In patients with peripheral vascular disease (PVD), mortality is high and renal artery stenosis (RAS) is a frequent incidental finding. RAS carries a high risk for mortality, but whether incidentally discovered RAS is a risk factor for mortality is unknown. The prognostic impact of incidental RAS for mortality was studied in 550 consecutive patients who underwent intra-arterial digital subtraction angiography for PVD in a single center between 1997 and 2000. In 491 patients (336 men, 155 women; mean follow-up 3.8 ؎ 1.9 yr), the renal arteries were visualized and follow-up data were available. RAS (diameter reduction >50%) was present in 26% of the patients. Mortality in the RAS group was 59 versus 28% in the non-RAS group (odds ratio 3.8; 95% confidence interval 2.5 to 5.7; P < 0.0001). Diabetes, previous myocardial infarction, history of PVD, stroke, and hypertension were more frequent in the RAS group; age was higher and GFR was lower in the RAS group. Therefore, RAS was associated with elevated mortality and increased prevalence of cardiovascular risk factors. Cox regression analysis showed that RAS was an independent predictor for mortality (P ‫؍‬ 0.005), along with age, diabetes, smoking, previous myocardial infarction, history of PVD, and stroke. In patients who were evaluated for PVD by digital subtraction angiography, mortality was high. Incidental RAS was a frequent finding and an independent predictor for mortality. Whether RAS is a marker for or, alternatively, a mediator of the poor prognosis and whether prognosis can be improved by specific intervention should be the subject of future prospective studies.

In PAD, incidental RAS predicts long-term mortality independent of other risk factors. The elevated mortality is not due to a higher postoperative risk. Subjects presenting with PAD and RAS can therefore undergo vascular procedures with the same risk as other patients.

I n our recently published paper in the Journal of Hypertension [1] we investigated the cross-sectional and longitudinal association of fatty liver disease (FLD) with blood pressure (BP) and hypertension in a general population cohort. Furthermore, we analyzed the specific contribution of alcohol consumption to this association. We drew four main conclusions: first, FLD as evidenced by liver hyperechogenicity and increased serum alanine aminotransferase (ALT) levels is associated with BP-related variables and hypertension at baseline. Second, FLD predicts the progression of BP and the development of hypertension after 5 years. Third, alcohol consumption has a minor contribution to the association of FLD with BP-related variables and hypertension. Fourth, the findings emphasize the necessity to implement liver ultrasound in routine medical care to detect FLD if ALT levels are elevated.Due to two errors in our analyses we have to withdraw the second and fourth conclusion. First, we mistakenly did not adjust for BP measurement at baseline or excluded prevalent cases at baseline. Therefore, no proper inferences were possible on any progression of BP and incident hypertension. Second, due to an error in the analysis syntax, an incomplete subset of individuals was included in regression models. We re-analyzed our data using appropriate methods. All corrected tables are displayed below.Whereas higher BP values and higher odds ratios for increased systolic BP, increased diastolic BP and hypertension in longitudinal analyses were observed among individuals with FLD as evidenced by liver hyperechogenicity and increased ALT levels compared to individuals without FLD, all effect sizes were small (Tables 1 and 2). The only statistically significant associations concerned diastolic BP in the whole study population (Table 1) and systolic BP in the subgroup of individuals not receiving antihypertensive medication (Table 2). In this subgroup, the association of FLD with diastolic BP was borderline significant (P ¼ 0.08). Although these results give some support to our hypothesis that FLD is associated with progression of BP and incident hypertension, we cannot maintain our previous conclusion that FLD is a strong risk factor for the progression of BP over TABLE 1. Association between baseline fatty liver disease and blood pressure-related variables at follow-up in the total sample (n ¼ 3210) USÀ and ALTÀ (N ¼ 1912) USÀ and ALTþ (N ¼ 342) USþ and ALTÀ (N ¼ 492) USþ and ALTþ (N ¼ 464) SBP; mmHg 132.6 (131.7-133.4) 132.0 (130.3-133.8) 132.6 (131.0-134.1) 134.2 (132.5-135.9) DBP; mmHg 81.2 (80.8-81.7) 80.4 (79.4-81.5) 81.2 (80.4-82.1) 82.4 (81.4-83.4) Ã Incident increased SBP (!140 mmHg) a Ref. 1.2 (0.7-1.8) 0.9 (0.6-1.4) 1.3 (0.8-2.0) Incident increased DBP (!90 mmHg) a Ref. 0.9 (0.5-1.4) 0.8 (0.5-1.3) 1.0 (0.8-1.6) Incident hypertension b,a Ref. 0.7 (0.4-1.2) 1.0 (0.6-1.7) 1.2 (0.7-2.2)ALT levels above the 75th percentile were considered increased. ALT, alanine aminotransferase; US, ultrasound. Ã P < 0.05 compared with individuals ...