Renal artery stenosis predicts adverse cardiovascular and renal outcome in patients with peripheral artery disease
Article first published online: 12 JUN 2009
DOI: 10.1111/j.1365-2362.2009.02180.x
© 2009 The Authors. Journal Compilation © 2009 Stichting European Society for Clinical Investigation Journal Foundation
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How to Cite
Amighi, J., Schlager, O., Haumer, M., Dick, P., Mlekusch, W., Loewe, C., Böhmig, G., Koppensteiner, R., Minar, E. and Schillinger, M. (2009), Renal artery stenosis predicts adverse cardiovascular and renal outcome in patients with peripheral artery disease. European Journal of Clinical Investigation, 39: 784–792. doi: 10.1111/j.1365-2362.2009.02180.x
Publication History
- Issue published online: 24 JUL 2009
- Article first published online: 12 JUN 2009
- Received 21 February 2009; accepted 18 May 2009
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Keywords:
- Outcome;
- peripheral artery disease;
- renal artery stenosis
Abstract
Background Patients with symptomatic peripheral artery disease (PAD) are considered cardiovascular high-risk patients. Our aim was to investigate whether incidental renal artery stenosis (RAS) increases the risk for adverse cardiovascular and renal outcomes in these patients.
Materials and methods We prospectively enrolled 487 consecutive patients admitted for revascularization of symptomatic PAD and performed a renal overview angiogram categorizing RAS as absent (0–29%), moderate (30–59%) and severe (≥ 60%) respectively. Clinical follow-up was for median 15 months (IQR 12–22) for the occurrence of major adverse events [MAE: composite of death, myocardial infarction (MI), stroke, percutaneous coronary intervention, coronary bypass surgery, amputation and kidney failure]. Glomerular filtration rates (GFR) were obtained at 12 months to quantify the course of renal function.
Results A severe RAS was found in 76 patients (15·6%). Overall MAE occurred in 121 patients (24·8%), the composite endpoint of MI, stroke, amputation and death occurred in 101 patients (20·7%). Patients with a severe RAS had a 1·87-fold increased adjusted risk for MAE (95% CI 1·12–3·12, P = 0·017), a 2·51-fold increased adjusted risk for occurrence of the composite endpoint of MI, stroke, amputation and death (95% CI 1·45–4·34, P = 0·001) and a 2·93-fold increased risk for death (95% CI 1·41–6·08, P = 0·004), compared to those of patients without RAS respectively. We observed a significant association between the decrease of GFR over the 12-month follow-up period and the severity of RAS by multivariable analysis (P = 0·044).
Conclusion Severe RAS in patients with symptomatic PAD is an independent predictor of major adverse cardiovascular events, adverse renal outcome and mortality.

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