[Associations of ICAM1 gene and VCAM1 promoter polymorphisms with transplanted kidney function].

INTRODUCTION

Transplantation is the preferred method of treatment of end-stage renal failure due to improvement in the quality of life and longer survival of patients. The process of graft rejection involves many mediators, including intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1). Recent research has revealed the genetic background of the synthesis ofadhesins. Several polymorphisms of genes coding for ICAM-1 and VCAM-1 have been described which may be functionally important through various rates of synthesis of the mediator. Genetic differences in the synthesis of adhesion molecules may affect graft function and predispose to acute or chronic rejection.

MATERIAL AND

METHODS

The study enrolled 270 Caucasian whites (104 females and 166 males), aged 21 to 76 years (mean 47.63 +/- 12.96), who underwent allogenic renal grafting. Groups of patients with delayed graft function (n = 85), acute rejection (n = 70), and chronic allograft nephropathy were formed (n = 62). Biopsy of the renal graft was done to verify progressive loss of function. Polymorphisms were identified with PCR-RFLP.

RESULTS AND

CONCLUSIONS

It was found that the GG genotype of the rs5498 polymorphisms of the ICAM1 gene is a significant risk factor of acute rejection and is correlated with elevated concentrations of creatinine in allogenic renal graft recipients. The TC genotype of the rs3170794 polymorphism of the VCAM1 promoter may be a risk factor of acute rejection in allogenic renal graft recipients. The G allele of the rs5498 polymorphism of the ICAM1 gene is significantly correlated with interstitial fibrosis and may also be correlated with other chronic histopathologic lesions seen in bioptates of the grafted kidney. There was no correlation of the rs1041163 and rs3170794 polymorphisms of the VCAM1 promoter with the severity of histopathologic lesions seen in bioptates of the grafted kidney.