title: [Clinic and morphologic evolution five years after a renal atherosclerotic artery stenosis (RAS): a study of twenty nine hypertensive patients population].
abstract: The indication of renal atherosclerotic artery stenosis revascularisation is always debated in clinical practices when arterial hypertension is stabilized by the treatment, especially if the stenosis is discovered fortuitously. The clinician needs clinical and morphological markers which will indicate or not the revascularisation in the situation of "nephronic protection". The benefits of angioplasty have been studied on the blood pressure, the creatinine clearance, the glomerular function analyzed by scintigraphy, the renal length and more recently on the mean cortical thickness (MCT). The follow-up of these studies is generally inferior to 2 years. In this work, we tried to estimate the clinic and morphologic evolution 5 years after a unilateral artery stenosis angioplasty. From a group of 249 patients who had a renal angioplasty between January 1995 and January 2000 (T0), 29 patients with refractory hypertension and with a unilateral atherosclerotic renal artery stenosis on spiral computed tomographic angiography (TCA) performed at T0 [17 M; 12 W; medium age 68.6 +/- 10 years] were included. The TCA performed at 5 years (T5) eliminated a new renal arterial stenosis or restenosis. We have analyzed 29 revascularized kidneys (kidney S) and 29 controlateral kidneys (kidney C), the blood pressure and renal function. The renal length (mm) was at T0: kidney C=99.4 +/- 13.5; kidney S=93.5 +/- 10.8 and at T5: kidney C=99.4 +/- 12.6; kidney S=94.2 +/- 10.7. MCT (mm) was at T0: kidney C=7 +/- 1.2; kidney S=6.6 +/- 1.1 and at T5: kidney C=6.2 +/- 1.2; kidney S5=6 +/- 1. The cortical atrophy got worse while the renal length and creatinine clearance were stable: only diastolic blood pressure was controlled (78.8 mmHg +/- 11.9). In spite of small strength, this study arguments the fact that the angioplasty isn't sufficient to control the arterial hypertension in an atheromatous context, not allowing to slow the evolution of distal cortical lesions with however a stability of creatinine clearance.
authors.affiliation: Service d'HTA et de médecine vasculaire, Lille.
authors.forename: S
authors.initials: S
authors.lastname: Duquenoy
authors.forename: C
authors.initials: C
authors.lastname: Mounier-Vehier
authors.forename: P
authors.initials: P
authors.lastname: Devos
authors.forename: V
authors.initials: V
authors.lastname: Boivin
authors.forename: J P
authors.initials: JP
authors.lastname: Beregi
mesh_terms: D000368:Aged; D017130:Angioplasty / Q000379:methods*; D001161:Arteriosclerosis / Q000209:etiology* / Q000601:surgery*; D003404:Creatinine / Q000378:metabolism; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000150:complications*; D007668:Kidney / Q000502:physiology; D008297:Male; D008875:Middle Aged; D012008:Recurrence; D012078:Renal Artery Obstruction / Q000209:etiology* / Q000601:surgery*; D016896:Treatment Outcome
chemical_list: D003404:Creatinine