Evidence Suggesting Persistence of Nephritogenic Immunopathologic Mechanisms in Patients Receiving Renal Allografts

Abstract

A B S T R A C T Direct immunofluorescent (IF)exami

Renal Transplantation in Systemic Lupus erythematosus

“…The possibility that glomerulonephritis can recur in kid ney allografts has always been a real concern among workers in renal transplantation since the initial clinical experience on renal transplantation carried out on identi cal twins [8], Since neither morphologic nor immunohisto chemical criteria alone can differentiate between recurrent glomerulonephritis and the glomerular lesion that occurs in chronic allograft rejection, the distinction had to await discovery of a marker that would be diagnostic of the origi nal disease [6,9], The demonstration of anti-GBM anti body deposits in the allografts of patients with Good pasture's syndrome was firm evidence for recurrent disease [9], Indeed, the presence of anti-GBM antibody in the serum of these patients at the time of transplantation was predictive of recurrence of the original lesion in the allo graft kidney [10]. Edington et al [II] have also demon strated that the recurrence of Heymann nephritis in iso geneic transplants in rats was associated with the deposi tion in the allograft kidneys of RTE-y5 and a-globuiin.…”

Evaluation of Percutaneous Kidney Biopsy in Advanced Renal Failure

“…D ixon et al [24] and others [25][26][27] have pointed to a similar situation in the case of those patients with crescentic glomerulonephritis and serum antibodies directed against glomerular basement membrane. Biopsy in these patients with crescentic or rapidly progressive glomerulonephritis of an idio pathic nature in whom anliglomerular basement membrane antibodies can be demonstrated, has the same prognostic and therapeutic implications in that reoccurrence of the original disease is likely to ensue in the graftedkidney.…”

Percutaneous renal graft biopsy: a clinical, laboratory and pathological analysis

“…Post-transplant glomerulonephritis is frequent, but classification as de novo, recurrent or indeterminate is difficult since the primary renal disease is rarely diagnosed. Such glomerulonephritis can be due to persistent systemic factors, 13 donor glomerular disease, 14 ischemic lesions, hypertension or secondary to acute rejection episodes. 8 Following its introduction, cyclosporine has been found to be a further factor causing glomerular lesions 15,16 Histologically, glomerular lesions can be superposed since, as with ischemia, hypertension and immunological or toxic factors, the pathogenic mechanisms can lead to endothelial injury 17 which in turn produces focal and segmental glomerulosclerosis, usually in the vascular pole of the glomerulus.…”