Circulating Endothelial Progenitor Cells After Kidney Transplantation

Soler, María José; Martínez-Estrada, Ofelia M.; Puig-Marí, Josep Maria; Marco-Feliu, D; Oliveras, Anna; Vila, Joan; Mir, Marisa; Orfila, A; Vilaró, Senén; Lloveras, J

doi:10.1111/j.1600-6143.2005.01010.x

Cited by 23 publications

(25 citation statements)

References 30 publications

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“…Wide literature described an impaired number of CAC colonies in cardiovascular disease and in T1D (7,17,46,47) concluding that an in vitro colony growth defect would represent their dysfunction. Furthermore 'early outgrowth' but not 'late outgrowth' angiogenic cells have been well studied in the presence of immunosuppressants (48,49) and it was found that addition of an mTOR inhibitor resulted in dramatic impairment in 'early outgrowth' angiogenic cell number (50,51). Thus, we focused on the number of colonies as a quantification of CAC function in T1D, in insulin-independent islettransplanted immunosuppressed patients and in controls.…”

Section: Discussionmentioning

confidence: 99%

Improved Function of Circulating Angiogenic Cells Is Evident in Type 1 Diabetic Islet-Transplanted Patients

Petrelli

Maestroni

Fadini

et al. 2010

American Journal of Transplantation

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Circulating angiogenic cells (CACs) are vascularcommitted bone marrow-derived cells that are dysfunctional in type 1 diabetes (T1D).Here we studied whether restoration of normoglycemia following islet transplantation is associated with better CAC function. We carried out a cross-sectional study of 18 T1D patients, 14 insulin-independent islet-transplanted patients (ITA) and 14 healthy controls (C) evaluating in vivo and in vitro CACs viability and function. We found that the percentage of CACs in vivo did not differ among the three groups while the number of CAC colonies obtained from T1D, but not from ITA, was reduced compared to C (C = 7.3 ± 1.9, T1D = 0.9 ± 0.4 and ITA = 4.7 ± 1.9; p < 0.05 T1D vs. all). In vitro CAC migration/differentiation were similar, while in vivo an improved angiogenic ability of ITA compared to T1D was shown (capillary density: C = 93.5 ± 22.1, T1D = 19.2 ± 2.8 and ITA = 44.0 ± 10.5, p < 0.05 T1D vs. all). Increased apoptosis and lesser IL-8 secretion were evident in CACs obtained from T1D compared to C and ITA. in vitro addition of anti-hIL-8 reduced the number of colonies obtained from C. Finally, T1D, but not ITA, had a lower endothelial-dependent dilatation (EDD) compared with C. These data suggest that CAC function is altered in T1D and may be improved after islet transplantation.

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Section: Discussionmentioning

confidence: 99%

Improved Function of Circulating Angiogenic Cells Is Evident in Type 1 Diabetic Islet-Transplanted Patients

Petrelli

Maestroni

Fadini

et al. 2010

American Journal of Transplantation

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“…Steiner et al and de Groot and coworkers observed normalized EPC numbers after KTx (17,18). In contrast, Soler et al reported significantly reduced EPC numbers in renal transplant recipients compared to control subjects (19). Furthermore, tests of functional features of EPC may be of importance too.…”

Section: Introductionmentioning

confidence: 96%

Kidney Transplantation Substantially Improves Endothelial Progenitor Cell Dysfunction in Patients with End-Stage Renal Disease

Herbrig¹,

Gebler²,

Oelschlaegel

et al. 2006

American Journal of Transplantation

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Endothelial progenitor cells (EPC) are involved in endothelial repair and maintenance. Dysfunction of EPC may contribute to accelerated arteriosclerosis in chronic kidney disease. Kidney transplantation (KTx) improves both survival and endothelial function of dialysis patients. In a prospective study, we tested to which extent KTx changes EPC biology. We studied number and function (migratory activity, adhesion to extracellular matrix proteins and to mature endothelial cells [EC]) of EPC in 20 patients during dialysis and 3, 6, 9 and 12 months after KTx. Twenty-two healthy volunteers served as matched controls. Circulating precursor populations were measured by flow cytometric analysis. Cytokines relevant for EPC mobilization were monitored. Compared to the dialysis state, KTx increased the migration of EPC to approximately 2-fold. Adhesion to fibronectin and to collagen type IV was significantly increased after KTx. An improved adhesion rate of EPC to mature EC was observed. The number of EPC decreased. The amount of precursor populations showed no difference compared to the pretransplant state. Our study shows an improved function of EPC after KTx. This finding indicates an improved potential for endothelial repair which in turn may contribute to enhanced endothelial function and reduced cardiovascular morbidity after KTx.

