Multiple factors contribute to the development of chronic allograft nephropathy (CAN) in renal transplant recipients, and atherogenesis is considered to be an important pathologic process contributing to the development of this disease. There is growing acknowledgment of the role of inflammation in the pathogenesis of atherosclerosis, and markers of inflammation, such as C-reactive protein (CRP), have been shown to predict atherosclerotic vascular disease in the general and end-stage renal disease populations. In this pilot study, we hypothesized that elevations in pretransplant concentrations of CRP predict an increased incidence of CAN after renal transplantation. This case-control study compared pretransplant CRP levels in patients with allograft dysfunction and biopsy-proven CAN (n = 15) with a control group of transplant recipients with normal allograft function (n = 43). The median concentration of serum CRP was significantly higher in the CAN versus the control patients (13.1 +/- 3.9 mg/L versus 3.5 +/- 2.5 mg/L; P = 0.01). This difference was sustained when restricting to patients who did not experience acute rejection. When dividing the patients into tertiles based on CRP concentration, the adjusted risk of CAN increased more than threefold with each increment in CRP by tertile (adjusted odds ratio, 3.16; P = 0.03). The findings of our pilot study show an association between pretransplant elevations of CRP and CAN in end-stage renal disease patients who go on to receive a renal transplant. Cohort studies in larger groups of transplant patients are needed to confirm a causal pathway between pretransplant inflammation, atherogenesis, and CAN.
Copyright 2002 by the National Kidney Foundation, Inc.