Definition and Background

Renal artery stenosis (RAS) is a reduction in the lumen of one or both renal arteries, and can be an important cause of renal failure and secondary hypertension. In >90% of cases the condition is due to atheroma of the renal arteries (atheromatous renovascular disease, or ARVD; Figure 8.1), and this is a disease of ageing. Patients usually have evidence of atheroma in other important vascular beds, such as coronary artery disease (CAD), cerebrovascular and peripheral vascular disease (PVD), and RAS involves the renal ostia (renal arterial origins) in 90% of cases. ARVD can be unilateral or bilateral and up to 50% of patients have renal artery occlusion (RAO) at diagnosis. It is very common: post-mortem studies indicate its presence in over 40% of older patients.

Figure 8.1 Renal arteriogram showing atheromatous renal artery stenosis. A flush aortogram: note the irregular shape of the aorta due to atheroma. The red arrow points to marked reduction in the arterial lumen of the renal artery. Atheromatous RAS typically involves the ostia of the renal arteries, as these are involved with aortic atherosclerotic lesions.

Approximately 5–10% of RAS cases are due to fibromuscular dysplasia (FMD; Figure 8.2), which, when it is discovered, is typically seen in hypertensive young women, most of whom have well-preserved renal function. In contrast to ARVD, angioplasty of FMD RAS lesions is usually associated with clinical improvement, such as cure of hypertension in a third of patients.

Figure 8.2 Renal arteriogram showing fibromuscular renal artery stenosis. A selective right renal artery angiogram in fibromuscular RAS (FMD). The aorta is not affected by atheroma. The red arrows point to multiple bead-like irregularities in the lumen of the renal artery well away from the ostium. A nephrogram can be seen, and there is contrast in the renal collecting system and ureter.

Although many patients with ARVD will have hypertension and/or chronic kidney disease (CKD), in the vast majority of patients it is likely to be incidental and pathophysiologically insignificant to these latter conditions. This explains the inconsistent results following renal artery intervention in ARVD, which has led to uncertainty in guidelines for its management. Assessing the severity of a stenosis and having a thorough understanding of the clinical context are essential to planning management. Most RAS will be suspected, diagnosed and treated in a hospital setting. One important exception is a change in renal function with the introduction of angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs), as numerically the majority of scripts for hypertension and heart failure are community-based.

Clinical Features

Although the majority of ARVD cases are asymptomatic, the condition should be suspected in patients presenting with renal dysfunction and hypertension who have evidence of atheromatous disease in other vascular beds. Particular clinical features include significant deterioration of renal function (e.g. ≥30% increase in serum creatinine or ≥ 25% fall in estimated glomerular filtration rate, or eGFR) accompanying use of ACEI or ARBs, or unexplained ‘flash’ (sudden onset) pulmonary oedema (Figure 8.3), but the presence of femoral, renal or aortic bruits and the coexistence of severe extra-renal vascular disease are the commonest clinical pointers to diagnosis. Hypertension may be absent, particularly in patients with chronic cardiac dysfunction, but a high index of suspicion for RAS diagnosis is advised in cases with severe (often systolic) hypertension, especially when unresponsive to three or more anti-hypertensive agents and with evidence of widespread vascular disease. Box 8.1 lists some of the important clinical clues to the presence of RAS.

Figure 8.3 ‘Flash’ pulmonary oedema. A chest X-ray showing shows florid bilateral pulmonary oedema, which was the presentation of severe RAS in this patient.