[Predictors of successful renal artery revascularization in atherosclerotic renovascular disease].
ABSTRACT Atherosclerotic renovascular disease (ARVD) is defined as a reduction in glomerular filtration rate in patient with significant renovascular bilateral occlusive disease or unilateral in a solitary kidney. ARVD is a frequent and potentially avoidable cause of end stage renal failure and the need for replacement therapy among person above 50 years old. Use of balloon angioplasty with stenting or surgical repair has been shown to improve renal potency, but there is no clear evidence that it prevents further progressive decline of renal function or blood pressure, compared to medical therapy alone. It is now recognized that severity of histopathologic damage is an important determinant and predictor of renal functional outcome. Proteinuria increases with declining renal failure and reflects the severity of parenchymal damage. Proteinuria and high renal resistance index are associated with glomerular damage and altered intrarenal perfusion. They aren't linked to renal artery stenosis (RAS) grade. Recent study indicate that abrupt decline in renal function reflects reversibility after revascularization. This should probably be undertaken in RAS patients with rapidly deteriorating renal function, refractory hypertension and in whom plasma creatinine concentration has increased by >20% during one month long administration of angiotensin-converting enzyme inhibitor. Renal biopsy may be useful to evaluate patient who will have advantage from revascularization.
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ABSTRACT: The intent of endovascular therapy for symptomatic atherosclerotic renal artery stenosis (ARAS) is to preserve parenchyma and avoid renal-related morbidity. The aim of this study is to examine the impact of renal artery intervention on parenchymal preservation. We performed a retrospective analysis of records from patients who underwent endovascular intervention for ARAS and were followed by duplex ultrasound between 1990 and 2008. Renal volume (in cm(3)) was estimated in all patients as renal length (cm) x renal width (cm) x renal depth (cm) x 0.5. The normal renal volume was calculated as 2 x body weight (kg) in cm(3). Failure of preservation was considered to be a persistent 10% decrease in volume. Clinical benefit defined as freedom from renal-related morbidity (increase in persistent creatinine >20% of baseline, progression to hemodialysis, death from renal-related causes) was calculated. Five hundred ninety-two renal artery interventions were performed. One hundred eighty-six kidneys suffered parenchymal loss (>5%) with an actuarial parenchymal loss rate of 29% +/- 1% at five years respectively. There were no significant differences in age, gender, starting renal volume, or kidney size. However, patients with parenchymal loss had lower eGFR (45 +/- 24 vs 53 +/- 24 mL/min/1.73 m(2); Loss vs noLoss, P = .0002, Mean +/- SD) higher resistive index (0.75 +/- 0.9 vs 0.73 +/- 0.10; P = .0001) and worse nephrosclerosis grade (1.43 +/- 0.55 vs 1.30 +/- 0.49; P = .006) then those not suffering parenchymal loss. Parenchymal loss was associated with significantly worse five-year survival (26% +/- 4% vs 48% +/- 2%; Loss vs noLoss; P < .001) and freedom from renal-related morbidity (70% +/- 5% vs 82% +/- 2%; P < .05) with increased numbers progressing to dialysis (17% vs 7%; P < .006). While parenchymal preservation occurs in most patients, parenchymal loss occurs in 31% of patients and is associated with markers of impaired parenchymal perfusion (resistive index and nephrosclerosis grade) at the time of intervention. Pre-existing renal size or volumes were not predictive of parenchymal loss. Parenchymal loss is associated with a significant decrease in survival and a marked increased renal related morbidity and progression to hemodialysis.Journal of vascular surgery: official publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter 02/2010; 51(5):1222-9; discussion 1229. DOI:10.1016/j.jvs.2009.09.050 · 2.98 Impact Factor