Elevated urinary sVCAM-1, IL6, sIL6R and TNFR1 concentrations indicate acute kidney transplant rejection in the first 2weeks after transplantation

Reinhold, Stephan W.; Straub, Rainer H.; Krüger, Bernd; Kaess, Bernhard M.; Bergler, Tobias; Weingart, Christian; Banas, Miriam C.; Krämer, Bernhard K.; Banas, Bernhard

doi:10.1016/j.cyto.2011.12.006

Cited by 25 publications

(27 citation statements)

References 37 publications

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“…The soluble TNFR levels have been reported to be increased during acute rejection. [20][21][22][23][24] In accordance with these studies, we observed significant elevation of serum TNFR2 levels in acute rejection. Regarding ROC analysis for estimating acute rejection, serum TNFR1 and TNFR2 levels determined on 7th day and first month have highest sensitivity and specificity in our study.…”

Section: Discussionsupporting

confidence: 78%

Association between graft function and serum TNF-α, TNFR1 and TNFR2 levels in patients with kidney transplantation

Yılmaz

Akbaş

et al. 2015

Renal Failure

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Introduction: This prospective observational study aimed to assess the relevance of serial postoperative serum TNF-a, TNFR1 and TNFR2 measurements for predicting graft function and acute rejection episodes (AR) after transplantation. Materials and methods: We studied 50 kidney transplant recipients (31 female, 19 male; mean age: 38.36 ± 12.88). Blood samples were collected immediately before and after surgery at day 7, month 1 and month 3. Serum TNF-a, TNFR1 and TNFR2 levels were measured by ELISA using a commercial kit (Invitrogen ELISA). Serum cystatin-C levels were measured by particle-enhanced immunonephelometric method. Glomerular filtration rate (GFR) was estimated by Chronic Kidney Disease-Epidemiology (CKD-EPI) equation. Patients were assigned to their transplant outcomes in terms of acute rejection [AR(+) and AR(À)] and slow (SGF) or immediate graft function (IGF). Results: Among 50 recipients, six had AR(+) and 44 had AR(À), depending on graft function: 17 had SGF and 33 had IGF. Serum creatinine, cystatin-C, TNF-a, TNFR1 and TNFR2 levels demonstrated consistent significantly decreases after transplantation while GFR values had consistent increases (p ¼ 0.001). Pretransplant levels were not statistically different between AR(+) and AR(À) groups (TNF-a: 30.79 ± 5.96 vs. 27.95 ± 2.43 pg/mL, TNFR1: 55.96 ± 21.6 vs. 40.52 ± 7.41 ng/mL, TNFR2: 58.31 ± 8.06 vs. 50.9 ± 3.34 ng/mL, respectively) (p40.05). Serum TNF-a, TNFR1 and TNFR2 levels on day 7 and month 1 were also significantly higher in AR(+) group compared to AR(À) (p ¼ 0.012, p ¼ 0.049 for TNF-a, p ¼ 0.001, p ¼ 0.002 for TNFR1, p ¼ 0.001, p ¼ 0.002 for TNFR2). Conclusions: Our preliminary findings suggest that serum TNF-a, TNFR1 and TNFR2 levels might be considered useful markers of evaluating graft function after renal transplantation.

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Section: Discussionsupporting

confidence: 78%

Association between graft function and serum TNF-α, TNFR1 and TNFR2 levels in patients with kidney transplantation

Yılmaz

Akbaş

et al. 2015

Renal Failure

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“…IL-6 and TNF-α) and soluble vascular cell adhesion molecules (sVCAM-1) promote B- and T-cell activation, the key reaction leading to acute and chronic renal allograft rejection [55]. During an acute cellular rejection, the influx of lymphocytes in the renal interstitium is accompanied by the detection of epithelial cells expressing upregulated TNF-α converting enzyme (TACE), which are surrounded by a higher level of TACE-activating molecules (histamine, protein kinase C activator, reactive oxygen species and IL-1), stimulating the local shedding of TNFR2.…”

