Renal Arterial Disease and Hypertension

Abstract

Renal artery disease produces a spectrum of progressive clinical manifestations ranging from minor degrees of hypertension to circulatory congestion and kidney failure. Moderate reductions in renal blood flow do not induce tissue hypoxia or damage, making medical therapy for renovascular hypertension feasible. Several prospective trials indicate that optimized medical therapy using agents that block the renin-angiotensin system should be the initial management. Evidence of progressive disease and/or treatment failure should allow recognition of high-risk subsets that benefit from renal revascularization. Severe reductions in kidney blood flow ultimately activate inflammatory pathways that do not reverse with restoring blood flow alone.

Keywords: Angiotensin; Hypertension; Ischemic nephropathy; Kidney; Renal artery stenosis; Renovascular.

Figure 1

Schematic view of progressively more severe clinical manifestations associated with occlusive renovascular disease (RVD). Minor degrees of lumen obstruction are manifest as “incidental” lesions of minimal hemodynamic importance. As obstruction leads to reduced pressures and flow beyond the lesion, renovascular hypertension and acceleration of cardiovascular events ensue, particularly when associated with impaired sodium excretion. Ultimately, severe and longstanding RVD activates injury pathways within the kidney parenchyma that may no longer depend primarily upon hemodynamic effects of stenosis and respond only partially to restoring vessel patency.

Figure 2

Examples of fibromuscular renovascular disease. Left panel depicts an angiogram with a typical “string-of-beads” appearance typical of medial fibroplasia. Indentation of the vessel wall represents a series of internal webs that reduce distal perfusion and trigger RVH. Such lesions can respond to intra-arterial balloon angioplasty (PTRA). Right panel depicts an angiogram with a focal stenosis causing severe hypertension. Recent classification schemes distinguish mainly between “multifocal” disease (left) and “focal” disease (right).

Figure 3

Tissue oxygenation as measured by Blood Oxygen Level Dependent (BOLD) MR remains stable during moderate reductions in renal blood flow in atherosclerotic renovascular disease. At some level, severe and prolonged blood flow reductions lead to overt tissue hypoxia associated with rarefication of small vessels, activation of inflammatory pathways and interstitial fibrosis. Eventually, restoration of large vessel patency no longer reverses this process.

Figure 4

CT angiogram from a patient with unilateral atherosclerotic RVD manifest by high Doppler velocities and recently progressive hypertension. This was treated with drug therapy including ACE inhibition with satisfactory BP levels and GFR (serum creatinine 1.1 mg/dL). Results of prospective, randomized trials indicate that little additional benefit is to be gained by further intervention, e.g. renal revascularization, so long as this remains stable (see text).

Figure 5

(A, left) Angiographic image of high-grade stenosis manifest by new-onset accelerated hypertension more than 20 years after mantel radiation for malignancy. Drug therapy was associated with declining kidney function. (B, right) Endovascular stent placement in the proximal right renal artery achieved excellent recovery of lumen patency. This maneuver was followed with normalization of blood pressure and withdrawal of medications over two months.

Figure 6

Schematic illustration of steps in the management of RVH and ischemic nephropathy. The foremost goals are to reduce morbidity associated with hypertension by reaching goal BP and to preserve kidney function. Should that not be achievable by medical therapy or should vascular disease progress, renal revascularization should be considered, either by endovascular or surgical intervention (see text).