CRP and acute renal rejection: a marker to the point

Roshdy, Amin; El-Khatib, Mohamed; Rizk, Mary N.; El-Shehaby, Amal

doi:10.1007/s11255-011-0098-4

Cited by 16 publications

(10 citation statements)

References 13 publications

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“…Consistent with previous clinical studies [9][10][11][12][13], we found that all 75 AKI patients with different causes of disease had elevated levels of serum CRP, which were accompanied by deterioration of renal function. Consistent with previous clinical studies [9][10][11][12][13], we found that all 75 AKI patients with different causes of disease had elevated levels of serum CRP, which were accompanied by deterioration of renal function.…”

Section: Discussionsupporting

confidence: 91%

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C-reactive protein promotes acute kidney injury by impairing G1/S-dependent tubular epithelium cell regeneration

Tang

Huang

et al. 2014

Clinical Science

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CRP (C-reactive protein) is regarded as an inflammatory biomarker in AKI (acute kidney injury), but its exact role in AKI remains unclear. Thus we sought to investigate the role of CRP in AKI. Clinically, elevated serum CRP levels were found to associate closely with increased serum creatinine and urea levels (P<0.01) in patients with AKI, which then fell after recovery from AKI. To determine the role of CRP in AKI, an ischaemia/reperfusion mouse model of AKI was developed using Tg (transgenic) mice that express human CRP. Compared with the WT (wild-type) mice, CRP Tg mice developed more severe renal injury at 24 h after ischaemia as determined by significantly increased serum creatinine and tubular necrosis. This was associated with an impaired TEC (tubular epithelium cell) regeneration as shown by an over 60% reduction in PCNA+ (proliferating-cell nuclear antigen) and BrdU+ (bromodeoxyuridine) TECs in CRP Tg mice with AKI. In vitro, the addition of CRP to a human TEC line (HK-2) also largely suppressed the proliferation of TECs. The functional role of CRP in AKI was demonstrated further by the blocking of CRP binding to the FcγRII (Fcγ receptor II) with a neutralizing anti-CD32 antibody, which restored TEC proliferation and prevented AKI in CRP Tg mice. Moreover, we found that impaired G1/S transition by suppression of the phosphorylation of CDK2 (cyclin-dependent kinase 2) and expression of cyclin E may be a key mechanism by which CRP inhibits TEC regeneration during the AKI repair process. In conclusion, CRP plays a pathogenic role in AKI by inhibiting G1/S-dependent TEC regeneration. The results of the present study suggest that targeting CRP signalling may offer a new therapeutic potential for AKI.

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Section: Discussionsupporting

confidence: 91%

“…Increased serum levels of CRP are also found in patients with AKI and have been suggested as a biomarker of inflammation in AKI [9][10][11][12][13]. Increased serum levels of CRP are also found in patients with AKI and have been suggested as a biomarker of inflammation in AKI [9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

C-reactive protein promotes acute kidney injury by impairing G1/S-dependent tubular epithelium cell regeneration

Tang

Huang

et al. 2014

Clinical Science

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“…Limited inflammatory disorders, 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 ).…”

Section: Discussionmentioning

confidence: 99%

The Role of Serum C-Reactive Protein Measured by High-Sensitive Method in Thyroid Disease

Czarnywojtek

Owecki

Zgorzalewicz-Stachowiak

et al. 2014

Arch. Immunol. Ther. Exp.

