ObjectivesAngiotensin II, in addition to having vasopressor effects, induces proteinuria in experimental models. Proteinuria has been reported, sometimes in the nephrotic range, in patients with chronic complete renal artery occlusion. We aimed to identify the factors associated with proteinuria in such cases.Design and main outcome measureComplete renal artery occlusion was detected by intra-arterial angiography in 96 patients referred for hypertension. We analysed patient characteristics at presentation to identify the factors associated with proteinuria.SettingA referral hypertension unit.ResultsMedian protein excretion was 0.25 g/day (range 0–11). Nine patients had nephrotic syndrome (proteinuria⩾3.5 g/day per 1.73 m2). Patients in the upper tertile for proteinuria differed from those with lower proteinuria in terms of total cholesterol levels (P<0.01), the proportion of diabetics (P<0.01) and supine active renin concentration (P= 0.02). They tended to have higher systolic blood pressure levels (P= 0.07), a lower frequency of contralateral renal artery stenosis (P= 0.09) and a longer contralateral kidney (P= 0.09). In multivariate logistic regression, the factors independently linked to proteinuria in the upper tertile were active renin concentration (P= 0.05) and contralateral kidney length (P= 0.02). Proteinuria significantly decreased in nephrotic patients (P<0.01) treated with revascularization or nephrectomy and/or angiotensin converting enzyme inhibition.ConclusionsProteinuria in renal artery occlusion is positively related to active renin concentration, which reflects plasma angiotensin II concentration. Therapy aimed at lowering angiotensin II levels decreased proteinuria in nephrotic patients. The positive relationship between proteinuria and contralateral kidney length may reflect compensatory hypertrophy in response to nephron function loss.