Post-Transplant C-Reactive Protein Predicts Arterial Stiffness and Graft Function in Renal Transplant Recipients

Demirci, Bahar Gürlek; Sezer, Sıren; Çolak, Turan; Sayin, Cihad Burak; Tutal, Emre; Haberal, Mehmet

doi:10.1016/j.transproceed.2014.10.064

Cited by 5 publications

(5 citation statements)

References 15 publications

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“…Several other cross-sectional studies demonstrated the link between metabolic syndrome, arterial stiffness, and inflammation ( 97 ). Increased CRP levels were associated with elevated PWV in patients after renal transplant , and overall CRP was suggested to be a useful marker to anticipate graft survival and cardiovascular morbidity in renal transplant recipients ( 102 ).…”

Section: Crp High-sensitivity C-reactive Protein (Hscrp) and Arterimentioning

confidence: 99%

“…C-reactive protein and hsCRP were associated with arterial stiffness in patients with metabolic syndrome, renal transplant, diabetes mellitus, and RA (Table 4 ) ( 7 , 21 , 102 , 104 ). Many interventions able to reduce cardiovascular risk have been associated with lower hsCRP values, such as weight loss, diet, exercise, smoking cessation, use of lipid-lowering drugs (statins, niacin, fibrates, gemfibrozil), aspirin, and thiazolidinediones ( 92 ).…”

Section: Crp High-sensitivity C-reactive Protein (Hscrp) and Arterimentioning

confidence: 99%

“…Most of the studies were cross-sectional, often with only a relatively small number of participants, and sometimes with just one measurement of inflammatory markers, all of which is unfavorable for the significance of results and their interpretation. The cross-sectional design of most studies cannot establish causality, it can only establish an association ( 102 ). Relatively small numbers of study participants, which are often a specific subgroup of patients with certain morbidities does not allow to extend conclusions to the general population; therefore, the results of many studies presented here need confirmation in larger studies.…”

Section: Study Limitationsmentioning

confidence: 99%

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Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

Malainer²,

et al. 2017

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Arterial stiffness predicts an increased risk of cardiovascular events. Inflammation plays a major role in large arteries stiffening, related to atherosclerosis, arteriosclerosis, endothelial dysfunction, smooth muscle cell migration, vascular calcification, increased activity of metalloproteinases, extracellular matrix degradation, oxidative stress, elastolysis, and degradation of collagen. The present paper reviews main mechanisms explaining the crosstalk between inflammation and arterial stiffness and the most common inflammatory markers associated with increased arterial stiffness, considering the most recent clinical and experimental studies. Diverse studies revealed significant correlations between the severity of arterial stiffness and inflammatory markers, such as white blood cell count, neutrophil/lymphocyte ratio, adhesion molecules, fibrinogen, C-reactive protein, cytokines, microRNAs, and cyclooxygenase-2, in patients with a broad variety of diseases, such as metabolic syndrome, diabetes, coronary heart disease, peripheral arterial disease, malignant and rheumatic disorders, polycystic kidney disease, renal transplant, familial Mediterranean fever, and oral infections, and in women with preeclampsia or after menopause. There is strong evidence that inflammation plays an important and, at least, partly reversible role in the development of arterial stiffness, and inflammatory markers may be useful additional tools in the assessment of the cardiovascular risk in clinical practice. Combined assessment of arterial stiffness and inflammatory markers may improve non-invasive assessment of cardiovascular risk, enabling selection of high-risk patients for prophylactic treatment or more regular medical examination. Development of future destiffening therapies may target pro-inflammatory mechanisms.

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Section: Crp High-sensitivity C-reactive Protein (Hscrp) and Arterimentioning

confidence: 99%

Section: Crp High-sensitivity C-reactive Protein (Hscrp) and Arterimentioning

confidence: 99%

Section: Study Limitationsmentioning

confidence: 99%

See 1 more Smart Citation

Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

Malainer²,

et al. 2017

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“…In greater detail, high plasma (as well as urinary) concentrations of tumor necrosis factor -α (TNF-a, a pro-inflammatory cytokine) have been related to higher risk of graft rejection and impaired graft function, through activation of T lymphocytes [8][9][10][11]. Elevated serum amyloid A (SAA, an acute phase protein) has also exhibited an association with kidney allograft rejection [12][13][14][15][16][17], while increased C-reactive protein (CRP, an acute phase protein, as well) is also considered a harbinger of chronic allograft dysfunction, graft rejection and cardiovascular mortality [6,7,[17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Changes of serum Amyloid-A (SAA), tumor necrosis factor-a (TNF-a), c-reactive protein (CRP) and association of CRP with cystatin-c in kidney transplantation