Section: Clinical Aspects Of Tnfr1 and Tnfr2 In Renal Pathology (Tablmentioning

confidence: 99%

Tumor Necrosis Factor Receptors: Biology and Therapeutic Potential in Kidney Diseases

Speeckaert

Laute³

et al. 2012

Am J Nephrol

105

101

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The major evolutionary advance represented in the human immune system is a mechanism of antigen-directed immunity in which tumor necrosis factor (TNF)-α and TNF receptors (TNFRs) play essential roles. Binding of TNF-α to the 55-kDa type I TNFR (TNFR1, TNFRSF1A, CD120a, p55) or the 75-kDa type II TNFR (TNFR2, TNFRSF1B, CD120b, p75) activates signaling pathways controlling inflammatory, immune and stress responses, as well as host defense and apoptosis. Multiple studies have investigated the role of TNFRs in the development of early and late renal failure (diabetic nephropathy, nephroangiosclerosis, acute kidney transplant rejection, renal cell carcinoma, glomerulonephritis, sepsis and obstructive renal injury). This article reviews the general characteristics, the analytical aspects and the biology of TNFRs in this domain. In addition, the potential therapeutic application of specific TNFR blockers is discussed.

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“…8 Increased urinary IL-6, tumor necrosis factor receptor 1, and vascular cell adhesion molecule 1 levels may predict early acute rejection. 9 Pentraxins are a group of multimeric proteins that are involved in acute immunologic responses. Short pentraxins (CRP and amyloid P protein) are synthesized by the liver in response to inflammatory signals such as IL-6.…”

Section: Introductionmentioning

confidence: 99%

Untitled

Gürsu

Çelik²,

Öztürk³

et al. 2014

Exp Clin Transplant

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Objectives: There are numerous changes in inflammatory status that occur after a kidney transplant. Pentraxin 3 is a marker of inflammation, but little information is available about pentraxin 3 levels after a kidney transplant. We evaluated the relation between pentraxin 3 and other inflammatory markers including high sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor α in kidney transplant recipients. Materials and Methods: Adult patients (40 patients; aged, 18-80 y; mean age, 38 ± 10 y) who had a kidney transplant from living-related donors were studied. Patients who had comorbidities associated with chronic inflammation were excluded. Blood samples were obtained before starting immunosuppressive treatment and 2 months after kidney transplant for measurement of pentraxin 3, high sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor α levels. Results: After transplant, mean levels of high sensitivity C-reactive protein and interleukin 6 decreased but levels of pentraxin 3 and tumor necrosis factor α did not change. There were significant correlations between interleukin 6 and high sensitivity C-reactive protein before transplant (r = 0.71; P ≤ .0001) and after transplant (r = 0.45; P ≤ .003). There was no correlation between tumor necrosis factor α and high sensitivity C-reactive protein before transplant, but there was a significant correlation between tumor necrosis factor α and high sensitivity C-reactive protein after transplant (r = 0.36; P ≤ .03). There was no correlation between interleukin 6 and pentraxin 3, tumor necrosis factor α and pentraxin 3, or high sensitivity C-reactive protein and pentraxin 3 before or after transplant. Conclusions: After a kidney transplant, pentraxin 3 may not be useful in determining inflammatory status, and high sensitivity C-reactive protein may be better than pentraxin 3 as a marker of inflammation.

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Elevated urinary sVCAM-1, IL6, sIL6R and TNFR1 concentrations indicate acute kidney transplant rejection in the first 2weeks after transplantation

Cited by 25 publications

References 37 publications

Association between graft function and serum TNF-α, TNFR1 and TNFR2 levels in patients with kidney transplantation

Association between graft function and serum TNF-α, TNFR1 and TNFR2 levels in patients with kidney transplantation

Tumor Necrosis Factor Receptors: Biology and Therapeutic Potential in Kidney Diseases

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