A clinicopathological study of IgA nephropathy in renal transplant recipients: beneficial effect of angiotensin-converting enzyme inhibitor

Citation
K. Oka et al., A clinicopathological study of IgA nephropathy in renal transplant recipients: beneficial effect of angiotensin-converting enzyme inhibitor, NEPH DIAL T, 15(5), 2000, pp. 689-695
Citations number
42
Categorie Soggetti
Urology & Nephrology
Journal title
NEPHROLOGY DIALYSIS TRANSPLANTATION
ISSN journal
09310509 → ACNP
Volume
15
Issue
5
Year of publication
2000
Pages
689 - 695
Database
ISI
SICI code
0931-0509(200005)15:5<689:ACSOIN>2.0.ZU;2-C
Abstract
Background. Prolonging the survival of transplant kidneys is a major task o f modern nephrology. It has recently been shown that deteriorating renal fu nction and substantial graft loss were observed in 55% of renal allograft r ecipients with recurrent IgA nephropathy (IgAN) at long-term follow-up. To gain a useful insight into the therapeutic approach towards protecting allo graft kidneys from deteriorating graft function, we compared the histologic al characteristics of post-transplant IgAN to primary IgAN and investigated the effects of an ACE inhibitor. Methods. Twenty-one patients with post-transplant IgAN and 63 patients with primary IgAN were included in the histopathological study. The effectivene ss of angiotensin-converting enzyme (ACE) inhibitor treatment in post-trans plant IgAN was also studied in 10 patients. Results. The prevalence of glomeruli with adhesions and/or cellular crescen ts in primary IgAN was significantly greater than in post-transplant IgAN ( P<0.05), but the proportion of glomeruli with segmental sclerosis was simil ar in both groups. The rate of global obsolescence, and the degree of inter stitial fibrosis in post-transplant IgAN were significantly greater than in primary IgAN (P<0.5). The degree of glomerular obsolescence and the severi ty of interstitial fibrosis correlated with the severity of glomerular lesi on in primary IgAN, but not in post-transplant IgAN. In primary IgAN, glome rular diameter significantly correlated with the proportions of glomerular obsolescence, but not in post-transplant IgAN, suggesting that allograft ki dneys may be in a hyperfiltration state. Both the blood pressure and the urinary protein excretion significantly imp roved after ACE-inhibitor treatment (P<0.001). Conclusion. In post-transplant IgAN, histopathological lesions indicative o f acute inflammatory insults were suppressed, and glomerular hypertrophy, w hich may relate to haemodynamic burden such as hyperfiltration, was promine nt. Preliminary study of ACE-inhibitor treatment in 10 patients showed favo urable effects. A future long-term follow-up study is required to establish the effectiveness of ACE inhibitors in treatment of post-transplant IgAN.