title: Post-transplant sCD30 and neopterin as predictors of chronic allograft nephropathy: impact of different immunosuppressive regimens.
abstract: Immunological monitoring for chronic allograft nephropathy (CAN) is of great potential interest. We assessed serum soluble CD30 (sCD30) together with in vitro Th2-type responses (IL-4, IL-10, CD4 helper activity) and neopterin in a prospective study of 84 renal transplant recipients with 2-year follow-up. Patients were randomized to CsA/Aza, CsA/MMF and Tacr/Aza, respectively, to analyze the effect of immunosuppression on posttransplant sCD30 and neopterin. ATG induction and acute rejections did not alter sCD30 levels whereas CMV disease was associated with transient upregulation of sCD30 (p = 0.003 at 4 months) and sustained upregulation of neopterin (corrected for graft function (Neo/CR) p = 0.005 at 2 years). Tacr versus CsA treatment proved to be an independent variable associated with downregulation of 1-year sCD30, which was positively related to Neo/CR (p = 0.007 and 0.01, respectively; logistic regression). Importantly, increased 1-year sCD30 and Neo/CR were associated with decreased glomerular filtration rate at 2 years (p = 0.02 and p < 0.0005, respectively) and evidence of CAN (p < 0.0005). High 1-year sCD30 could not be attributed to enhanced Th2-type responses and was not associated with HLA antibody formation. Our data suggest that elevated sCD30 and neopterin predict graft deterioration by CAN. Tacr effectively downregulates these responses and might be of advantage in patients with elevated sCD30 or neopterin.
authors.affiliation: Department of Internal Medicine, University Clinic of Giessen and Marburg, Germany. rolf.weimer@innere.med.uni-giessen.de
authors.forename: R
authors.initials: R
authors.lastname: Weimer
authors.forename: C
authors.initials: C
authors.lastname: Süsal
authors.forename: S
authors.initials: S
authors.lastname: Yildiz
authors.forename: A
authors.initials: A
authors.lastname: Staak
authors.forename: S
authors.initials: S
authors.lastname: Pelzl
authors.forename: F
authors.initials: F
authors.lastname: Renner
authors.forename: H
authors.initials: H
authors.lastname: Dietrich
authors.forename: V
authors.initials: V
authors.lastname: Daniel
authors.forename: S
authors.initials: S
authors.lastname: Kamali-Ernst
authors.forename: W
authors.initials: W
authors.lastname: Ernst
authors.forename: W
authors.initials: W
authors.lastname: Padberg
authors.forename: G
authors.initials: G
authors.lastname: Opelz
mesh_terms: D000328:Adult; D000906:Antibodies / Q000276:immunology; D015415:Biomarkers; D002908:Chronic Disease; D003181:Complement C4 / Q000378:metabolism; D005260:Female; D006084:Graft Rejection / Q000276:immunology / Q000517:prevention & control; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D017730:Ki-1 Antigen / Q000032:analysis* / Q000097:blood / Q000276:immunology; D007674:Kidney Diseases / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016030:Kidney Transplantation / Q000276:immunology* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D019798:Neopterin / Q000276:immunology*; D011379:Prognosis; D012995:Solubility; D018418:Th2 Cells / Q000276:immunology; D014184:Transplantation, Homologous / Q000276:immunology; D016896:Treatment Outcome
chemical_list: D000906:Antibodies; D015415:Biomarkers; D003181:Complement C4; D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II; D007166:Immunosuppressive Agents; D017730:Ki-1 Antigen; D019798:Neopterin