Many primary glomerular diseases can recur in the allograft. Before making such a diagnosis, it is necessary to exclude donor transmitted disease, and glomerular pathology developing de novo after transplantation. The incidence and severity of disease recurrence varies with the native disease.

Focal segmental glomerulosclerosis (FSGS) recurs in 30 to 50% of cases. Clinical onset of proteinuria is usually within the first few months of transplantation, and in some cases, within a few days of surgery, suggesting the involvement of a circulating factor in the pathogenesis of this disease. Graft loss occurs at a variable rate, and may be as early as within a year of diagnosis.

Membranous glomerulonephritis (MGN) recurs in 25 to 50% of patients, typically a year or more after transplantation. It is associated with gradual graft loss occurring over 2-7 years. The occurrence of denovo MGN after renal transplantation should prompt investigations for Hepatitis B and C infection. A history of horse anti-thymocyte globulin therapy can be elicited in some patients.

Membranoproliferative glomerulonephritis (MPGN) type 1 reportedly recurs in 30 to 40% of renal allografts. The recurrence may be asymptomatic in up to 30% of individuals, but typically leads to slowly progressive graft loss. Recurrent MPGN type 2 (dense deposit disease) has a 90% incidence of recurrence ultrastructurally: immune complex deposits can be seen in the GBM lamina densa within 6-9 months of transplantation. Approximately 30-40% of patients remain clinically asymptomatic. The remainder show 40-50% graft loss within 2 years. The light microscopic appearance in MPGN type 2 is indistinguishable from MPGN type 1.

Renal transplantation for IgA nephropathy is followed by recurrent disease in up to 50% of the cases, consistent with the notion that the disease is a manifestation of excessive IgA immune complex production at mucosal surfaces. Since this basic immune dysfunction is not altered by the transplant procedure, IgA immune complexes get readily re-deposited within the allograft. Clinical manifestations are noted 3 months to 4 years after surgery, and generally consist of only mild proteinuria. Progressive disease is relatively uncommon.

Diabetes mellitus is a common indication for renal transplantation. Since the underlying metabolic defect is not corrected by transplantation, progressive structural changes are demonstrable in serial allograft biopsies examined by ultrastructural and morphometric techniques. However, clinically significant recurrent diabetic nephropathy develops very slowly.


  1. Mathew TH. Recurrence of disease following renal transplantation. Am J Kidney Dis 12(2):85-96, 1988.
  2. Verani R and Dan M. Membranous glomerulonephritis in renal transplant. A case report and review of the literature. Am J Nephrol 2(6):316-320, 1982.
  3. Moritz MJ, Burke JF, Jarrell BE, et al. The incidence of membranoproliferative glomerulonephritis in renal allografts. Transplant Proc 19(1 Pt 3):2206-2207, 1987.
  4. Bennett WM, Fassett RG, Walker RG, et al. Mesangiocapillary glomerulonephritis type II (dense-deposit disease): clinical features of progressive disease. Am J Kidney Dis 13(6):469-476, 1989.
  5. Suganuma T, Morozumi K, Satoh K, et al. Studies of IgA nephropathy in renal transplantation. Transplant Proc 21(1 Pt 2):2123-2127, 1989.
  6. Osterby R, Nyberg G, Persson H, et al. Early glomerulopathy in kidneys transplanted into diabetic patients. Transplant Proc 23(1 Pt 2):1270, 1991.
  7. Porter KA. Renal transplantation. In: Pathology of the Kidney Ed. RH Heptinstall. Little Brown & Co. Boston 1799-1934, 1992.

Please mail comments, corrections or suggestions to the TPIS administration at the UPMC.

University of Pittsburgh. All rights reserved. Unauthorized redistribution prohibited.

Last Modified: Thu Jun 18 10:14:08 EDT 2009


Please give your feedback about this page here:


If you have more questions, you can always email TPIS Administration.