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Zonal distribution of glomerular collapse in renal allografts: possible role of vascular changes
Tibor Nadasdy1, Carol Allen, Martin S Zand
1Department of Pathology, The Johns Hopkins University, Baltimore, MD, USA.
Insights
Collapsing glomerulopathy in kidney transplants may differ from native kidney disease. These cases suggest collapsing glomerular changes represent a pattern of injury, not a distinct disease entity.
Area of Science:
- Nephrology
- Transplant Pathology
- Renal Histology
Background:
- Collapsing glomerulopathy (CG) is an aggressive kidney disease characterized by proteinuria and rapid renal failure, often resembling HIV-associated nephropathy but occurring in HIV-negative individuals.
- The characteristic lesion involves glomerular capillary loop collapse and podocyte proliferation within Bowman's space, typically with severe tubulointerstitial injury.
- CG has been observed de novo in renal allografts, but its presentation and association with proteinuria in transplants may differ from native kidneys.
Observation:
- This study reports on three allograft nephrectomy specimens exhibiting zonal collapsing glomerular changes and tubulointerstitial injury.
- Allograft specimens demonstrated obliterative vascular changes, including chronic transplant arteriopathy, acute vascular rejection, and thrombotic microangiopathy.
- Notably, none of the patients with these allograft findings presented with severe proteinuria.
Findings:
- The morphologic pattern of collapsing glomerulopathy in renal allografts may represent a distinct process compared to CG in native kidneys.
- Collapsing glomerular changes in allografts, particularly when associated with vascular pathology, do not consistently correlate with severe proteinuria.
- These findings challenge the notion that collapsing glomerular changes alone define the disease entity of CG.
Implications:
- Collapsing glomerular changes in renal allografts may indicate a pattern of injury rather than a specific disease entity, potentially influenced by factors like hemodynamic disturbances.
- Further research is needed to elucidate the specific pathogenetic mechanisms of CG in the context of renal transplantation.
- Distinguishing CG in allografts from native kidneys is crucial for accurate diagnosis and management of kidney transplant recipients.
Abstract:
Collapsing glomerulopathy (CG), an aggressive variant of focal segmental glomerular sclerosis, is a renal disease with severe proteinuria and rapidly progressive renal failure. The pathogenesis of CG is unknown. It strongly resembles human immunodeficiency virus (HIV)-associated nephropathy, but the patients are HIV negative. The characteristic glomerular lesion is capillary loop collapse with prominent podocytes filling Bowman's space. Interestingly, these glomerular changes are usually associated with severe tubulointerstitial injury, including tubular epithelial degenerative changes, microcystic dilation of several tubules, and interstitial inflammatory cell infiltrate. Recently, it became evident that the morphologic pattern of CG may appear not only in native kidneys, but also de novo in renal allografts, and that the pattern of CG in renal transplants is not always associated with severe proteinuria. Studies describing CG in renal allografts are all based on biopsies. We report 3 allograft nephrectomy specimens that showed a zonal distribution of the characteristic collapsing glomerular changes with associated tubulointerstitial injury. All 3 kidneys had obliterative vascular changes. One nephrectomy specimen had chronic obliterative transplant arteriopathy, 1 had acute vascular rejection, and 1 had thrombotic microangiopathy. None of the patients had severe proteinuria. Our cases suggest that the morphologic pattern of CG in renal allografts may not represent the same disease process as CG in native kidneys and provide further evidence that collapsing glomerular changes do not define the disease entity of CG, but rather represent a pattern of renal injury. Among other factors, hemodynamic disturbance may play a role in the development of the pattern of CG in renal allografts.