Renal Artery Stenosis

Background

Specialists have known for a long time that renal artery stenosis (RAS) is the major cause of renovascular hypertension and that it may account for 1-10% of the 50 million people in the United States who have hypertension.

Apart from its role in the pathogenesis of hypertension, renal artery stenosis is also being increasingly recognized as an important cause of chronic renal insufficiency and end-stage renal disease. In older individuals, atherosclerosis (ATH) is by far the most common etiology of renal artery stenosis.[1, 2] As the renal artery lumen progressively narrows, renal blood flow decreases and eventually compromises renal function and structure.

With the increase in the elderly population and the possible increase in the prevalence of renal artery stenosis and ischemic nephropathy, clinicians dealing with renovascular disease (RVD) need noninvasive diagnostic tools and effective therapeutic measures to resolve the problem successfully. This article explores the natural history of this disorder, the value of a variety of invasive and noninvasive diagnostic procedures, and the consequence of allowing the artery to remain obstructed versus reversing renal artery occlusion.

NextPathophysiology

In patients with ATH, the initiator of endothelial injury is not clear; however, dyslipidemia, hypertension, cigarette smoking, diabetes mellitus, viral infection, immune injury, and increased homocysteine levels may contribute to endothelial injury. In the atherosclerotic lesion site, endothelium permeability to plasma macromolecules (eg, low-density lipoprotein [LDL]) increases, turnover of endothelial cells and smooth muscle cells increases, and intimal macrophages increase. When atherogenic lipoproteins exceed certain critical levels, the mechanical forces may enhance lipoprotein insudation in these regions, leading to early atheromatous lesions.

Renal blood flow is 3- to 5-fold greater than the perfusion to other organs because it drives glomerular capillary filtration. Both glomerular capillary hydrostatic pressure and renal blood flow are important determinants of the glomerular filtration rate (GFR).[3]

In patients with renal artery stenosis, the chronic ischemia produced by the obstruction of renal blood flow produces adaptive changes in the kidney that are more pronounced in the tubular tissue. These changes include atrophy with decreased tubular cell size, patchy inflammation and fibrosis, tubulosclerosis, atrophy of the glomerular capillary tuft, thickening and duplication of the Bowman capsule, and intrarenal arterial medial thickening. In patients with renal artery stenosis, the GFR is dependent on angiotensin II and other modulators that maintain the autoregulation system between the afferent and efferent arteries and can fail to maintain the GFR when renal perfusion pressure drops below 70-85 mm Hg. Significant functional impairment of autoregulation, leading to a decrease in the GFR, is not likely to be observed until arterial luminal narrowing exceeds 50%.

The degree of renal artery stenosis that would justify any attempt at either surgical intervention or radiologic intervention is not known. One study suggested that a ratio of pressure, measured distal to renal artery stenosis, less than 90% relative to aortic pressure, was found to be associated with significant renin release from the affected kidney, renin being measured in the ipsilateral renal vein. This might be useful as a functional measurement of significant renovascular stenosis leading to hypertension and, thus, a marker of those individuals more likely to benefit from angioplasty and stenting.[4, 5]

PreviousNextEpidemiologyFrequencyUnited States

Studies suggest that ischemic nephropathy may be responsible for 5-22% of advanced renal disease in all patients older than 50 years.

Mortality/Morbidity

The consequences of renal artery stenosis are hypertension, which may be particularly difficult to control or may require multiple antihypertensive agents (with increased adverse effects), and progressive loss of renal function (ischemic nephropathy).

In addition, the discovery of atherosclerotic RVD frequently occurs in the setting of generalized vascular disease (ie, cerebral, cardiac, peripheral), with the co-morbidity associated with disease in those vascular beds. Thus, any therapeutic intervention for renal artery stenosis should logically take into account the underlying prognosis associated with these co-morbidities.

Race

RVD is less common in African American patients. The incidence rate in 2 studies of patients with severe hypertension was 27-45% in white persons compared to 8-19% in African American persons.[6]

Sex

While the incidence of atherosclerotic RVD is independent of sex, Crowley et al showed that female sex (as well as older age, elevated serum creatinine level, coronary artery disease, peripheral vascular disease, hypertension, and cerebrovascular disease) is an independent predictor of RVD progression.[7]

Age

In 1964, Holley et al reported data from 295 consecutive autopsies performed in their institution during a 10-month period.[8] The mean age at death was 61 years. The prevalence rate of renal artery stenosis was 27% of 256 cases identified as having history of hypertension, while 56% showed significant stenosis (>50% luminal narrowing), and, among normotensive patients, 17% had severe renal artery stenosis (>80% luminal narrowing). Among those older than 70 years, 62% had severe renal artery stenosis.

Another similar autopsy study reported similar results, with 5% of patients older than 64 years showing severe stenosis; this figure increased to 18% for patients aged 65-74 years and 42% for patients older than 75 years.

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