Surgical correction of atherosclerotic renovascular disease can retrieve excretory renal function in selected hypertensive patients with ischemic nephropathy. Patients with improved renal function had a significant and independent increase in dialysis-free survival in comparison with patients whose function was unchanged and patients whose function was worsened after operation. These results add further evidence in support of a prospective, randomized trial designed to define the value of renal artery intervention in patients with ischemic nephropathy.

Main renal artery interrogation is an accurate screening test to detect significant stenosis or occlusion of the main renal artery. Hilar analysis alone does not provide sufficient sensitivity to be used as a sole screening study. Neither method detects the presence of renovascular disease associated with polar vessels.

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Abstract-Determinants of restenosis after angioplasty include constrictive remodeling and intimal hyperplasia. Both processes require extensive matrix turnover, so matrix metalloproteinases (MMPs) have become potential targets of antirestenosis therapies. We studied the effects of RO113-2908, a broad-spectrum MMP inhibitor (MMPI), on the response to iliac artery angioplasty and stenting in atherosclerotic cynomolgus monkeys. Lumen diameter (LD) was measured angiographically, and artery wall geometry was assessed after perfusion-fixation at 4 weeks. Angiogenesis was measured in subcutaneous polyvinyl alcohol disks. Key Words: restenosis Ⅲ constrictive remodeling Ⅲ metalloproteinases Ⅲ angioplasty Ⅲ stents E ach year, Ϸ3 million patients undergo reconstruction of atherosclerotic arteries, and many subsequently develop recurrent stenoses at the sites of repair. Restenosis after angioplasty or stenting is due primarily to constrictive artery wall remodeling or intimal hyperplasia, respectively. These processes involve extensive reorganization of extracellular matrix to facilitate changes in artery wall geometry and accumulation of new intimal mass.Matrix degradation is tightly regulated in the normal artery wall through a balance between matrix metalloproteinases (MMPs) and their endogenous inhibitors (eg, TIMPs). Atherosclerosis shifts the balance toward degradation, as MMPs are produced by accumulating macrophages and activated smooth muscle cells (SMCs). 1-3 Angioplasty further increases MMP production, 4 -7 and matrix turnover and maturation continue for months after angioplasty in all layers of the arterial wall, likely contributing to SMC proliferation, migration, and remodeling. 7-9 These observations have led to speculation that inhibiting MMP activity could limit restenosis. However, experiments with MMP inhibitors to prevent intimal hyperplasia in animal models have shown mixed results, and effects on remodeling have not been well characterized. 5,6,10 -13 Whether this approach can improve the response to angioplasty or stenting in human beings with advanced atherosclerosis is yet to be defined.To extend this approach to a preclinical model, we treated atherosclerotic cynomolgus monkeys with a broad-spectrum MMPI for 4 weeks after angioplasty and stent-angioplasty to determine the impact on restenosis. Treatment provided continuous, systemic MMP inhibitory activity and inhibited angiogenesis, but artery wall remodeling and intimal hyperplasia were not improved. Additional preclinical research is needed to define the spectrum of matrix-degrading proteases critical in constrictive remodeling and intimal hyperplasia of atherosclerotic arteries after angioplasty. Methods Animal ModelThirty-one adult male monkeys (Macaca fascicularis; mean age, 13.5 years) consumed an atherogenic diet (0.28 mg cholesterol/kcal) for 2.5Ϯ0.1 years to induce advanced iliac artery lesions. 8,14 -17 Animals were then randomized into MMPI (nϭ16) or control (nϭ15) groups based on diet duration and the ratio of total to HDL choleste...