Published online Dec 24, 2017. doi: 10.5500/wjt.v7.i6.285
Peer-review started: September 15, 2017
First decision: October 24, 2017
Revised: November 2, 2017
Accepted: November 10, 2017
Article in press: November 10, 2017
Published online: December 24, 2017
Processing time: 101 Days and 10.6 Hours
The glomerular diseases after renal transplantation can occur de novo, i.e., with no relation to the native kidney disease, or more frequently occur as a recurrence of the original disease in the native kidney. There may not be any difference in clinical features and histological pattern between de novo glomerular disease and recurrence of original glomerular disease. However, structural alterations in transplanted kidney add to dilemma in diagnosis. These changes in architecture of histopathology can happen due to: (1) exposure to the immunosuppression specifically the calcineurin inhibitors (CNI); (2) in vascular and tubulointerstitial alterations as a result of antibody mediated or cell-mediated immunological onslaught; (3) post-transplant viral infections; (4) ischemia-reperfusion injury; and (5) hyperfiltration injury. The pathogenesis of the de novo glomerular diseases differs with each type. Stimulation of B-cell clones with subsequent production of the monoclonal IgG, particularly IgG3 subtype that has higher affinity to the negatively charged glomerular tissue, is suggested to be included in PGNMID pathogenesis. De novo membranous nephropathy can be seen after exposure to the cryptogenic podocyte antigens. The role of the toxic effects of CNI including tissue fibrosis and the hemodynamic alterations may be involved in the de novo FSGS pathophysiology. The well-known deleterious effects of HCV infection and its relation to MPGN disease are frequently reported. The new concepts have emerged that demonstrate the role of dysregulation of alternative complement pathway in evolution of MPGN that led to classifying into two subgroups, immune complex mediated MPGN and complement-mediated MPGN. The latter comprises of the dense deposit disease and the C3 GN disease. De novo C3 disease is rather rare. Prognosis of de novo diseases varies with each type and their management continues to be empirical to a large extent.
Core tip: The role of post-transplant glomerulonephritis in affecting both patient and allograft survival is well documented. For decades recurrent glomerular diseases after renal transplantation have been thoroughly investigated. On the other hand a group of a newly classified de novo glomerular diseases attained an increasing interest. However, the paucity of data concerned with de novo glomerular diseases after renal transplantation have been shown to be a great obstacle necessitating more active cooperation between transplant centers. A thorough work up is clearly warranted to declare not only their pathogenesis, but also to draw the proper therapeutic plan.