Assessment of sICAM-1 and sVCAM-1 in Patients with Chronic Renal Allograft Dysfunction.
- Author:
Yu Seun KIM
1
;
Hyun Ok KIM
;
Kyu Hun CHOI
;
Hyeon Joo JEONG
;
Taec Kyun KIM
;
Soon Il KIM
;
Myoung Soo KIM
;
Jang Il MOON
;
Eun Mi LEE
;
Ki Il PARK
Author Information
1. Department of Surgery, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Soluble adhesion molecule;
Renal transplantation
- MeSH:
Allografts*;
Biopsy;
Creatinine;
Cyclosporine;
Hematuria;
Humans;
Intercellular Adhesion Molecule-1;
Kidney Transplantation;
Proteinuria;
Renal Insufficiency;
Transplantation;
Transplants;
Vascular Cell Adhesion Molecule-1
- From:The Journal of the Korean Society for Transplantation
1997;11(1):41-48
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
AIMS: To examine the relationship between soluble adhesion molecules ICAM-1 and VCAM-1, and chronic renal allograft dysfunction METHODS: Serum samples taken on the day of renal biopsy from renal allograft recipients showing chronic graft dysfunction(n=31), at least one year after renal transplantation, were examined and compared with those from healthy control(n=20), or end stage renal failure patients(n=18), for the measurement of sICAM-1 and sVCAM-1. Specific enzyme-linked immunometric method were used. No pateints was experiencing concurrent infection. The indications of the biopsy were slow increment of serum creatinine, significant proteinuria(over 1 gram per day) or newly-developed microscopic hematuria with or without small amount of proteinuria. RESULTS: sVCAM-1 was increased in end stage renal failure patients as well as transplant recipients as compared with the healthy controls. However, sICAM-1 was not increased either in end stage renal failure patients or renal allograft recipients. The degree of chronic rejection and cyclosporine toxicity did not correlate with the serum level of sVCAM-1. The level of serum creatinine did not correlate with the serum levels of either sICAM-1 or sVCAM-1. CONCLUSION: Increase of sVCAM-1 but not of sICAM-1 may have some role in the mechanism of chronic renal allograft dysfunction.