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“…Impaired endothelial vasodilation seems to be related to oxidative stress (159) and reduced levels of nitric oxide (160), likely as a result if accumulation in renal failure of an inhibitor of nitric oxide synthase, asymmetrical dimethylarginine (161)(162)(163)(164)(165)(166). In addition, reduced levels of circulating endothelial progenitor cells and increased numbers of mature endothelial cells have been noted in renal failure and have been hypothesized to reflect ongoing endothelial injury and perhaps poor repair function (167)(168)(169)(170)(171)(172)(173).…”

Section: Pathophysiology Of Cvd In Ckdmentioning

confidence: 99%

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Nogueira

Weir

2007

Clinical Journal of the American Society of Nephrology

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D uring the past several decades, the advent and refinement of maintenance dialysis and kidney transplantation have essentially eliminated kidney failure per se as a cause of death in developed countries. However, as patients survive many years after the development of renal failure, comorbidities develop, progress, and ultimately cause death in these individuals. Cardiovascular disease (CVD) has ranked prominent among these comorbidities, accounting for nearly half of the deaths (1). All along the continuum of chronic kidney disease (CKD)-from microalbuminuria to ESRD-a higher risk for CVD has been observed (see Epidemiology of CVD in CKD). In fact, individuals with early CKD are more likely to die of CVD than to develop ESRD (2,3). Then, among those who survive to ESRD, the all-cause CVD mortality in patients with ESRD is many-fold higher than in the general population (4). Unfortunately, the reasons for the association of CKD with CVD are not clearly understood, and the role of various clinical interventions in stemming the CVD epidemic are not well defined. Complicating the issue is the potential variation in the pathophysiology and clinical behavior of CVD through the stages of CKD.3-Hydroxyl-3-methylglutaryl CoA reductase inhibitors (statins) and other lipid-lowering drugs (LLD) have been clearly demonstrated to lessen the morbidity and mortality of CVD in the general population; therefore, there is hope that the use of these drugs may likewise help patients with CKD (In addition, it has been theorized that dyslipidemia may contribute to the progression of CKD, such that LLD may prove to slow CKD progression.) Nevertheless, given differences in epidemiology and pathophysiology of CVD in CKD, there are reasons to question whether the cardiovascular benefits of LLD that are observed in the general population will also be realized in the CKD population. It is widely acknowledged that the current medical literature provides insufficient data to guide the use of LLD in the CKD population, in large part because renal insufficiency has been an exclusion criterion for most of the randomized, controlled studies that have addressed this issue. Although consensus-based guidelines on the treatment of dyslipidemias in individuals with CKD and with kidney transplants have been published by the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) Work Groups, the nephrology and cardiology communities recognize the urgent need for high-quality clinical studies on this issue, and this has fueled the publication of subgroup analyses of previous large studies in the general population and the launching of large-scale clinical trials in the CKD population, as summarized in Table 1. To provide the reader with a better appreciation of the important issues that are germane to management of dyslipidemia in CKD, this article (1) briefly summarizes the literature on the benefits of LLD in the general population, (2) demonstrates the limited involvement of individuals with CKD in the studies in the ge...

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Circulating Endothelial Progenitor Cells After Kidney Transplantation

Cited by 23 publications

References 30 publications

Improved Function of Circulating Angiogenic Cells Is Evident in Type 1 Diabetic Islet-Transplanted Patients

Improved Function of Circulating Angiogenic Cells Is Evident in Type 1 Diabetic Islet-Transplanted Patients

Kidney Transplantation Substantially Improves Endothelial Progenitor Cell Dysfunction in Patients with End-Stage Renal Disease

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

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