Activated cells in urine and monocyte chemotactic peptide-1 (MCP-1) — Sensitive rejection markers in renal graft recipients

Dubiński, B.; Boratyńska, Maria; Kopeć, W; Szyber, P; Patrzałek, D.; Klinger, Marian

doi:10.1016/j.trim.2007.07.005

Cited by 26 publications

(22 citation statements)

References 17 publications

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“…MCP-1 is a chemokine that attracts monocytes and is elevated in patients with ureteropelvic junction obstruction (19) and renal transplant rejection (20). CD14 is expressed on many cells and has been found to be elevated in the blood of patients with chronic renal disease, possibly as a marker for increased risk of death in patients on dialysis (21).…”

Section: Articlesmentioning

confidence: 99%

Evolution of the urinary proteome during human renal development and maturation: variations with gestational and postnatal age

et al. 2012

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Background: Low birth weight is associated with deficits in nephron number in the infant kidney and increased risk of adulthood hypertension and renal dysfunction. Urinary biomarkers may be potential indicators of renal reserve, but little is known about the influence of gestational and postnatal age on the expression of urinary proteins. The aims of this study were to determine the relationships between selected urinary proteins and renal maturation. We hypothesized that urinary protein patterns would change over time during late nephrogenesis and renal maturation. Methods: Urine samples were collected at birth and over 12 mo from preterm (33-35 wk) and term (38-40 wk) infants. candidate urinary proteins were identified by antibody array and quantified with enzyme-linked immunosorbent assay. results: Preterm infants at birth were found to have relatively elevated levels of insulin-like growth factor binding protein-1, -2, and -6, monocyte chemotactic protein-1, cD14, and sialic acid-binding Ig-like lectin 5. These markers gradually decline to levels similar to those of full-term infants by 2-6 mo of life. In contrast, many urinary markers in healthy full-term infants remain stable over the first year of life. conclusion: Gestational and postnatal age must be considered when evaluating the utility of urinary biomarkers. P remature infants are challenged to adapt to an ex utero environment while organogenesis remains incomplete. In humans, ~60% of nephrons develop during the third trimester (1) with nephrogenesis complete at 32-36 wk gestation (2). Although the kidney continues to mature for an additional 1-2 y, full-term infants have a complete endowment of nephrons, varying widely from 250,000 to 1.8 million per kidney, by 36 wk gestation (2,3) and do not form new nephrons after birth. However, the duration of nephrogenesis and the health of the nephrons in infants born prematurely remain unknown. There appears to be a correlation between gestational age and nephron number in large animal species. Studies in baboons demonstrate a direct correlation between gestational age and nephron number (4). Moreover, prematurely delivered baboons continue to develop nephrons after birth, but the length of gestation inversely correlates with the number of abnormal nephrons (4) (the lower the gestational age the higher the number of abnormal nephrons). There may be a limited window for nephrogenesis to continue postnatally in humans. A single autopsy study has shown that nephrogenesis appears to continue for 40 postnatal days in extremely preterm human infants and then cease (5). A smaller complement of nephrons may not be reflected by renal dysfunction in the preterm infant. However, adults born at a low birth weight, with a reduced number of nephrons, are at increased risk of hypertension, impaired kidney function, and cardiovascular disease (6).As the overall mortality of the premature population decreases, the risk of long-term morbidity in this population emerges (7). Barker and Martyn (8) established a framework for th...

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Section: Articlesmentioning

confidence: 99%

Evolution of the urinary proteome during human renal development and maturation: variations with gestational and postnatal age

et al. 2012

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“…CCL2/MCP-1 was the first CC chemokine to be discovered, acting as a potent chemotactic factor for monocytes, and has been one of the most studied biomarkers [6,10,13,[17][18][19][20][21][22][23][24][25][26][27][28]. Many studies have associated CCL2/MCP-1 with glomerulopathies [6,13,[19][20][21][22][23][24][25][26] and with renal transplantation [10,27,28].…”

Section: Chemokines In Renal Diseasesmentioning

confidence: 99%

“…Many studies have associated CCL2/MCP-1 with glomerulopathies [6,13,[19][20][21][22][23][24][25][26] and with renal transplantation [10,27,28]. Wada and coworkers found significantly elevated urinary levels of this chemokine in adults with diabetic nephropathy, whereas serum levels remained similar to those of healthy volunteers [21].…”

Section: Chemokines In Renal Diseasesmentioning

confidence: 99%

“…Taken together, these studies pointed to a potential role for CCL2/MCP-1 in glomerular inflammation. Concerning renal transplantation, it was previously reported that urinary levels of CCL2/MCP-1 were significantly higher in patients with acute rejection and a significant reduction of this chemokine was found in patients who responded to antirejection treatment [27]. In addition, increased urinary levels of CCL2/MCP-1 at 6 months after renal transplantation might predict renal allograft loss [28].…”

