Journal Article

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

Kazumasa Oka, Enyu Imai, Toshiki Moriyama, Yoshitaka Akagi, Akio Ando, Masatsugu Hori, Akihiko Okuyama, Kiyohide Toki, Masahiro Kyo, Yukito Kokado and Shiro Takahara

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 15, issue 5, pages 689-695
Published in print May 2000 | ISSN: 0931-0509
Published online May 2000 | e-ISSN: 1460-2385 | DOI:
A clinicopathological study of IgA nephropathy in renal transplant recipients: beneficial effect of angiotensin‐converting enzyme inhibitor

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Background. Prolonging the survival of transplant kidneys is a major task of modern nephrology. It has recently been shown that deteriorating renal function and substantial graft loss were observed in 55% of renal allograft recipients with recurrent IgA nephropathy (IgAN) at long‐term follow‐up. To gain a useful insight into the therapeutic approach towards protecting allograft kidneys from deteriorating graft function, we compared the histological 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 effectiveness of angiotensin‐converting enzyme (ACE) inhibitor treatment in post‐transplant IgAN was also studied in 10 patients.

Results. The prevalence of glomeruli with adhesions and/or cellular crescents in primary IgAN was significantly greater than in post‐transplant IgAN (P<0.05), but the proportion of glomeruli with segmental sclerosis was similar in both groups. The rate of global obsolescence, and the degree of interstitial fibrosis in post‐transplant IgAN were significantly greater than in primary IgAN (P<0.05). The degree of glomerular obsolescence and the severity of interstitial fibrosis correlated with the severity of glomerular lesion in primary IgAN, but not in post‐transplant IgAN. In primary IgAN, glomerular diameter significantly correlated with the proportions of glomerular obsolescence, but not in post‐transplant IgAN, suggesting that allograft kidneys may be in a hyperfiltration state.

Both the blood pressure and the urinary protein excretion significantly improved after ACE‐inhibitor treatment (P<0.001).

Conclusion. In post‐transplant IgAN, histopathological lesions indicative of acute inflammatory insults were suppressed, and glomerular hypertrophy, which may relate to haemodynamic burden such as hyperfiltration, was prominent. Preliminary study of ACE‐inhibitor treatment in 10 patients showed favourable effects. A future long‐term follow‐up study is required to establish the effectiveness of ACE inhibitors in treatment of post‐transplant IgAN.

Keywords: ACE inhibitors; graft function loss; hyperfiltration; kidney allograft; post‐transplant IgA nephropathy

Journal Article.  4219 words.  Illustrated.

Subjects: Nephrology

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