No effect of C-reactive protein (CRP) haplotypes on CRP levels and post-transplant morbidity and mortality in renal transplantation

Krueger, Bernd and Boeger, Carsten A. and Schroeppel, Bernd and Farkas, Stefan and Schnitzbauer, Andreas A. and Hoffmann, Ute and Obed, Aiman and Murphy, Barbara T. and Banas, Bernhard and Kraemer, Bernhard K. (2008) No effect of C-reactive protein (CRP) haplotypes on CRP levels and post-transplant morbidity and mortality in renal transplantation. TRANSPLANT INTERNATIONAL, 21 (5). pp. 452-458. ISSN 0934-0874, 1432-2277

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Abstract

Increased serum C-reactive protein (CRP) levels have been associated with all-cause and cardiovascular mortality after kidney transplantation. As genetic variations within the CRP gene determine CRP serum levels, we analyzed the association of both serum CRP levels, and post-transplant morbidity/mortality with CRP-genotypes/haplotypes. We determined CRP levels pretransplant, at 3 and 6 months post-transplant in 402 first kidney recipients, gencityped the three functionally distinct polymorphisms, and subsequently reconstructed the different haplotypes. Four different CRP-haplotypes were observed with a frequency >1%: CGC (33.3%), CGT (30.2%), CAT (29.7%) and GGT (6.8%). CRP levels pretransplantation or 3 and 6 months post-transplant were not different in patients with different CRP-haplotypes. Furthermore, no association of CRP-haplotypes/diplotypes was found with acute rejection, delayed graft function, all-cause mortality or cardiovascular events. In our renal transplant population, we found no association of CRP-haplotypes/diplotypes with either CRP levels or with post-transplant morbidity/mortality. In this inflammation-prone population, rather small genetically determined differences in serum CRP observed in normal populations presumably are overridden by background inflammation. Life long genetically determined increased serum CRP levels appear not to have an impact in our study, implying that CRP is more likely only a marker of current inflammation than a causative agent of cardiovascular morbidity and mortality.

Item Type: Article
Uncontrolled Keywords: CORONARY-HEART-DISEASE; CARDIOVASCULAR MORTALITY; PROMOTER REGION; GRAFT FUNCTION; ALL-CAUSE; GENE; INFLAMMATION; POLYMORPHISM; SURVIVAL; ATHEROSCLEROSIS; cardiovascular disease; C-reactive protein; haplotype; renal function; renal transplantation
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Chirurgie
Medicine > Lehrstuhl für Innere Medizin II
Depositing User: Dr. Gernot Deinzer
Date Deposited: 04 Nov 2020 07:06
Last Modified: 04 Nov 2020 07:06
URI: https://pred.uni-regensburg.de/id/eprint/31026

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