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Immune Complex-Type Deposits in the Fischer-344 to Lewis Rat Model of Renal Transplantation and a Subset of Human Transplant Glomerulopathy

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Immune Complex-Type Deposits in the Fischer-344 to Lewis Rat Model of Renal Transplantation and a Subset of Human Transplant Glomerulopathy. / Grau, Veronika; Zeuschner, Philip; Immenschuh, Stephan; Bockmeyer, Clemens Luitpold; Zell, Stefanie; Wittig, Juliane; Säuberlich, Karen; Abbas, Mahmoud; Padberg, Winfried; Meyer-Schwesinger, Catherine; von Brandenstein, Melanie; Schlosser, Monika; Dieplinger, Georg; Galliford, Jack; Clarke, Candice; Roufosse, Candice; Becker, Jan Ulrich.

In: TRANSPLANTATION, Vol. 100, No. 5, 05.2016, p. 1004-14.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Grau, V, Zeuschner, P, Immenschuh, S, Bockmeyer, CL, Zell, S, Wittig, J, Säuberlich, K, Abbas, M, Padberg, W, Meyer-Schwesinger, C, von Brandenstein, M, Schlosser, M, Dieplinger, G, Galliford, J, Clarke, C, Roufosse, C & Becker, JU 2016, 'Immune Complex-Type Deposits in the Fischer-344 to Lewis Rat Model of Renal Transplantation and a Subset of Human Transplant Glomerulopathy', TRANSPLANTATION, vol. 100, no. 5, pp. 1004-14. https://doi.org/10.1097/TP.0000000000001068

APA

Grau, V., Zeuschner, P., Immenschuh, S., Bockmeyer, C. L., Zell, S., Wittig, J., Säuberlich, K., Abbas, M., Padberg, W., Meyer-Schwesinger, C., von Brandenstein, M., Schlosser, M., Dieplinger, G., Galliford, J., Clarke, C., Roufosse, C., & Becker, J. U. (2016). Immune Complex-Type Deposits in the Fischer-344 to Lewis Rat Model of Renal Transplantation and a Subset of Human Transplant Glomerulopathy. TRANSPLANTATION, 100(5), 1004-14. https://doi.org/10.1097/TP.0000000000001068

Vancouver

Grau V, Zeuschner P, Immenschuh S, Bockmeyer CL, Zell S, Wittig J et al. Immune Complex-Type Deposits in the Fischer-344 to Lewis Rat Model of Renal Transplantation and a Subset of Human Transplant Glomerulopathy. TRANSPLANTATION. 2016 May;100(5):1004-14. https://doi.org/10.1097/TP.0000000000001068

Bibtex

@article{bf4f391a10184dd09ea56b05bff27af8,
title = "Immune Complex-Type Deposits in the Fischer-344 to Lewis Rat Model of Renal Transplantation and a Subset of Human Transplant Glomerulopathy",
abstract = "BACKGROUND: Antibody-mediated rejection is a leading cause for renal transplant loss. Rodent models are useful to dissect pathomechanisms and to develop treatment strategies. Although used for decades as a model, glomerular histopathological findings of Fischer-344 kidneys transplanted into Lewis rats have never been comprehensively described.METHODS: Kidneys from Fischer-344 rats were transplanted into Lewis rats as life-sustaining allografts without immunosuppression. Lewis isografts and normal Fischer-344 kidneys served as controls. Grafts were harvested at 9 days, 6 and 26 weeks. Histopathological examination included light microscopy, immunohistochemistry, and morphometry. Findings were compared with 51 human biopsies with transplant glomerulopathy.RESULTS: Most glomerular findings in rat allografts resembled human acute and chronic antibody-mediated rejection with glomerulitis, microthrombosis, microaneurysms, glomerular hypertrophy, podocyte loss, glomerular basement membrane splitting, and secondary focal and segmental glomerulosclerosis. In line with previous reports on nonendothelial antigens, glomerular immunoglobulin and C4d deposition was mostly nonendothelial. Only in 26-week allografts, we found mesangial and subendothelial immune complex-type electron-dense deposits. Similar deposits were found in 8 of 51 human biopsies with transplant glomerulopathy after rigorous exclusion of immune complexes of other cause, particularly recurrent glomerulonephritis and hepatitis C.CONCLUSIONS: Thus, our model closely reflects the glomerular changes of acute antibody-mediated rejection in humans and of a special subset of human transplant glomerulopathy. The significance of alloimmune immune complex-type deposits in human transplants deserves further investigation.",
author = "Veronika Grau and Philip Zeuschner and Stephan Immenschuh and Bockmeyer, {Clemens Luitpold} and Stefanie Zell and Juliane Wittig and Karen S{\"a}uberlich and Mahmoud Abbas and Winfried Padberg and Catherine Meyer-Schwesinger and {von Brandenstein}, Melanie and Monika Schlosser and Georg Dieplinger and Jack Galliford and Candice Clarke and Candice Roufosse and Becker, {Jan Ulrich}",
year = "2016",
month = may,
doi = "10.1097/TP.0000000000001068",
language = "English",
volume = "100",
pages = "1004--14",
journal = "TRANSPLANTATION",
issn = "0041-1337",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

