Changes of Kidney Injury Molecule-1 Expression and Renal Allograft Function in Protocol and for Cause Renal Allograft Biopsy.
10.4285/jkstn.2014.28.3.135
- Author:
Yonhee KIM
1
;
A Lan LEE
;
Myoung Soo KIM
;
Dong Jin JOO
;
Beom Seok KIM
;
Kyu Ha HUH
;
Soon Il KIM
;
Yu Seun KIM
;
Hyeon Joo JEONG
Author Information
1. Department of Pathology, Yonsei University College of Medicine, Seoul, Korea. jeong10@yuhs.ac
- Publication Type:Original Article
- Keywords:
Kidney injury molecule-1;
Acute kidney injury;
Graft dysfunction;
Histology
- MeSH:
Acute Kidney Injury;
Allografts*;
Biopsy*;
Delayed Graft Function;
Fibrosis;
Follow-Up Studies;
Humans;
Inflammation;
Kidney*;
Male;
Necrosis;
Tissue Donors;
Transplants
- From:The Journal of the Korean Society for Transplantation
2014;28(3):135-143
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Kidney injury molecule-1 (KIM-1) is known as a good ancillary marker of acute kidney injury (AKI) and its expression has also been observed in acute rejection and chronic graft dysfunction. We tested usefulness of KIM-1 as an indicator of acute and chronic renal graft injury by correlating KIM-1 expression with renal graft function and histology. METHODS: A total of 133 zero-time biopsies and 42 follow-up biopsies obtained within 1 year posttransplantation were selected. Renal tubular KIM-1 staining was graded semiquantitatively from 0 to 3 and the extent of staining was expressed as the ratio of KIM-1 positive/CD10 positive proximal tubules using Image J program. RESULTS: KIM-1 was positive in 39.8% of zero-time biopsies. KIM-1 positive cases were predominantly male and had received grafts from donors with older age, deceased donors, and poor renal function at the time of donation, compared with KIM-1 negative cases. KIM-1 expression showed correlation with delayed graft function and acute tubular necrosis. In comparison of KIM-1 expression between stable grafts (n=23) and grafts with dysfunction (n=19) at the time of repeated biopsy, the intensity/extent of KIM-1 staining and renal histology at zero-time did not differ significantly between the two groups. Histologically, KIM-1 expression was significantly increased with both acute and chronic changes of glomeruli, tubules and interstitium, peritubular capillaritis, and arteriolar hyalinosis. CONCLUSIONS: KIM-1 can be used as an ancillary marker of AKI and a nonspecific indicator of acute inflammation and tubulointerstitial fibrosis. However, KIM-1 expression at zero-time is not suitable for prediction of long-term graft dysfunction.
