CRP and acute renal rejection: A marker to the point

ArticleinInternational Urology and Nephrology 44(4):1251-5 · January 2012with34 Reads
Impact Factor: 1.52 · DOI: 10.1007/s11255-011-0098-4 · Source: PubMed

C-reactive protein (CRP) is increased in end-stage renal disease patients. Recent studies have shown positive associations between inflammatory markers and cardiovascular mortality in kidney transplant recipients. The aim of the present study was to examine the correlation between CRP and early detection of renal allograft rejection. Furthermore, investigate the association between pretransplant levels of CRP with the development of acute renal allograft rejection as a possible predictive marker. Ninety-one renal transplant recipients were sequentially analyzed. The median follow up of patients was 8 weeks. Basal and 8 weeks post transplant CRP levels were assessed. CRP levels were significantly higher in allograft rejection both in the pretransplant (n = 25, P = 0.001) and postransplant (n = 33, P = 0.001) phases when compared to those without rejection. By stepwise multiple regression analysis, rejection in transplanted patients was independently correlated to albumin/creatinine ratio and CRP 8 weeks after transplantation. Elevated pretransplant serum CRP level is a risk predictor for acute rejection episodes and may be a useful predictive marker in the follow-up of post-transplantation patients.

    • "(2014) 62:501–509 505 such as Crohn's disease, are better managed with the implementation of a regular Hs-CRP measurement (Erlinger et al. 2004; Owczarek et al. 2012). Hs-CRP is also useful in determining renal transplant rejection (Grebe et al. 2011; Roshdy et al. 2012). A moderate increase in the concentration of Hs-CRP occurs in liver diseases (Komoriya et al. 2012), autoimmune diseases (Rezaieyazdi et al. 2011), and neoplasms (Hopkins et al. 2012). "
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  • [Show abstract] [Hide abstract] ABSTRACT: C-reactive protein (CRP) is regarded as a inflammatory biomarker in acute kidney injury (AKI), but its exact role in AKI remains unclear. Thus, we sought to investigate the role of CRP in AKI. Clinically, elevated serum CRP were closely associated with an increased serum creatinine and urea (p<0.01) in patients with AKI, which was declined when AKI recovered. To determine the role of CRP in AKI, an ischemia-reperfusion mouse model of AKI was induced in transgenic (Tg) mice that express human CRP. Compared to wild type mice, CRP Tg mice developed more severe renal injury at 24h after ischemia determined by significantly increased serum creatinine and tubular necrosis. This was associated with impaired tubular epithelial cells (TEC) regeneration as evidenced by over 60% reduction in PCNA+ and BrdU+ TEC in CRP Tg mice with AKI. In vitro, addition of CRP to a human TEC line (HK-2) also largely suppressed the proliferation of TEC. The functional role of CRP in AKI was further demonstrated by the blocking CRP binding to its FcγRII with a neutralizing anti-CD32 antibody restoring the TEC proliferation and preventing AKI in CRP Tg mice. Moreover, we found that impaired G1/S transition by suppressing phosphorylation of CDK2 and expression of cyclin E may be a key mechanism by which CRP inhibited TEC regeneration during the AKI repair process. Conclusively, CRP plays a pathogenic role in AKI by inhibiting G1/S-dependent TEC regeneration. Results from this study suggest that targeting CRP signaling may offer a new therapeutic potential for AKI.
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  • [Show abstract] [Hide abstract] ABSTRACT: We previously reported that compared to standard glycemic control [blood glucose (BG): 70-180 mg/dL], patients randomized to intensive glycemic control (BG: 70-110 mg/dL) were at increased risk of graft rejection in renal transplantation. However, the underlying mechanisms that associate the effect of intensive glycemic control with renal transplant outcomes have not been identified. A secondary data analysis of 93 participants (n=44 intensive, n=49 control) was conducted using data from a previous randomized controlled clinical trial. We examined inflammatory biomarkers, glycemic variability, hypoglycemia, and hyperglycemia as potential contributing etiologies by assessing the effect of intensive glycemic control on these characteristics, and evaluate the association of these variables with graft rejection. Intensive glycemic control had no appreciable effect on highly sensitive C-reactive protein, interleukin (IL)-6, tumor necrosis factor alpha, IL-1β, or IL-10 levels at all time points after transplantation. Moreover, neither inflammatory biomarkers nor increased glycemic variability were associated with graft rejection. However, intensive treatment increased the risk of hypoglycemia (BG <70 mg/dL, 84% vs. 25%, P<0.001). In sub-analysis, compared to non-rejecters, rejecters demonstrated higher rates of blood glucose below 70 mg/dL (90% vs. 49%, P=0.02). Inflammatory biomarkers and increased glycemic variability lack correlation with clinical outcomes in renal transplant, but importantly, increased perioperative hypoglycemic episodes (BG <70mg/dL) may be a salient etiology that contributed to the increased risk for acute allograft rejection related to intensive glycemic control. Further research is needed to confirm a causal association.
    No preview · Article · May 2014 · Transplantation
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