| Autor: |
Tominaga K; Department of Nephrology, Self-Defense Forces Central Hospital, Setagaya 154-8532, Japan.; Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Hachioji 193-0998, Japan., Oda T; Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Hachioji 193-0998, Japan., Iwama S; Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Hachioji 193-0998, Japan., Kojima T; Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Hachioji 193-0998, Japan., Konno O; Department of Kidney Transplantation Surgery, Kidney Disease Center, Tokyo Medical University Hachiouji Medical Center, Hachioji 193-0998, Japan., Yamada M; Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Hachioji 193-0998, Japan., Nakabayashi I; Department of Nephrology, Fussa Hospital, Fussa 197-8511, Japan., Iwamoto H; Department of Kidney Transplantation Surgery, Kidney Disease Center, Tokyo Medical University Hachiouji Medical Center, Hachioji 193-0998, Japan. |
| Abstrakt: |
We report the histological changes over time for a patient with infection-related glomerulonephritis (IRGN) that developed in a transplanted kidney. A 47-year-old man had undergone renal transplantation 3 years ago for end-stage kidney disease (ESKD). After several episodes of acute rejection, the patient was in a stable CKD condition. The abrupt development of severe microscopic hematuria and renal dysfunction was observed approximately 2 weeks after the onset of a phlegmon in his right leg. An allograft biopsy showed prominent glomerular endocapillary proliferation on light microscopy, granular C3 deposition on immunofluorescent microscopy, and subepithelial electron-dense deposits on electron microscopy, suggesting IRGN accompanied by moderate interstitial fibrosis and tubular atrophy (IFTA). Positive glomerular staining for nephritis-associated plasmin receptor (NAPlr) and plasmin activity, which are biomarkers of bacterial IRGN, supported the diagnosis. Although the infection was completely cured with antibiotic therapy, renal dysfunction persisted. A re-biopsy of the allograft 2 months later revealed resolution of the glomerular endocapillary proliferation and negative staining for NAPlr/plasmin activity, with worsening IFTA. We showed, for the first time, the chronological changes in infiltrating cells and histological markers of IRGN in transplanted kidneys. Glomerular changes, including NAPlr/plasmin activity staining, almost disappeared after the cessation of infection, while interstitial changes continuously progressed, contributing to ESKD progression. |
