Prevalence of atherosclerotic renal artery stenosis in patients starting dialysis.

BACKGROUND: Atherosclerotic renal artery stenosis (ARAS) can lead to end-stage renal failure (ESRF). We determined the prevalence of ARAS in patients 45 years of age or older starting renal replacement therapy. METHODS: Forty-nine of 80 consecutive patients (37 males, 12 females) starting renal replacement therapy in our centre gave informed consent and underwent spiral computed tomographic angiography of their renal arteries. A renal artery diameter reduction of 50% or more assessed by two radiologists was considered as a significant stenosis. RESULTS: Twenty of 49 patients (41%) had an ARAS, and in eight cases (16%) this was bilateral or unilateral with a single kidney. Women were more likely to have an ARAS than men; 75 (9/12) vs 30% (11/37, P<0.01). However, relatively more women declined participation. Non-participants and participants did not differ in respect to other relevant clinical data. Nonetheless, findings in these patients would be negative, the prevalence of ARAS would still be 31% in women and 22% in men (NS). In 13 patients with ARAS the registered diagnosis of ESRF either was hypertension, renovascular disease or unknown. Assuming that in these patients atherosclerotic renovascular disease was the cause of renal failure, a total of 13 patients (13/49, 27%) entered the dialysis programme because of this problem. CONCLUSIONS: These results suggest that ARAS is an important cause of ESRF.

Long-term effects of arterial stenting on kidney function for patients with ostial atherosclerotic renal artery stenosis and renal insufficiency.

It is uncertain whether renal artery stent placement in patients with atherosclerotic renovascular renal failure can prevent further deterioration of renal function. Therefore, the effects of renal artery stent placement, followed by patency surveillance, were prospectively studied in 63 patients with ostial atherosclerotic renal artery stenosis and renal dysfunction (i.e., serum creatinine concentrations of >120 micromol/L (median serum creatinine concentration, 171 micromol/L; serum creatinine concentration range, 121 to 650 micromol/L). Pre-stent renal (dys) function was stable for 28 patients and declining for 35 patients (defined as a serum creatinine concentration increase of > or =20% in 12 mo). The median follow-up period was 23 mo (interquartile range, 13 to 29 mo). Angioplasty to treat restenosis was performed in 12 cases. Five patients reached end-stage renal failure within 6 mo, and this was related to stent placement in two cases. Two other patients died or were lost to follow-up monitoring within 6 mo, with stable renal function. For the remaining 56 patients, the treatment had no effect on serum creatinine levels if function had previously been stable; if function had been declining, median serum creatinine concentrations improved in the first 1 yr [from 182 micromol/L (135 to 270 micromol/L ) to 154 micromol/L (127 to 225 micromol/L ); P < 0.05] and remained stable during further follow-up monitoring. In conclusion, stent placement, followed by patency surveillance, to treat ostial atherosclerotic renal artery stenosis can stabilize declining renal function. For patients with stable renal dysfunction, the usefulness is less clear. The possible advantages must be weighed against the risk of renal failure advancement with stent placement.

Vascular Effects of ACE Inhibition Independent of the Renin-Angiotensin System in Hypertensive Renovascular Disease : A Randomized, Double-Blind, Crossover Trial.

-To evaluate whether ACE inhibition and angiotensin II type 1 blockade exert beneficial effects on NO availability independent of their blood pressure-lowering effect, we used a double-blind crossover design to study vascular function in 18 patients with hypertensive renovascular disease during 6 weeks of therapy with enalapril (Ena) and valsartan (Val) compared with non-renin-angiotensin system-mediated treatment with the alpha(1)-blocker doxazosin (Dox). Control measurements were performed in 13 age-matched volunteers. Forearm blood flow was assessed with venous occlusion plethysmography, and serotonin and nitroprusside were used as endothelium-dependent and -independent vasodilators, respectively. Blood pressure was similar during all treatment periods. Serotonin-induced vasodilation was decreased in patients during Dox treatment (n=12) compared with control subjects (n=13) (increase 42+/-20% versus 107+/-65%, P:<0.05). Crossover from Dox to Val (n=6) had no effect on serotonin response (increase 50+/-14%), but crossover to Ena (n=6) caused a significant improvement (increase 79+/-39%, P:<0.05 versus Dox). In an assessment of all patients, serotonin-induced vasodilation during Ena (n=12, increase 75+/-31%) was increased compared with both Val and Dox (43+/-14% and 42+/-20%, respectively; both P:<0.05 versus Ena). The nitroprusside response remained unaltered during all treatment periods. In conclusion, ACE inhibition improves the impaired endothelium-dependent vascular function in patients with hypertensive renovascular disease. This effect is unrelated to blood pressure-lowering or angiotensin II-mediated effects.