Many renal transplants undergo gradual deterioration in structure and
function in the months or years after transplantation. The processes t
hat underlie this progressive decline have not been defined, and may i
nclude immunological and nonimmunological mechanisms. The present expe
riments were designed to investigate the glomerular capillary hydrosta
tic pressure in long-surviving rat renal transplants with or without c
hronic rejection. Stop-flow glomerular pressures were measured in F344
renal allografts with chronic rejection, syngeneic F344 grafts, and l
ong-surviving syngeneic and allogeneic LEW grafts without chronic reje
ction; control measurements were done in nontransplanted intact animal
s or after subtotal renal ablation. Renal ablation or transplantation
resulted in increased glomerular pressure in F344 but not LEW kidneys;
the glomerular pressure in syngeneic F344 grafts was not different fr
om that in allogeneic F344 grafts. There was no correlation between th
e mean arterial pressure and the glomerular capillary pressure. Our da
ta suggest that the glomerular capillary pressure is determined by loc
al intrarenal factors. The glomerular capillary pressure in allotransp
lanted kidneys resembles that of the donor kidney after subtotal renal
ablation. The importance of increased glomerular pressure in the prog
ressive decline of graft function of chronic rejection remains to be e
stablished.