Multiple anti-slit autoantibodies in post-transplant recurrent focal segmental glomerulosclerosis.

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Abstract Title *

Multiple anti-slit autoantibodies in post-transplant recurrent focal segmental glomerulosclerosis.

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Co-author 1

Yoko Shirai shirai.yoko@twmu.ac.jp Tokyo Women’s Medical University Department of Pediatric Nephrology Tokyo Japan *

Co-author 2

Kenichiro Miura kmiura@twmu.ac.jp Tokyo Women’s Medical University Department of Pediatric Nephrology Tokyo Japan -

Co-author 3

Naoko Ito ito.naoko@twmu.ac.jp Tokyo Women’s Medical University Department of Surgical Pathology Tokyo Japan -

Co-author 4

Sekiko Taneda taneda.sekiko@twmu.ac.jp Tokyo Women’s Medical University Department of Surgical Pathology Tokyo Japan -

Co-author 5

Junki Koike j2koike@marianna-u.ac.jp St. Marianna University Department of Pathology Kanagawa Japan -

Co-author 6

Kazuho Honda kzhonda@med.showa-u.ac.jp Showa University School of Medicine Department of Anatomy Tokyo Japan -

Co-author 7

Motoshi Hattori hattori@twmu.ac.jp Tokyo Women’s Medical University Department of Pediatric Nephrology Tokyo Japan - Tokiwa Fondation, Jyoban Hospital, Iwaki, Kidney Disease Research Institute Fukushima Japan

Co-author 8

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Introduction

We previously reported that anti-nephrin autoantibodies may act as a circulating factor responsible for post-transplant recurrent focal segmental glomerulosclerosis (rFSGS) (Hattori M, et al., Am J Transplant, 2022; Shirai Y, et al., Kidney Int, 2024). Recently, autoantibodies targeting slit diaphragm molecules other than nephrin have been described (Raglianti V, et al. Kidney Int, 2024; Shirai Y, et al., Kidney Int, 2025).

Methods

We analyzed 19 cases of rFSGS who underwent kidney transplantation, in which allograft biopsy specimens during recurrence were available. Among these, 10 achieved complete remission, 4 partial remission, and 5 were non-responders. Dual staining of IgG with nephrin, podocin, or Kirrel1 was evaluated by structured illumination microscopy. Anti-nephrin, anti-podocin and anti-Kirrel1 autoantibodies were quantified by ELISA in available plasma samples.

Results

IgG depositions on podocytes were observed in 18 of 19 cases (95%). IgG was co-localized with nephrin, podocin, and Kirrel1 in 15 (79%), 8 (42%), and 10 (53%) cases, respectively. One case (5%) showed IgG deposition, but without co-localization of IgG with any slit diaphragm–associated molecules (Figure). In all cases with available plasma samples, circulating autoantibodies against nephrin, podocin and Kirrel1 were detected, corresponding to the colocalization of IgG with these molecules. Co-localization of IgG with two or three slit diaphragm molecules was observed in 10 cases (Figure). Notably, nephrin co-localized with IgG exhibited altered localization to the intracellular areas of podocytes, whereas podocin and Kirrel1 remained localized to the slit diaphragm despite IgG binding. No clear correlations were observed between IgG deposition patterns or co-localization profiles and treatment response.

Conclusion

Multiple anti-slit autoantibodies were commonly identified in rFSGS. Difference in localizations of slit diaphragm molecules may provide insights into the pathogenesis of rFSGS.

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