Mast cells in human allografted kidney: correlation with interstitial fibrosis.
BACKGROUND
Chronic allograft nephropathy is the major cause of long-term graft failure in human allografted kidney transplantation. In addition to macrophages and T lymphocytes, mast cells have been shown to increase in chronic allograft nephropathy. The present study examined tryptase-positive mast cells and microvessels in the allografted kidney.


METHODS
We selected 131 biopsy specimens obtained from 100 allografted, 14 non-grafted renal biopsy specimens and nine nephrectomy specimens due to renal cell carcinomas. Formalin-fixed, paraffin- embedded specimens were immunostained using primary antibodies for mast cell tryptase, mast cell chymase and CD34. The number of the mast cells and microvessels was counted in at least 20 high-power fields (10 x 40).


RESULTS
Tryptase-positive mast cells outnumbered chymase, toluidine blue or naphthol-AS-D choloacetate-positive mast cells. The mean number of the tryptase-positive mast cells was significantly higher in the 36 specimens with chronic allograft nephropathy (5.1 +/- 3.5) among the grafted kidneys with other disease categories (P < 0.001). In the chronic allograft nephropathy, the mean numbers of mast cells was significantly higher in Ci 2 + Ci 3 (n = 20; 6.4 +/- 3.89) than in Ci 1 (n = 16; 3.6 +/- 2.65) (P < 0.01). In the non-grafted kidney, the number of mast cells was highest in the four specimens with diabetic nephropathy. Mast cells and microvessels were analysed in the two representative cases, which subsequently developed chronic allograft nephropathy. Both of the cases showed the highest number of mast cells in chronic allograft nephropathy. In contrast, the mean number of microvessels tended to decrease along with interstitial fibrosis.


CONCLUSIONS
This study demonstrated clearly a close association between renal interstitial fibrosis and mast cells, which might play an important role in the development of chronic allograft nephropathy.
Goto
Eizo
E
Division of Organ Pathology, Department of Microbiology and Pathology, Faculty of Medicine, Tottori University, Yonago, Japan.
Honjo
Soichiro
S
Yamashita
Hideki
H
Shomori
Kohei
K
Adachi
Hironobu
H
Ito
Hisao
H
D002452:Cell Count; D002908:Chronic Disease; D003928:Diabetic Nephropathies / Q000473:pathology; D005355:Fibrosis / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D007668:Kidney / Q000473:pathology*; D007674:Kidney Diseases / Q000473:pathology; D016030:Kidney Transplantation; D008407:Mast Cells / Q000473:pathology*; D008833:Microcirculation / Q000473:pathology; D011183:Postoperative Complications; D014184:Transplantation, Homologous