Zonal distribution of glomerular collapse in renal allografts: Possible role of vascular changes

Nádasdy, Tibor; Allen, C A; Zand, Martin S.

doi:10.1053/hupa.2002.124333

Cited by 63 publications

(36 citation statements)

References 10 publications

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“…Especially for FSGS NOS, careful attention is required for exclusion of another primary disease associated with FSGS and FSGS secondary to chronic allograft nephropathy or calcineurin inhibitors. 11 Howie et al 12 showed that FSGS NOS could occur in a later stage of patients with tip lesions. In our study, only one patient had the tip lesion variant of FSGS in the native kidney.…”

Section: Discussionmentioning

confidence: 99%

Fidelity and Evolution of Recurrent FSGS in Renal Allografts

IJpelaar¹,

Farris²,

Goemaere³

et al. 2008

Journal of the American Society of Nephrology

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Five pathologic variants of FSGS were recently defined ("Columbia classification"), but the stability of these phenotypes in renal allografts remains unknown. We hypothesized that if the variants represent distinct diseases, then the pattern of recurrent FSGS in renal allografts will mimic the original disease in the native kidney. This multicenter study included 21 cases of recurrent FSGS from 19 patients who had both native and transplant biopsy samples available for analysis. These results support the Columbia classification, because 81% recurred in the same pattern as the original disease, but three variants manifested plasticity from native to allograft kidneys or in the pattern of recurrence (four FSGS, not otherwise specified [NOS] to collapsing variant, two collapsing variant to FSGS NOS, and one cellular variant to FSGS NOS). No transitions between the cellular and the collapsing variants were observed, supporting the view that these are separate entities. Three categories of recurrence were observed: Type I, recurrence of the same variant of FSGS; type II, recurrence of the same FSGS variant, preceded by a minimal change-like lesion; and type III, recurrence of a different FSGS variant in the allograft. Thus, potential evolution of the pathologic phenotype should be considered in pathologic interpretation and clinical trials. Clinical features and prognosis differ for these FSGS variants. 5 For example, patients with a tip lesion generally present with severe nephrotic syndrome but are steroid sensitive and have the highest

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Section: Discussionmentioning

confidence: 99%

Fidelity and Evolution of Recurrent FSGS in Renal Allografts

IJpelaar¹,

Farris²,

Goemaere³

et al. 2008

Journal of the American Society of Nephrology

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“…More recently, a direct causal relationship between patchy infarction and de novo CG in transplanted kidneys has been reported by percutaneous imaging-directed needle biopsies [4]. Similarly, a direct topographic relationship between ischemia and CG has only been reported in transplanted kidneys by Nadasdy et al [5]. To date, no such direct relationship has been reported in native kidney specimens.…”

Section: To the Editormentioning

confidence: 95%

Glomerular collapse in a direct topographic relationship with patchy cortical infarction in a native nephrectomy specimen

Mubarak

Kazi

2012

Clin Exp Nephrol

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“…52 There is evidence that CIs can be associated with a de novo collapsing variant of FSGS in renal allografts. 53,54 This lesion may be augmented by hyperlipidemia and hypertension and may be a response to glomerular injury from ischemia, augmented by CsA. Clinically, patients have a heterogeneous presentation with massive proteinuria and graft dysfunction.…”

Section: Complications Of Therapeutic Agentsmentioning

confidence: 97%

“…55 This glomerular lesion has been observed to be focal in allograft nephrectomies. 54 Microcystic tubular dilatation, tubular epithelial degenerative change, and interstitial inflammation accompany the collapsing FSGS lesion.…”

Section: Complications Of Therapeutic Agentsmentioning

confidence: 99%

Renal Pathology in the Pediatric Transplant Patient

Vogler¹,

Wang²,

Brink³

et al. 2007

Advances in Anatomic Pathology

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Renal transplantation is a therapeutic goal for children with advanced chronic kidney disease. There are many causes of renal dysfunction in children with allografts--the transplanted kidney can develop a variety of morphologic alterations leading to dysfunction. Evaluation of the kidney biopsy is one of the best methods of determining the cause of graft dysfunction. Rejection is a major cause of renal allograft failure in children. The morphologic hallmarks of acute antibody-mediated and cell-mediated rejection and chronic allograft nephropathy have been codified in classification strategies that are useful in adults and children. Viral infection and Epstein-Barr virus-driven posttransplant lymphoproliferative disease also occur in the pediatric transplanted kidney. Drug toxicity from immunosuppressive agents also causes characteristic morphologic alterations in the renal allograft. As the survival of pediatric heart and liver transplant patients improves, the incidence of immunosuppression therapy-related disease in the native kidney in these patients will likely become more important clinically. In addition to renal lesions related to the allograft state, glomerular disease can recur or occur de novo in renal allografts. Here, we describe the pathology of the more common morphologic lesions in kidneys of children with a renal allograft.

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Zonal distribution of glomerular collapse in renal allografts: Possible role of vascular changes

Cited by 63 publications

References 10 publications

Fidelity and Evolution of Recurrent FSGS in Renal Allografts

Fidelity and Evolution of Recurrent FSGS in Renal Allografts

Glomerular collapse in a direct topographic relationship with patchy cortical infarction in a native nephrectomy specimen

Renal Pathology in the Pediatric Transplant Patient

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