Literature survey, thus far, has shown a decrease in the excretion of
urinary tissue kallikrein (TK) in transplant patients with a further r
eduction of the enzyme during episodes of acute rejection. The study a
ims were to compare, at cellular and subcellular levels, the localisat
ion of tissue kallikrein in biopsies of the transplant kidney to autop
sy derived normal renal tissue. Renal biopsies from eighteen transplan
t patients with deteriorating renal function were obtained. Immunolabe
lling for tissue kallikrein, using a polyclonal goat anti-TK, antibody
raised against recombinant TK, was performed following routine enzyma
tic, immunofluorescence and electron microscopic techniques. In normal
kidney tissue, TK was immunolocalised in the distal connecting tubule
s and collecting ducts. By comparison the renal transplant tissue show
ed a reduction in the intensity of label, but maintained the sites of
localisation. In the sections examined by electron microscopy, althoug
h TK was confined mainly at the luminal side of the cell, some label w
as noted along the basolateral membranes. In the transplant kidneys, t
here was a reduction in the overall number of gold particles counted,
which correlated with the decreased intensity observed on immunocytoch
emistry. In addition, there was a shift to a basolateral orientation o
f the immunolabel, Acute rejection is characterised by oedema, tubulit
is and vasculitis. Destruction of the tubule cells and leakage of TK i
nto the interstitial tissue space and the resultant effect of the form
ed kinins on renal capillary vasculature could explain the observed re
nal parenchymal oedema and transplant rejection.