In summary, this is a 62-year-old man with inadequately controlled hypertension despite the usage of three anti-hypertensive agents, who has a small left kidney resulting from left renal artery occlusion, a reasonable sized right kidney although the upper pole artery is occluded resulting from failed angioplasty. The kidneys appear to have preserved renal function of 17 ml/min and 18 ml/min respectively and a serum creatinine of 249 µmol/l. The sizes of the renal arteries are not clarified. Is the lower or upper pole right renal artery the main arterial blood supply or are they of equal size? Also, we do not know the quality of the aorta, is it heavily diseased or not.
It is important to bear in mind that the current problem is the patient’s difficult to control hypertension and not the level of renal function, which appears to be stable despite the occluded renal arteries. Clearly, blood supply to the kidneys from capsular and ureteric blood arteries is currently sufficient to provide an adequate combined GFR. What is not absolutely clear is whether the occlusion of the renal arteries will allow long-term adequacy of blood supply to the kidneys, now that the latter are in the main protected from cholesterol emboli from the aorta. Whether the kidneys continue to shrink down in size is not, therefore, certain. All kidneys that I have biopsied when operating on for renovascular disease, have exhibited considerable damage due to ischaemia and cholesterol embolisation. These renal changes may, and often do, progress despite surgical, radiological or medical management of hypertension.

It is important to recognise that both kidneys are a problem and any management needs to deal with both. The right kidney is, however, within normal size limits and preservation of that kidney is vital for long-term renal preservation of function. There are several options available to manage this patient:

1. Increase anti-hypertensive medication using additional calcium channel blocker, metolazone or minoxidil etc. This should resolve the hypertension although at the expense of taking more tablets with increased chances of side-effects. Using ACEI or angiotensin II inhibitor is likely to cause a reduction in renal blood flow and will result in an increase in serum creatinine once again. Of course the blood supply to the kidneys would remain indirect apart from that to the lower pole of the right kidney.
   
2. Surgical options are also available. Revascularisation of both kidneys is possible although we do not know whether the right upper pole renal artery supplies a sufficient amount of renal parenchyma to be worthwhile revascularising. Clearly, if the lower artery is the main supply to the right kidney, then the loss of the parenchyma supplied by upper pole artery can be ignored. The surgical options also depend also on the quality of the aortic wall – is it safe to clamp the aorta or is it too diseased to use?

The safest option is to perform an extra-anatomical bypass to the renal arteries. The right upper pole artery could be revascularised by a saphenous vein bypass from the hepatic artery and the left renal artery by using the splenic artery. Neither of these procedures involves clamping the aorta and hence avoids left heart strain. The spleen continues to be supplied by the short gastric arteries from the stomach. Alternatively, only one of these procedures may be necessary. If the right kidney upper polar vessel is large, then revascularising this kidney would be most valuable and a hepato-renal bypass may be best. The left kidney could be left alone since it is quite small. In this situation, the left kidney would still cause hypertension but this could be managed using an ACI.

Another extra-anatomical bypass could be performed from the common iliac arteries to the renal arteries. Again, aortic clamping would not be necessary. These bypasses would be longer in length and would depend on the quality of the inflow iliac arteries for blood supply.

If the patient is without significant cardiovascular risk then an aortic procedure can be contemplated. The first option would be to consider renal artery endarterectomy. This involves clamping the aorta above and below the renal arteries and removing the intimal atherosclerotic layer from the aortic ostia and the origins of the occluded renal arteries. This technique is practised in a few centres only. There is a danger of intimal dissection down the renal arteries and aorta if the endarterectomies are not performed properly and hence most surgeons avoid this method.

The next alternative is a bilateral aorto-renal saphenous vein bypass. This procedure involves using one saphenous vein and its major branch, thus only a single anastomosis onto the aorta is required. Provided the aorta is not heavily diseased, this option is attractive with only short bypasses being necessary.

It is imperative that further investigations to exclude significant cardiac disease is undertaken before surgery should be contemplated. Patients with renovascular disease often have extensive other vascular disease, including the coronary, carotid and peripheral arteries. A MIBI scan/treadmill exercise test would be useful to exclude such high risk cases. One of the problems of surgical intervention remains post-operative myocardial infarction or stroke. Pre-operative risk assessment and full discussion with patient and physician is mandatory before embarking on surgery. The mortality of past series of surgical series reflects the degree of pre-operative co-morbid assessment of patients. If best risk cases are undertaken then a durable long-term result can ensue. However, there will remain a need for long-term anti-hypertensive medication since the already damaged kidneys will not return to normal. However, the number of drugs used to control hypertension would be reduced. In addition, ACEI could be tentatively prescribed following surgery.