Mast cells (MCs), few in the normal kidney, are found in increased num
ber in the renal parenchyma in diseases associated with persistent chr
onic inflammation. MCs are not easily identified in routinely processe
d archival tissue sections with histochemical stains. A more reliable
method of detection was provided with the introduction of MC tryptase-
specific monoclonal antibodies. To determine the possible role of MCs
in renal allograft rejection, we studied 28 biopsy specimens from rena
l allografts that had been in place for various lengths of time (from
3 days to 40 months) in patients whose primary diagnosis was acute int
erstitial rejection; die specimens were associated with varying degree
s of interstitial fibrosis, edema, and hemorrhage. The specimens were
graded on a semiquantitative scale (from 0 to 3+) for the severity of
rejection, the degree of interstitial fibrosis, interstitial edema, an
d interstitial hemorrhage. Eosinophils, plasma cells, and MCs were qua
ntitatively evaluated in these biopsy specimens. MCs were detected by
use of a commercially available anti-MG tryptase monoclonal antibody,
which proved to be an excellent tool to detect MCs in routinely proces
sed paraffin sections. A positive correlation was found between the nu
mber of MCs and the time since transplantation (R = 0.841, P < 0.005)
and between the number of MCs and the severity of interstitial fibrosi
s (R = 0.489, P < 0.005), as well as with interstitial edema (R = 0.51
7, P < 0.005). MCs were increased in number in patients with moderate
(n = 18; mean, 18.00 MCs per 10 high power fields [HPFs]) and severe (
n = 5; mean, 12.20 MCs per 10 HPFs) acute rejection compared with pati
ents with mild (n = 5; mean, 2.44 MCs per 10 HPFs) acute rejection and
normal kidneys (n = 6; mean, 1.75 MCs per 10 HPFs). These results sug
gested that MCs might play a role in the process of acute rejection of
renal allografts and in the development of interstitial fibrosis.