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Updated: Feb 15, 2026
Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases?
Fedaey Abbas1, Mohsen El Kossi2, Jon Kim Jin2
1Department of Nephrology, Jaber El Ahmed Military Hospital, Safat 13005, Kuwait.
Insights
Glomerular diseases post-renal transplant can be new or recurrent, presenting diagnostic challenges. Understanding their distinct paths, like PGNMID, CNI effects in FSGS, and complement dysregulation in MPGN, is key.
Area of Science:
- Nephrology
- Transplantation Immunology
- Pathology
Background:
- Glomerular diseases after renal transplantation are a significant clinical concern.
- These diseases can arise de novo or as a recurrence of the original native kidney disease.
- Distinguishing between de novo and recurrent glomerular disease is often challenging due to similar clinical and histological features, compounded by structural changes in the transplanted kidney.
Purpose of the Study:
- To explore the diverse pathogenesis of de novo glomerular diseases following renal transplantation.
- To highlight the diagnostic complexities arising from structural alterations in transplanted kidneys.
- To review the specific mechanisms involved in various de novo glomerular diseases, including PGNMID, membranous nephropathy, FSGS, and MPGN.
Main Methods:
- Review of existing literature on de novo and recurrent glomerular diseases post-renal transplantation.
- Analysis of pathogenetic mechanisms for specific types of de novo glomerular diseases.
- Discussion of factors contributing to diagnostic challenges, including immunosuppression effects and post-transplant complications.
Main Results:
- De novo glomerular diseases have varied etiologies, distinct from recurrence.
- Pathogenesis includes B-cell stimulation (PGNMID), podocyte antigens (membranous nephropathy), calcineurin inhibitor (CNI) toxicity and hemodynamic changes (FSGS), and HCV infection or complement dysregulation (MPGN).
- Structural alterations from CNI, immunological injury, viral infections, ischemia-reperfusion, and hyperfiltration complicate diagnosis.
Conclusions:
- De novo glomerular diseases represent a heterogeneous group with distinct pathogenetic pathways.
- Accurate diagnosis is crucial but challenging due to superimposed structural changes in the allograft.
- Management remains largely empirical, underscoring the need for further research into specific disease mechanisms and targeted therapies.
Abstract:
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.
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