Angiotensin-converting enzyme inhibition in experimental in-situ immune complex glomerulonephritis: influence on renal function, proteinuria, and morphology

Background. Converting enzyme inhibition (CEI) ameliorates progressive loss of function in nonimmune-mediated renal diseases and experimental hypertension. Little, however, is known on the potential role of CEI in established experimental chronic glomerular immune injury. We therefore studied the effect of the CEI ramipril on renal function and morphology in a model of immune mediated glomerular injury. Methods. The immune complex glomerulonephritis was induced in uninephrectomized rats by intrarenal perfusion with the cationized antigen followed by an intravenous application of the antibody. This disease is characterized by the development of progressive albuminuria and a nephrotic syndrome (albuminuria: immune complex glomerulonephritis 342 + 58, control 76±18mg/24h; /> <0.01) when compared with untreated nephritic rats. Ramipril, however, did not significantly change inulin clearances (immune complex glomerulonephritis 224 + 67, immune complex glomerulonephritis + CEI 278 ±48 ul/min/lOOg bw). Glomerular structural damage expressed as glomerular damage index was significantly greater in rats with immune complex glomerulonephritis when compared with controls (immune complex glomerulonephritis 0.91+0.13; control 0.60±0.08; P<0.05), but was uneffected by the treatment with the CEI (immune complex glomerulonephritis + CEI 1.02 ±0.26; control + CEI 0.63±0.11).