CD44 as a pathological marker for the early detection of calcineurin inhibitor-induced nephrotoxicity after kidney transplantation

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CD44 as a pathological marker for the early detection of calcineurin inhibitor-induced nephrotoxicity after kidney transplantation

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Co-author 1

Asako Hayashi asako-hayashi@hoku-iryo-u.ac.jp Hokkaido University Graduate School of Medicine Pediatrics Sapporo Japan *

Co-author 2

Kiyohiko Hotta hotta1125@gmail.com Hokkaido University Graduate School of Medicine Renal Genitourinary Surgery Sapporo Japan -

Co-author 3

Asahi Yamamoto asahi.y1992@gmail.com Hokkaido University Graduate School of Medicine Pediatrics Sapporo Japan -

Co-author 4

Ryosuke Yokokawa ryosuke.yokokawa@med.hokudai.ac.jp Hokkaido University Graduate School of Medicine Pediatrics Sapporo Japan -

Co-author 5

Ryota Suzuki ryota.s.1987@gmail.com Hokkaido University Graduate School of Medicine Pediatrics Sapporo Japan -

Co-author 6

Toshiyuki Takahashi t-toshi@med.hokudai.ac.jp Hokkaido University Graduate School of Medicine Pediatrics Sapporo Japan -

Co-author 7

Yasuyuki Sato fcsatoyasu@med.hokudai.ac.jp Hokkaido University Graduate School of Medicine Pediatrics Sapporo Japan -

Co-author 8

Takayuki Okamoto okamon@med.hokudai.ac.jp Hokkaido University Graduate School of Medicine Pediatrics Sapporo Japan -

Co-author 9

Co-author 10

Co-author 11

Co-author 12

Co-author 13

Co-author 14

Co-author 15

Introduction

Long-term administration of calcineurin inhibitors (CNI) can cause irreversible nephrotoxicity. Therefore, early detection of CNI-induced nephrotoxicity is essential in patients who require prolonged CNI administration. However, few pathological indicators for the early phase of CNI-induced nephrotoxicity have been identified.

Methods

We retrospectively analyzed kidney transplant recipients at Hokkaido University Hospital between 2004 and 2014. All patients received CNIs after transplantation, and protocol biopsies were performed at the time of transplantation and at 1 year, 3-4 years, and 5-7-years post-transplantation to evaluate histopathological changes. The following cases were excluded: patients with focal segmental glomerulosclerosis (FSGS) before transplantation, antibody-mediated rejection, recurrent FSGS after transplantation, post-transplant infection, or post-transplant diabetes.

Results

Compared with findings at 1 year after transplantation, glomerular CD44 expression significantly increased from 3-4 years after CNI administration and continued to rise thereafter(p<0.05). Podocyte injury, immunostaining for podocyte markers such as WT-1 and podocin decreased from 5-7 years after CNI administration. Tubular atrophy/interstitial fibrosis, arterial hyaline thickening, and FSGS also increased during 5-7 years period compared with findings at 1 year.

Conclusion

We previously demonstrated that CD44-positive parietal epitherial cells (PECs) play pivotal roles in FSGS development in rodent models of CNI-induced nephrotoxicity. Our present findings suggest that CD44 could serve as a useful pathological marker for the early detection of CNI-induced nephrotoxicity after kidney transplantation in humans.

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