Wegener's granulomatosis: Inflammatory cells and markers of repair and fibrosis in renal biopsies - A clinicopathological study

Citation
K. Aasarod et al., Wegener's granulomatosis: Inflammatory cells and markers of repair and fibrosis in renal biopsies - A clinicopathological study, SC J UROL N, 35(5), 2001, pp. 401-410
Citations number
58
Categorie Soggetti
Urology & Nephrology
Journal title
SCANDINAVIAN JOURNAL OF UROLOGY AND NEPHROLOGY
ISSN journal
00365599 → ACNP
Volume
35
Issue
5
Year of publication
2001
Pages
401 - 410
Database
ISI
SICI code
0036-5599(200110)35:5<401:WGICAM>2.0.ZU;2-7
Abstract
Objective: This study aimed to quantitate inflammatory cells in renal biops ies from patients with Wegener's granulomatosis (WG) and to identify cells participating in early fibrogenesis. The goal was to determine whether thes e cells correlated with the severity of renal disease and whether their pre sence had a hearing on renal prognosis. Material and Methods: Sixty-one patients with WG who had a renal biopsy tak en at the time of diagnosis were included in the study. Immunostaining with monoclonal antibodies towards macrophages (CD68), T- and B-lymphocytes, al pha -smooth muscle actin (alpha -SMA) and vimentin was done. Results: The dominating intraglomerular leucocytes were macrophages (29.9 /- 15 cells/glomerular cross-section) and to a lesser extent T-cells (2.57 +/- 1.8 cells/glomerular cross-section). No B-lymphocytes were detected in the glomeruli. More than two-thirds of the T-cells were CD8(+) (cytotoxic) cells. Macrophages and T-lymphocytes were distributed equally in the renal interstitium. and were numerous around crescentic glomeruli. Glomerular and interstitial macrophages and interstitial T-cells correlated significantly with serum (S-) creatinine at the time of biopsy but not after 1 year. S-c reatinine at the time of biopsy and after 1 year differed significantly amo ng the three levels of interstitial alpha -SMA staining. S-creatinine at bi opsy was highest when tubular vimentin staining was strongest, and tubular vimentin staining was strongest in patients with acute tubular damage. Conclusions: Evidence was found for a cellular type IV immune response in W G, with CD8(+) T-lymphocytes and macrophages dominating the cellular infilt rate. The detection of interstitial alpha -SMA, probably staining myofibrob lasts implicated in renal fibrogenesis, indicated a low glomerular filtrati on rate 1 year after renal biopsy.