RIS

TY - JOUR

T1 - Immune Complex-Type Deposits in the Fischer-344 to Lewis Rat Model of Renal Transplantation and a Subset of Human Transplant Glomerulopathy

AU - Grau, Veronika

AU - Zeuschner, Philip

AU - Immenschuh, Stephan

AU - Bockmeyer, Clemens Luitpold

AU - Zell, Stefanie

AU - Wittig, Juliane

AU - Säuberlich, Karen

AU - Abbas, Mahmoud

AU - Padberg, Winfried

AU - Meyer-Schwesinger, Catherine

AU - von Brandenstein, Melanie

AU - Schlosser, Monika

AU - Dieplinger, Georg

AU - Galliford, Jack

AU - Clarke, Candice

AU - Roufosse, Candice

AU - Becker, Jan Ulrich

PY - 2016/5

Y1 - 2016/5

N2 - BACKGROUND: Antibody-mediated rejection is a leading cause for renal transplant loss. Rodent models are useful to dissect pathomechanisms and to develop treatment strategies. Although used for decades as a model, glomerular histopathological findings of Fischer-344 kidneys transplanted into Lewis rats have never been comprehensively described.METHODS: Kidneys from Fischer-344 rats were transplanted into Lewis rats as life-sustaining allografts without immunosuppression. Lewis isografts and normal Fischer-344 kidneys served as controls. Grafts were harvested at 9 days, 6 and 26 weeks. Histopathological examination included light microscopy, immunohistochemistry, and morphometry. Findings were compared with 51 human biopsies with transplant glomerulopathy.RESULTS: Most glomerular findings in rat allografts resembled human acute and chronic antibody-mediated rejection with glomerulitis, microthrombosis, microaneurysms, glomerular hypertrophy, podocyte loss, glomerular basement membrane splitting, and secondary focal and segmental glomerulosclerosis. In line with previous reports on nonendothelial antigens, glomerular immunoglobulin and C4d deposition was mostly nonendothelial. Only in 26-week allografts, we found mesangial and subendothelial immune complex-type electron-dense deposits. Similar deposits were found in 8 of 51 human biopsies with transplant glomerulopathy after rigorous exclusion of immune complexes of other cause, particularly recurrent glomerulonephritis and hepatitis C.CONCLUSIONS: Thus, our model closely reflects the glomerular changes of acute antibody-mediated rejection in humans and of a special subset of human transplant glomerulopathy. The significance of alloimmune immune complex-type deposits in human transplants deserves further investigation.

AB - BACKGROUND: Antibody-mediated rejection is a leading cause for renal transplant loss. Rodent models are useful to dissect pathomechanisms and to develop treatment strategies. Although used for decades as a model, glomerular histopathological findings of Fischer-344 kidneys transplanted into Lewis rats have never been comprehensively described.METHODS: Kidneys from Fischer-344 rats were transplanted into Lewis rats as life-sustaining allografts without immunosuppression. Lewis isografts and normal Fischer-344 kidneys served as controls. Grafts were harvested at 9 days, 6 and 26 weeks. Histopathological examination included light microscopy, immunohistochemistry, and morphometry. Findings were compared with 51 human biopsies with transplant glomerulopathy.RESULTS: Most glomerular findings in rat allografts resembled human acute and chronic antibody-mediated rejection with glomerulitis, microthrombosis, microaneurysms, glomerular hypertrophy, podocyte loss, glomerular basement membrane splitting, and secondary focal and segmental glomerulosclerosis. In line with previous reports on nonendothelial antigens, glomerular immunoglobulin and C4d deposition was mostly nonendothelial. Only in 26-week allografts, we found mesangial and subendothelial immune complex-type electron-dense deposits. Similar deposits were found in 8 of 51 human biopsies with transplant glomerulopathy after rigorous exclusion of immune complexes of other cause, particularly recurrent glomerulonephritis and hepatitis C.CONCLUSIONS: Thus, our model closely reflects the glomerular changes of acute antibody-mediated rejection in humans and of a special subset of human transplant glomerulopathy. The significance of alloimmune immune complex-type deposits in human transplants deserves further investigation.

U2 - 10.1097/TP.0000000000001068

DO - 10.1097/TP.0000000000001068

M3 - SCORING: Journal article

C2 - 26895216

VL - 100

SP - 1004

EP - 1014

JO - TRANSPLANTATION

JF - TRANSPLANTATION

SN - 0041-1337

IS - 5

ER -