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Fidelity and Evolution of Recurrent FSGS in Renal Allografts

Daphne H.T. IJpelaar^*, Alton B. Farris, Natascha Goemaere, Kerstin Amann, Roel Goldschmeding^||, Tri Q. Nguyen^||, Evan Farkash, Marius C. van den Heuvel^¶, Emile de Heer^*, Jan A. Bruijn^*, Robert B. Colvin and Ingeborg M. Bajema^*

^* Department of Pathology, Leiden University Medical Center, Leiden, Netherlands; Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; Department of Pathology, Erasmus University Medical Center, Rotterdam, Netherlands; Department of Pathology, University of Erlangen-Nürnberg, Erlangen, Germany; ^|| Department of Pathology, University Medical Center Utrecht, Utrecht, Netherlands; and ^¶ Department of Pathology, University Medical Center Groningen, Groningen, Netherlands

Correspondence: Dr. Daphne H.T. IJpelaar, Leiden University Medical Center, Department of Pathology, Building 1, L1Q, P.O. Box 9600, 2300 RC Leiden, Netherlands. Phone: +31-71-526-6574; Fax: +31-71-524-8158; E-mail: d.ijpelaar{at}lumc.nl

Received for publication December 22, 2007. Accepted for publication May 1, 2008.

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.

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673