Effect of cytomegalovirus infection on long-term renal allograft function.
- Author:
Bin TANG
1
;
Pei-yan LV
;
Feng-ying XU
;
Ke-li ZHENG
;
Dong LIU
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Creatinine; blood; Cytomegalovirus Infections; blood; metabolism; physiopathology; Female; Humans; Kidney; metabolism; physiopathology; virology; Kidney Transplantation; Leukocytes, Mononuclear; metabolism; Male; RNA, Messenger; genetics; metabolism; Transforming Growth Factor beta1; genetics; Transplantation, Homologous
- From: Journal of Southern Medical University 2009;29(8):1588-1591
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the effect of cytomegalovirus (CMV) infection following kidney transplantation on long-term renal function and its mechanism.
METHODSNinety-six patients undergoing kidney transplantation between March 2000 and December 2005, who completed a 3-year follow-up investigation, were divided into 3 groups according CMV-pp65 antigenemia and clinical symptoms. Group A consisted of 33 recipients with symptomatic active CMV infection, group B included 33 with asymptomatic active CMV infection and group C included 30 with inactive infection. The relation of CMV infection, transforming growth factor-beta1 (TGF-beta1) mRNA in the peripheral blood mononuclear cells (PBMCs) and serum creatinine (Scr) were analyzed, and the grafts in 6 cases with renal dysfunction were biopsied.
RESULTSThe expression of TGF-beta1 mRNA in PBMCs was significantly higher in group A than in the other two groups 6 months after the transplantation (P<0.01), while Scr levels showed no significant difference between the 3 groups (P>0.05). Three years later, Scr levels in group A were significantly increased as compared with those in the other two groups (P<0.01), and the rate of renal dysfunction in group A (10/33) was significantly higher than those in group B (3/33) and C(3/30) (P<0.05). In the 16 with renal dysfunction, the expression of TGF-beta1 mRNA in PBMCs significantly higher than that in the other 80 patients with normal renal function (P<0.01). Renal allograft biopsies demonstrated mild or severe interstitial fibrosis, tubular atrophy and mononuclear cell infiltration in the 6 patients with renal graft dysfunction, supporting the diagnosis of chronic allograft nephropathy (CAN).
CONCLUSIONSymptomatic active CMV infection in renal allograft recipients is an important factor contributing to the occurrence of CAN. Monitoring of TGF-beta1 mRNA expression in PBMCs proves useful in identifying patients at risk of CAN.