Section: Chemokines In Renal Diseasesmentioning

confidence: 99%

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Chemokines as Potential Markers in Pediatric Renal Diseases

Silva¹,

Pereira²,

Teixeira³

et al. 2016

Biomarkers in Kidney Disease

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Glomerular diseases and obstructive uropathies are the two most frequent causes of chronic kidney disease (CKD) in children. Recently, biomarkers have become a focus of clinical research as potentially useful diagnostic tools in pediatric renal diseases. Among several putative biomarkers, chemokines emerge as promising molecules since they play relevant roles in the pathophysiology of pediatric renal diseases. The evaluation of these inflammatory mediators might help in the management of diverse renal diseases in children and the detection of patients at high risk to develop CKD. The aim of this paper is to revise general aspects of chemokines and the potential link between chemokines and the most common pediatric renal diseases by including experimental and clinical evidence.

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“…57 MCP-1 also plays an important contributory role in the pathogenesis of acute organ rejection and GAD. 63 Interestingly, statins attenuate the production of these chemokines in ECs, SMCs, and monocytes, 19,64 and also reduce CCR2 and CCR5 expression by both ECs and macrophages, attenuating GAD. 65 …”

Section: Chemokines and Ecsmentioning

confidence: 99%

The Role of Chemokines in Transplant Graft Arterial Disease

Shimizu

Mitchell

2008

ATVB

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Abstract-Despite the development of effective immunosuppressive therapy, transplant graft arterial disease (GAD) remains the major limitation to long-term graft survival. Multiple immune and nonimmune risk factors contribute to this vasculopathic intimal hyperplastic process. Thus, initial interplay between host inflammatory cells and donor endothelial cells triggers alloimmune responses, whereas alloantigen-independent factors such as prolonged ischemia, surgical manipulation, ischemia-reperfusion injury, and hyperlipidemia enhance the antigen-dependent events. Intrinsic to all stages of this process are chemokines, a family of 8-to 10-kDa proteins mediating directional migration of immune cells to sites of inflammation and injury. Beyond their role in immune-cell chemotaxis, chemokines also contribute to cellular activation, vascular remodeling, and angiogenesis. Expression of chemokines and their cognate receptors in allografts correlates with acute organ rejection, as well as GAD. Moreover, chemokine or chemokine receptor blockade prolongs graft survival and attenuates GAD in experimental models. Further studies will likely confirm a substantial utility for antichemokine therapy in human organ transplantation. Key Words: atherosclerosis pathophysiology Ⅲ other arteriosclerosis Ⅲ transplantation Ⅲ vascular biology, smooth muscle proliferation and differentiation G raft arterial disease (GAD), also termed allograft arteriopathy, graft vasculopathy, or transplant-associated arteriosclerosis is a vascular intimal proliferative process leading to ischemia and the progressive deterioration of allograft function. GAD is the major limitation to long-term graft and recipient survival after heart transplantation. 1 One-year, 3-year, 5-year, and 10-year survival afte adult heart transplantation is 92%, 80%, 73%, and 49%, respectively, 2 with the majority of mortality attributable to GAD. Intimal thickening, medial attenuation, adventitial fibrosis, and vasoconstriction characterize GAD lesions. 3 These can develop and progress at any time and at variable rates; significant vasculopathy can develop as early as 6 to 12 months posttransplant. Intravascular ultrasound (IVUS) demonstrates GAD in 75% of patients at 3 years after transplantation. 4 Clinical diagnosis of GAD is limited by the lack of ischemic symptoms in the largely denervated allograft, by the relative insensitivity of coronary angiography-which frequently underestimates the extent and severity of diffuse disease-and by the extensive involvement of small intramyocardial vessels. For most cases, retransplantation is the only effective therapy for established GAD, because disease diffuseness usually precludes angioplasty, endarterectomy, or bypass grafting.The mechanisms underlying GAD include antibodymediated and cell-mediated inflammation, followed by tissue remodeling. T cells, B cells, macrophages, dendritic cells, platelets, natural killer (NK) cells, or neutrophils, and vascular cells such as endothelial cells (ECs) and smooth muscle cells (SMCs) all co...

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Activated cells in urine and monocyte chemotactic peptide-1 (MCP-1) — Sensitive rejection markers in renal graft recipients

Cited by 26 publications

References 17 publications

Evolution of the urinary proteome during human renal development and maturation: variations with gestational and postnatal age

Evolution of the urinary proteome during human renal development and maturation: variations with gestational and postnatal age

Chemokines as Potential Markers in Pediatric Renal Diseases

The Role of Chemokines in Transplant Graft Arterial Disease

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