Peritubular capillary basement membrane reduplication in allografts and native kidney disease - A clinicopathologic study of 278 consecutive renal specimens

Citation
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
Citations number
18
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
TRANSPLANTATION
ISSN journal
00411337 → ACNP
Volume
71
Issue
10
Year of publication
2001
Pages
1390 - 1393
Database
ISI
SICI code
0041-1337(20010527)71:10<1390:PCBMRI>2.0.ZU;2-C
Abstract
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.