Several general considerations are worth stating before considering the clinical problem of hypertension resulting from (or exacerbated by) occlusive renal arterial disease.

First, occlusive renal arterial lesions occur in normotensive as well as hypertensive individuals, especially if these patients have other occlusive atherosclerotic lesions elsewhere in the circulation. Thus, atherosclerotic renal arterial lesions are not infrequently observed in normotensive patients undergoing renal arteriography for a comprehensive assessment of atherosclerotic disease of other organs. This concept is worth considering at this point since renal arteriography is frequently obtained as a more comprehensive study associated with coronary and peripheral arteriography.

Second, renal arterial disease associated with elevated arterial pressure (i.e. renovascular hypertension) is often said to be a rare secondary cause of systemic arterial hypertension and yet it occurs in 3—5% of all patients with hypertension. Using a conservative estimate of the current prevalence of hypertension in the USA, upwards of 2.5 million patients with hypertension may have renal arterial disease. And, of course, the disease occurs with increasing frequency in elderly patients since atherosclerotic lesions and hypertensive blood pressure levels are more frequent in this age group.

Third, renal arterial disease may complicate the course of essential hypertension, especially in those older people whose blood pressure has become more difficult to control (Table 7.1).

As suggested above, since both normotensive and hypertensive patients may have renal arterial lesions, they become clinically significant only when the lesions compromise renal and intrarenal haemodynamics sufficiently to stimulate the renopressor system or to adversely affect renal parenchymal function. When renal haemodynamics is sufficiently compromised, release of renin from the juxtaglomerular apparatus is increased and this, in turn, generates the production of angiotensin II. The increased angiotensin II generated raises arterial pressure through two mechanisms: (1) arteriolar constriction, which increases total peripheral resistance; and (2) secondarily by promoting aldosterone release from the adrenal cortex, leading to the specific metabolic changes of secondary hyperaldosteronism manifested primarily by hypokalaemic alkalosis. This is established by demonstrating increased plasma renin activity (PRA), increased circulating aldosterone concentration and urinary secretion, and sodium and water retention.

In our experience, if the renin concentration in blood sampled from the renal veins is higher in the affected kidney than in the unaffected kidney by a factor of 1.6 or more, then this is strongly suggestive of a unilateral lesion. However, evaluation of bilateral renal arterial disease is less clear-cut. In addition, one must bear in mind that there often are multiple renal arteries and veins or there may be multiple or bilateral lesions. For this reason, additional markers associated with renal arterial lesions are actively being sought. Factors under active study in our institution include the elevation of brain natriuretic peptide (BNP), angiotensinogen and other factors.

Clearly, the patient’s clinical history is extremely valuable, since renal involvement is the most common secondary form of hypertension (excluding over-the-counter and street drugs). A number of screening laboratory tests have been made available for the diagnosis of significant renal arterial disease, each with varying sensitivity and specificity. However, the ‘gold standard’ for the clinical diagnosis (in our opinion) resides with careful selective renal arteriography since it confirms the presence of disease and the extent of renal arterial involvement, and provides an excellent means of assessing anatomy and haemodynamic function and natural history.

The size of the kidneys also provides an excellent index of the significance of the lesions. A smaller kidney suggests significant occlusive disease, although unilateral renal atrophy should always be considered. In this regard, the left kidney is normally 0.5 cm longer than the right; thus, a 1.0-1.5 cm difference in the length of the kidneys should arouse suspicion. The delayed appearance of radiographic contrast material on intravenous urography with hyperconcentration and delay of disappearance should also provoke some suspicion; however, intravenous urography is less frequently used today.

Radioactive renography may also be helpful, with a delayed appearance and disappearance of the tagged radionuclide being of some value although this study is, at best, a ‘screening test’. However, preoperative and postoperative isotopic renography (with renal flow and scan) may be useful procedures in order to help evaluation of postoperative increased arterial pressure. Renographic studies before and after administration of a rapidly acting ACE inhibitor (i.e. captopril) associated with measurements of PRA may suggest a significant lesion, but again this approach is less useful nowadays. Finally, measurement of PRA (indexed to daily sodium intake) may also be of value but may be fraught with pitfalls and can be affected by diet and concurrent therapy. In summary, if one is seriously considering renal arterial disease, we believe that visualization of the renal arteries is in order and, overall, this is, in our opinion, probably the most cost-effective study.

The pathological nature of renal arterial lesions has an important bearing on the natural history of the disease. Identification of the renal arterial lesion arteriographically should be of great value in defining the pathological type of the lesion.

If the renal arterial disease is unilateral, treating the patient with an ACE inhibitor will inhibit the amount of angiotensin II that will be generated and, therefore, will reduce the level of the arterial pressure. However, if the patient has bilateral occlusive disease of the renal arteries, both kidneys will become ischaemic and will release increased amounts of renin. As a result, renal parenchymal function may become impaired. Arterial lesions may broadly be considered to be either atherosclerotic or nonatherosclerotic (or fibrosing); and the latter lesions are variable (Table 7.2).

In evaluating the patient with a renal arterial lesion, consideration should be given to several potential complications (Table 7.3).

In this discussion, we shall rely greatly on the older techniques of aortography as well as selective renal arteriography as earlier studies from the Cleveland Clinic employing careful arteriographic, pathological and clinical correlations provided much important information on the natural history of the disease produced by these lesions (in particular, the fibrosing lesions). Hence, this discussion is unique since clinical studies and treatment today do not usually include removal of renal arterial segments to correlate with the arteriographic and clinical pictures.