6533b7cffe1ef96bd1258e87

RESEARCH PRODUCT

Screening for congenital renovascular hypoplasia and renal artery stenosis by acute converting enzyme inhibition.

G. MercadanteG GiuntiniG CerasolaA RabioloSantina CottoneMangano MtContorno A

subject

AdultMalemedicine.medical_specialtyCaptoprilAdolescentUrologyAdministration OralAngiotensin-Converting Enzyme Inhibitorsurologic and male genital diseasesRenal artery stenosisKidneyRenal Artery ObstructionPlasma renin activityDiagnosis DifferentialRenin-Angiotensin SystemInternal medicinemedicine.arteryReninmedicineHumansRenal arteryScreening proceduresAgedKidneybusiness.industryKidney metabolismCaptoprilMiddle Agedmedicine.diseasefemale genital diseases and pregnancy complicationsHypoplasiaRadiographymedicine.anatomical_structureEndocrinologyHypertension RenovascularFemaleKidney Diseasesbusinesshormones hormone substitutes and hormone antagonistscirculatory and respiratory physiologymedicine.drug

description

To evaluate the usefulness of the captopril test for identifying renal artery stenosis (RAS) and renovascular hypoplasia (RAH), we studied 48 hypertensive patients. In 20 hypertensives with screening procedures indicating renovascular disease and in 28 essential hypertensives (EH), the plasma renin activity (PRA) responses to an oral test dose of captopril (50 mg) were studied. A 60-min post-captopril PRA increase of 150% (or 400% if baseline PRA < or = 3 ng/ml/h) was considered as positive. Renal angiography was performed in all cases. Among the 20 renovascular hypertensive patients, RAH in 9 and RAS in 11 subjects were proved by angiography. The captopril test in all patients with RAH resulted negative (mean PRA increase 50%); furthermore, the test identified 7 of the 11 RAS (mean PRA increase 477.6%); sensitivity and specificity for RAS were 64 and 88.8%, respectively. In the EH group, there were 3 false-positive subjects (mean PRA increase 122%). This study demonstrates that the PRA responses to a test dose of captopril are a useful screening test for distinguishing RAH from RAS, and for identifying the latter in hypertensive patients. These data also suggest that in subjects with RAH, hypertensive disease may not renin dependent.

10.1159/000187143https://pubmed.ncbi.nlm.nih.gov/8446252