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  • Title: Passive Heymann nephritis: evidence that angiotensin-converting enzyme inhibition reduces proteinuria and retards renal structural injury.
    Author: Zoja C, Corna D, Bruzzi I, Foglieni C, Bertani T, Remuzzi G, Benigni A.
    Journal: Exp Nephrol; 1996; 4(4):213-21. PubMed ID: 8983642.
    Abstract:
    In nonimmunological models of renal damage, abnormal traffic of proteins through the glomerular capillary is one of the possible causes of renal disease progression. Here we investigated whether in a model of immune-mediated glomerulonephritis long-lasting proteinuria resulted in renal structural damage and whether chronic treatment with perindopril, an angiotensin-converting enzyme (ACE) inhibitor, lowered proteinuria and retarded disease progression. Passive Heymann nephritis (PHN), a model of human membranous nephropathy, was induced with 0.5 ml/100 g of rabbit anti-Fx1 A antibody in 26 male Sprague-Dawley rats. Animals were then divided into two groups of 13 rats each, given daily vehicle or perindopril (1 mg/kg p.o). Treatment started at day 7 when proteinuria was already present and lasted 12 months. An additional group of normal rats was used as control. Renal biopsies were taken at months 8 and 12. Untreated PHN rats showed a significant increase in systolic blood pressure starting from month 8, that was normalized by perindopril administration. Urinary protein excretion progressively increased with time in untreated PHN rats that developed focal and segmental glomerulosclerosis and tubulointerstitial damage. Perindopril significantly reduced proteinuria and limited glomerular and tubulointerstitial injury. Urinary excretion of endothelin-1 (ET-1) and transforming growth factor-beta 1 (TGF-beta 1), two major mediators of renal damage in other models of glomerulonephritis, increased with time in PHN but only the former correlated with the degree of glomerulosclerosis. The effect of perindopril on proteinuria and renal structural damage was associated with a significant reduction in urinary ET-1 but not TGF-beta 1, suggesting that ET-1 may be an important determinant of disease progression in experimental membranous nephropathy.
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