Does captopril cause renal damage in hypertensive patients? Report from the Captopril Collaborative Study Group.
Renal biopsy material was studied from 38 hypertensive patients, 19 of whom had received captopril for at least six months. Comparable immunofluorescence findings and prominent arteriolar and mesangial deposits of C3 and IgM were noted equally in all patients. Within the non-captopril group one biopsy showed mesangial IgA glomerulonephritis and, in another, microscopy revealed typical membranous glomerulonephritis. The biopsy specimens from 4 patients in the captopril group showed evidence of glomerular deposits and 2 had typical membranous glomerulonephritis. Small, spherical electron-dense deposits were seen with equal frequency along the outer aspect of the glomerular basement membrane in both groups, but were not thought to be immune deposits. Renal biopsy material from hypertensive patients may have ultrastructural and immunohistological abnormalities which cannot be ascribed to captopril. Subclinical glomerulonephritis appears to exist in the hypertensive population. The membranous glomerulonephritis could be drug-related, but this cannot be determined with certainty from the small sample studied. Caution must be shown in attributing glomerulonephritis to any drug without information about the kidneys before treatment.
D001706:Biopsy; D002216:Captopril / Q000009:adverse effects*; D003176:Complement C3 / Q000032:analysis; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D007070:Immunoglobulin A / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D011392:Proline / Q000031:analogs & derivatives*
D003176:Complement C3; D007070:Immunoglobulin A; D007075:Immunoglobulin M; D011392:Proline; D002216:Captopril