Ultrastructural Features and Expression of Cytoskeleton Proteins of Podocyte from Patients with Minimal Change Disease and Focal Segmental Glomerulosclerosis

Shi, Sufang; Zhang, Youkang; Zhao, Ming‐Hui; Zou, Wan-zhong

doi:10.1080/08860220802060497

Cited by 10 publications

(10 citation statements)

References 25 publications

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“…Recurrent FSGS in renal transplants provides a unique opportunity to study the pathology of FSGS in human. Pathologically, MCD is usually the main histological feature at time of recurrence, with widespread foot process effacement and microvillous transformation of the podocytes (36, 37, 40–42). Serial biopsies taken 2–6 months after recurrence show reduced incidence of MCD over time, compared with increased incidence of FSGS with segmental FSGS lesion, podocyte detachment and epithelial hypercellularity, and accumulation of intracapillary foam cells (Fig.…”

Section: Recurrence Of Fsgs After Renal Transplantationmentioning

confidence: 99%

“…Thus, structural and functional abnormalities of podocytes cause permeability changes associated with proteinuria as well as glomerular capillary collapse with segmental sclerosis in FSGS. The morphological findings of podocyte injuries in FSGS are characterized by diffuse effacement of podocyte foot processes, detachment from GBM and loss of podocytes, and epithelial hyperplasia in glomeruli (40, 41). Recurrent FSGS with nephrotic syndrome frequently occurs within weeks of kidney transplantation, but the typical histopathological lesion of FSGS might not be observed until 4–6 wk after the transplantation (36, 37, 40).…”

Section: Pathogenesis Of Recurrent Fsgs After Transplantationmentioning

confidence: 99%

“…Recurrent FSGS with nephrotic syndrome frequently occurs within weeks of kidney transplantation, but the typical histopathological lesion of FSGS might not be observed until 4–6 wk after the transplantation (36, 37, 40). However, electron microscopic evaluation of the glomeruli often reveals diffuse effacement of the podocyte foot processes within days after the onset of proteinuria (40–42). Subsequently, detachment and loss of podocytes and epithelial cell hyperplasia occur with the development of segmental FSGS lesions.…”

Section: Pathogenesis Of Recurrent Fsgs After Transplantationmentioning

confidence: 99%

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Focal segmental glomerulosclerosis after renal transplantation

Shimizu¹,

Higo²,

Fujita

et al. 2011

Clinical Transplantation

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Shimizu A, Higo S, Fujita E, Mii A, Kaneko T. Focal segmental glomerulosclerosis after renal transplantation. Clin Transplant 2011: 25 (Suppl. 23): 6–14. © 2011 John Wiley & Sons A/S. Abstract: Focal segmental glomerulosclerosis (FSGS) is a clinicopathologic syndrome of proteinuria, usually of nephrotic range, associated with focal and segmental sclerotic glomerular lesions. Therefore, FSGS is diagnosed by clinical features and histopathological examination of renal biopsy. The natural history of the condition varies, and although it may respond to treatment, FSGS is an important disease in the etiology of end‐stage renal disease (ESRD). Furthermore, after kidney transplantation, approximately 30% of patients with FSGS develop recurrent FSGS. The risk factors for recurrence of FSGS include childhood onset and age <15 yr, rapid progression of the primary FSGS to ESRD, recurrence of FSGS in a previous allograft, diffuse mesangial hypercellularity in the native kidney, collapsing FSGS, and podocin gene mutation. In addition, after kidney transplantation, de novo FSGS also develops in approximately 10–20% of allografts, associated with a complication of hyperfiltration injury, chronic transplant glomerulopathy, and calcineurin inhibitor toxicity. FSGS is considered a podocyte disease, and the pathology is characterized by segmental FSGS lesion with glomerular epithelial hypercellularity. The pathological diagnosis of FSGS is based on the 2004 Columbia classification system. In the present minireview, we discuss the pathology of recurrence and de novo FSGS after kidney transplantation.

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Section: Recurrence Of Fsgs After Renal Transplantationmentioning

confidence: 99%

Section: Pathogenesis Of Recurrent Fsgs After Transplantationmentioning

confidence: 99%

Section: Pathogenesis Of Recurrent Fsgs After Transplantationmentioning

confidence: 99%

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Focal segmental glomerulosclerosis after renal transplantation

Shimizu¹,

Higo²,

Fujita

et al. 2011

Clinical Transplantation

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“…However, compared to MCD, more severe alterations in podocyte were identified, which are characterized by a higher frequency of detachment of the foot process from GBM, leading to a synechia and, finally, sclerosis in FSGS [24,25]. Recently, we reported that FSP1 expression was identified in injured podocytes of diabetic nephropathy [19], suggesting podocyte mesenchymal transition could be a potential pathway leading to podocyte dysfunction and detachment from GBM.…”

Section: Discussionmentioning

confidence: 99%

Clinical Significance of Fibroblast-Specific Protein-1 Expression on Podocytes in Patients with Focal Segmental Glomerulosclerosis

et al. 2011

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Backgrounds/Aims: We previously reported that fibroblast-specific protein 1 (FSP1) is a marker of epithelial-mesenchymal transition (EMT) in tubulointerstitial fibrosis. The EMT-like changes observed in podocytes are reportedly associated with podocyte detachment which may cause focal glomerulosclerosis. Methods: In cross-sectional studies, we analyzed podocyte expression of FSP1 immunohistochemically using renal biopsy specimens from 31 patients with focal segmental glomerulosclerosis (FSGS) and 39 patients with minimal change disease (MCD). We also semiquantitatively analyzed glomerular expression of FSP1 mRNA using laser capture microdissection and real-time PCR. Results: We found that FSP1 was localized to podocytes in both FSGS and MCD patients; however, the number of FSP1⁺ podocytes per glomerular profile was significantly higher in patients with FSGS than in those with MCD, and there was a corresponding difference in the levels of FSP1 mRNA. FSP1⁺ podocyte counts per glomerular profile in FSGS patients correlated significantly with the prevalence of glomerulosclerosis and the extent of interstitial type-I collagen-positive areas. Conclusion: Taken together, these data suggest that podocyte expression of FSP1 could shed light on the potential linkage between EMT-like changes, detachment of podocytes from the glomerular basal membrane and the pathophysiology underlying FSGS.

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“…This finding, if confirmed by western blot analysis and further characterized, might become very valuable. In fact, actin isoform disarrangement is thought to be pivotal in podocyte dysfunction, where severe cytoskeletal ultrastructural alterations are clearly associated with focal segmental glomerulosclerosis [35,36], the initial lesion of glomerular scarring. If confirmed, γ-smooth increase might reflect a mesangial cell dysfunction, playing a core role in diabetic nephropathy.…”

Section: Protein Idmentioning

confidence: 99%