J Korean Soc Transplant.  2014 Sep;28(3):135-143. 10.4285/jkstn.2014.28.3.135.

Changes of Kidney Injury Molecule-1 Expression and Renal Allograft Function in Protocol and for Cause Renal Allograft Biopsy

Affiliations
  • 1Department of Pathology, Yonsei University College of Medicine, Seoul, Korea. jeong10@yuhs.ac
  • 2Department of Surgery, Yonsei University College of Medicine, Seoul, Korea.
  • 3Research Institute for Transplantation, Yonsei University, Seoul, Korea.
  • 4Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.

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.

Keyword

Kidney injury molecule-1; Acute kidney injury; Graft dysfunction; Histology

MeSH Terms

Acute Kidney Injury
Allografts*
Biopsy*
Delayed Graft Function
Fibrosis
Follow-Up Studies
Humans
Inflammation
Kidney*
Male
Necrosis
Tissue Donors
Transplants

Figure

  • Fig. 1. Scoring of renal tubular kidney injury molecule-1 expression: (A) 0.5, focal staining, (B) 1, weak and entire staining, (C) 2, moderate and entire staining. and (D) 3, strong and entire staining (×400).

  • Fig. 2. Renal tubular kidney injury molecule-1 (KIM-1) expression in patients with stable graft function and dysfunction (×200). (A, B) In a patient with stable renal function, tubular KIM-1 expression increased in the repeat biopsy (B, score 2) compared with zero time (A, score 0.5). (C, D) Tubular KIM-1 expression became prominent in the repeat biopsy (D, score 3) in a patient with graft dysfunction, who showed negative KIM-1 staining at zero time (C).


Reference

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