Gompou,

Perrea,

Karatzas

et al. 2023

Hematol Med Oncol

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Objective: This study was performed to determine whether renal function and graft origin affect serum levels of tumor necrosis factor-a (TNF-a), serum amyloid A (SAA) and C-reactive protein (CRP), among individuals having undergone renal transplantation (Tx). Methods:In a sample of fifty kidney recipients, serum creatinine (Cr), SAA, TNF-α and CRP were quantitatively determined at several time-points, pre-and post-Tx (2nd, 6th, 14th day, 3 months post-Tx). Patients were grouped as follows: those presenting restored renal function (<1.5mg/dl three months post-Tx) versus those with mild renal dysfunction (>1.5mg/dl three months post-Tx), patients having received allograft from living donors versus patients having received cadaveric grafts.Results: A total of 32 participants received grafts from living donor while 18 received cadaveric transplants. Two evenly numbered groups (N=25) were formed according to the presence of mild renal dysfunction. The differences of SAA values between those with and without restored renal function, as well as between living versus cadaveric graft recipients, were not significant at any time point. Similarly, no disparities were detected in TNF-a levels, between patients with serum Cr<1.5mg/dl and those with Cr>1.5mg/dl, or between recipients of living and cadaveric donors. Finally, serum CRP levels were homogeneous in individuals with and without mild renal dysfunction, as well as in patients receiving grafts from living and cadaveric donors throughout the three-month follow-up. In an exploratory analysis, serum CRP and cystatin-c were not correlated, at any of the time-points.Conclusions: SAA, TNF-α and CRP are not differentiated by renal function and graft origin after renal transplantation.

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“…Arterial stiffness is a biologic process related to ageing [ 13 , 14 ] and blood pressure [ 15 ], but also with inflammation [ 16 , 17 ], arterial calcification [ 18 ] and stage of chronic kidney disease (CKD) [ 19 ]. In kidney transplant recipients, several studies have also associated arterial elasticity with donor age [ 20 ], donor vascular stiffness (in the case of living donors) [ 21 ], new-onset diabetes post-transplantation [ 22 ], cold ischaemia time [ 23 ], renal graft function [glomerular filtration rate (GFR)] [ 24 ], hypomagnesaemia [ 25 ] and resistance training [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Impact of immunosuppressive therapy on arterial stiffness in kidney transplantation: are all treatments the same?

Melilli

Manonelles

Montero

et al. 2017

Clinical Kidney Journal

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Arterial stiffness is a biologic process related to ageing and its relationship with cardiovascular risk is well established. Several methods are currently available for non-invasive measurement of arterial stiffness that provide valuable information to further assess patients’ vascular status in real time. In kidney transplantation recipients, several factors could accelerate the stiffness process, such as the use of calcineurin inhibitors (CNIs), the presence of chronic kidney disease and other classical cardiovascular factors, which would explain, at least in part, the high cardiovascular mortality and morbidity. Despite the importance of arterial stiffness as a biomarker of cardiovascular risk, and unlike other cardiovascular risk factors (e.g. left ventricular hypertrophy), only a few clinical trials or retrospective studies of kidney recipients have evaluated its impact. In this review we describe the clinical impact of arterial stiffness as a prognostic marker of cardiovascular disease and the effects of different immunosuppressive regimens on its progression, focusing on the potential benefits of CNI-sparing protocols and supporting the rationale for individualization of immunosuppression in patients with lower arterial elasticity. Among the immunosuppressive drugs, a belatacept-based regimen seems to offer better vascular protection compared with CNIs, although further studies are needed to confirm the preliminary positive results.

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Post-Transplant C-Reactive Protein Predicts Arterial Stiffness and Graft Function in Renal Transplant Recipients

Cited by 5 publications

References 15 publications

Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

Changes of serum Amyloid-A (SAA), tumor necrosis factor-a (TNF-a), c-reactive protein (CRP) and association of CRP with cystatin-c in kidney transplantation

Impact of immunosuppressive therapy on arterial stiffness in kidney transplantation: are all treatments the same?

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