Peritubular capillary basement membrane reduplication in allografts and native kidney disease - A clinicopathologic study of 278 consecutive renal specimens
J. Gough et al., Peritubular capillary basement membrane reduplication in allografts and native kidney disease - A clinicopathologic study of 278 consecutive renal specimens, TRANSPLANT, 71(10), 2001, pp. 1390-1393
Background. An association has been found between transplant glomerulopathy
(TG) and reduplication of peritubular capillary basement membranes (PTCR).
Although such an association is of practical and theoretical importance, o
nly one prospective study has tried to confirm it.
Methods. We examined 278 consecutive renal specimens (from 135 transplants
and 143 native kidneys) for ultrastructural evidence of PTCR, In addition t
o renal allografts with TG, we also examined grafts with acute rejection, r
ecurrent glomerulonephritis, chronic allograft nephropathy and stable graft
s ("protocol biopsies"). Native kidney specimens included a wide range of g
lomerulopathies as well as cases of thrombotic microangiopathy, malignant h
ypertension, acute interstitial nephritis, and acute tubular necrosis.
Results. We found PTCR in 14 of 15 cases of TG, in 7 transplant biopsy spec
imens without TG, and in 13 of 143 native kidney biopsy specimens. These 13
included cases of malignant hypertension, thrombotic microangiopathy, lupu
s nephritis, Henoch-Schonlein nephritis, crescentic glomerulonephritis, and
cocaine-related acute renal failure. Mild PTCR in allografts without TG di
d not predict renal failure or significant proteinuria after follow-up peri
ods of between 3 months and 1 year.
Conclusions. We conclude that in transplants, there is a strong association
between well-developed PTCR and TG while the significance of mild PTCR and
its predictive value in the absence of TG is unclear. PTCR also occurs in
certain native kidney diseases, though the association is not as strong as
that for TG. We suggest that repeated endothelial injury, including immunol
ogic injury, may be the cause of this lesion both in allografts and native
kidneys.