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The aim of this study was the evaluation of serum C-reactive protein (CRP) concentration as a marker of the inflammatory state in many different thyroid diseases and its dependence on the stage and duration of disease. We conducted a retrospective analysis of 444 randomly selected patients with different kinds of thyroid disease (106 men and 338 women, ranging 18–72 years of age; mean 56.2 ± 5.0 years; median 52 years). Group 1 (G1) comprised 250 patients with hyperthyroidism. Group 2 (G2) consisted of 72 euthyroid patients. Group 3 (G3) consisted of 122 patients with hypothyroidism. Free T4, free T3, and thyrotropin (TSH) levels were measured using the electrochemiluminescent method. Human serum thyroglobulin autoantibodies (Tg-Abs), thyroperoxidase autoantibodies (TPO-Abs), and autoantibodies against the thyrotropin receptor (TSHR-Abs) levels were measured by radioimmunoassay. The high-sensitive CRP (Hs-CRP) level (reference range <3 mg/L) was determined with a highly sensitive latex-based immunoassay. The mean value of Hs-CRP in G1 was 3.6 ± 2.8 mg/L, in G2 2.5 ± 1.5 mg/L and in G3 5.9 ± 5.8 mg/L. Hs-CRP (in mg/L) medians, interquartile and the total ranges in G1 were 3.0 (2.0 [0.1–21.0] 4.0); in G2: 2.3 [1.8 (0.2–9.2) 3.2]; and in G3: 4.3 [2.2 (0.3–31.5) 7.8]. We found statistically significant differences (Kruskal–Wallis test) in serum Hs-CRP values between G1 and G2 (P = 0.007), G1 and G3 (P = 0.001), G2 and G3 (P < 0.001). In G1, statistically significant correlation was confirmed between Hs-CRP and Tg-Abs (r = −0.22, P = 0.0016), CRP and TPO-Abs (r = −0.26, P < 0.001), and also between Hs-CRP and TSHR-Abs (r = −0.18, P = 0.02). In the remaining cases, differences between Hs-CRP and TSH levels (r = −0.09, P = 0.16) were not statistically significant. In G2, no statistically significant correlation was observed: Hs-CRP and Tg-Abs (r = −0.18, P = 0.13), Hs-CRP and TPO-Abs (r = −0.17, P = 0.15), Hs-CRP and TSH (r = 0.01, P = 0.91), Hs-CRP and TSHR-Abs (r = −0.19, P = 0.17). In G3, a statistically significant correlation was confirmed between Hs-CRP and Tg-Abs (r = 0.22, P = 0.012), Hs-CRP and TSH (r = −0.28, P = 0.001). No statistically significant correlation was observed between Hs-CRP and TPO-Abs (r = 0.20, P = 0.06) and between Hs-CRP and TSHR-Abs (r = −0.23, P = 0.11). Hs-CRP is increased in various types of hypothyroidism. This is particularly relevant in postpartum thyroiditis and in patients after radioiodine treatment. The impact of this situation on human health requires further research, however, one might assume that some types of thyroid disease may lead to systemic inflammatory reactions that are reflected in elevated CRP levels.

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“…From the standard markers of inflammation, pretransplant CRP was reported to be a risk factor for acute rejection episodes [ 5 ] or not to influence graft function and survival among children [ 23 ] or adults [ 24 ]. In the present study we also found no influence of pretransplant CRP levels on the rate of delayed graft function or acute rejection and allograft function.…”

Section: Discussionmentioning

confidence: 99%

“…While the immune response shift is well described in the literature, still it is not clear whether the pretransplant chronic inflammation affects posttransplant outcome. From routine blood tests CRP (C-reactive protein) and albumin levels were shown not only to reflect the general immune response in uremic patients [ 3 ] but also to predict kidney outcome [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Pretransplant Immune- and Apoptosis-Related Gene Expression Is Associated with Kidney Allograft Function

Kamińska

Kościelska‐Kasprzak

Chudoba

et al. 2016

Mediators of Inflammation

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Renal transplant candidates present immune dysregulation, caused by chronic uremia. The aim of the study was to investigate whether pretransplant peripheral blood gene expression of immune factors affects clinical outcome of renal allograft recipients. Methods. In a prospective study, we analyzed pretransplant peripheral blood gene expression in87 renal transplant candidates with real-time PCR on custom-designed low density arrays (TaqMan). Results. Immediate posttransplant graft function (14-day GFR) was influenced negatively by TGFB1 (P = 0.039) and positively by IL-2 gene expression (P = 0.040). Pretransplant blood mRNA expression of apoptosis-related genes (CASP3, FAS, and IL-18) and Th1-derived cytokine gene IFNG correlated positively with short- (6-month GFR CASP3: P = 0.027, FAS: P = 0.021, and IFNG: P = 0.029) and long-term graft function (24-month GFR CASP3: P = 0.003, FAS: P = 0.033, IL-18: P = 0.044, and IFNG: P = 0.04). Conclusion. Lowered pretransplant Th1-derived cytokine and apoptosis-related gene expressions were a hallmark of subsequent worse kidney function but not of acute rejection rate. The pretransplant IFNG and CASP3 and FAS and IL-18 genes' expression in the recipients' peripheral blood is the possible candidate for novel biomarker of short- and long-term allograft function.

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CRP and acute renal rejection: a marker to the point

Abstract: 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.

Cited by 16 publications

References 13 publications

C-reactive protein promotes acute kidney injury by impairing G1/S-dependent tubular epithelium cell regeneration

C-reactive protein promotes acute kidney injury by impairing G1/S-dependent tubular epithelium cell regeneration

The Role of Serum C-Reactive Protein Measured by High-Sensitive Method in Thyroid Disease

Pretransplant Immune- and Apoptosis-Related Gene Expression Is Associated with Kidney Allograft Function

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