of the renal artery lesion and the renal function on that side.
- Even when the anatomical result is good, the response (blood pressure and protection/ improvement of renal function) is uncertain. This may be because of pathology distal to the stenosis, caused by atheroembolism (cholesterol embolisation) or ischaemia. A small kidney or one with abnormal peripheral vessels is unlikely to be improved by revascularisation, but a ‘normal’ kidney may not be improved either.
- There is a significant risk of renal artery occlusion as a result of the procedure, and because atherosclerosis is often severe and widespread, of atheroembolism affecting kidneys, lower limbs, gut and elsewhere. This can occasionally be fatal.
Alternative medical management involves giving low-dose aspirin and lipid-lowering therapy, treat hypertension and monitor function. Where the benefit from revascularisation is uncertain (most cases), this therapy may be prescribed without angiography when the diagnosis is thought likely or possible.
Small vessel diseases
- Thrombotic microangiopathy, disseminated intravascular coagulation – see Hahaemaematology.
- Malignant hypertension – See Hypertension.
- Systemic sclerosis (scleroderma renal crisis) – very similar to malignant hypertension; prompt treatment with ACE inhibitors may arrest the disease. More on systemic sclerosis (edren.org/info)