title: Proteinuria in renal artery occlusion is related to active renin concentration and contralateral kidney size.
abstract: OBJECTIVE
  Angiotensin 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 MEASURE: Complete 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.
  
  
  METHODS
  A referral hypertension unit.
  
  
  RESULTS
  Median 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.
  
  
  CONCLUSIONS
  Proteinuria 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.
authors.affiliation: Hypertension Unit, Hôpital Européen Georges Pompidou, 20 rue Leblanc, 75908 Paris cedex 15, France.
authors.forename: Patrick
authors.initials: P
authors.lastname: Rossignol
authors.forename: Gilles
authors.initials: G
authors.lastname: Chatellier
authors.forename: Michel
authors.initials: M
authors.lastname: Azizi
authors.forename: Pierre-François
authors.initials: PF
authors.lastname: Plouin
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000450:Aldosterone / Q000097:blood; D001161:Arteriosclerosis / Q000097:blood / Q000150:complications; D001794:Blood Pressure / Q000502:physiology; D002784:Cholesterol / Q000097:blood; D003404:Creatinine / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007668:Kidney / Q000254:growth & development* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000097:blood / Q000150:complications; D010297:Paris / Q000453:epidemiology; D011507:Proteinuria / Q000097:blood / Q000150:complications* / Q000628:therapy; D012078:Renal Artery Obstruction / Q000097:blood / Q000150:complications* / Q000628:therapy; D012083:Renin / Q000097:blood*; D012307:Risk Factors
chemical_list: D000450:Aldosterone; D002784:Cholesterol; D003404:Creatinine; D012083:Renin