End-stage renal disease causes an imbalance between endothelial and smooth muscle progenitor cells

Westerweel, Peter E.; Hoefer, Imo E.; Bree, Petra de; Groeneveld, Dafna; Oostrom, Olivia van; Braam, Branko; Koomans, Hein A.; Verhaar, Marianne C.

doi:10.1152/ajprenal.00163.2006

Cited by 78 publications

(76 citation statements)

References 44 publications

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“…Here, we tested the ability of CKD patient-derived EPC to adhere to fibronectin-coated PCLdiUPy and found a high reduction in the number of adhering cells (up to 78%) compared with EPC from healthy controls. This reduction in adherent EPC numbers was not caused by EPC apoptosis in CKD patients (45), since apoptosis frequencies were comparable in CKD patients and healthy controls. Moreover, endothelial outgrowth of adherent EPC was also highly reduced (up to 80%) in patients with CKD compared with healthy controls.…”

Section: Discussionmentioning

confidence: 74%

“…Similarly, others have described decreases in erythropoiesis (11,13), increases in progenitor cell apoptosis (45) and impairment of EPC migration (6,9) caused by uremic toxins present in serum from CKD patients. However, we cannot exclude interference of antihypertensive drugs as confounder in our analysis, since all CKD patients were kept on their regular medication.…”

Section: Discussionmentioning

confidence: 83%

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Endothelial progenitor cell dysfunction in patients with progressive chronic kidney disease

Krenning¹,

Dankers²,

Drouven³

et al. 2009

American Journal of Physiology-Renal Physiology

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Endothelial progenitor cells (EPC) contribute to repair and maintenance of the vascular system, but in patients with chronic kidney disease (CKD), the number and function of EPC may be affected by kidney dysfunction. We assessed numbers and the angiogenic function of EPC from patients with CKD in relation to disease progression. In a cross-sectional, prospective study, 50 patients with varying degrees of CKD, including 20 patients undergoing dialysis and 10 healthy controls, were included. Mononuclear cells were isolated, and circulating EPC were quantified by flow cytometry based on expression of CD14 and CD34. EPC were cultured on fibronectin-coated supramolecular films of oligocaprolactone under angiogenic conditions to determine their angiogenic capacity and future use in regenerative medicine. CKD patients had normal numbers of circulating CD14+ EPC but reduced numbers of circulating CD34+ EPC. Furthermore, EPC from patients with CKD displayed functional impairments, i.e., hampered adherence, reduced endothelial outgrowth potential, and reduced antithrombogenic function. These impairments were already observed at stage 1 CKD and became more apparent when CKD progressed. Dialysis treatment only partially ameliorated EPC impairments in patients with CKD. In conclusion, EPC number and function decrease with advancing CKD, which may hamper physiological vascular repair and can add to the increased risk for cardiovascular diseases observed in CKD patients.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 83%

Endothelial progenitor cell dysfunction in patients with progressive chronic kidney disease

Krenning¹,

Dankers²,

Drouven³

et al. 2009

American Journal of Physiology-Renal Physiology

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“…Although there is no study reporting endothelial dysfunction in patients with haematuria and/or renal infections, several studies have reported that EPCs are numerically and functionally impaired in patients with acute 29 or chronic renal failure, 30 as compared with healthy subjects, and mechanisms such as inflammation or uraemic toxins have been given as potential explanations for the observed EPC dysfunction. 30 More clear and direct is the relationship between miscarriages and possible endothelial dysfunction, given that development, maturation and maintenance of a neovascular network are necessary for successful haemochorial placentation as well as normal embryonic development and growth.…”

Section: Discussionmentioning

confidence: 99%

Extended extraocular phenotype of PROM1 mutation in kindreds with known autosomal dominant macular dystrophy

et al. 2010

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Mutations in prominin 1 (PROM1) have been shown to result in retinitis pigmentosa, macular degeneration and cone-rod dystrophy. Because of the putative role of PROM1 in hippocampal neurogenesis, we examined two kindreds with the same R373C PROM1 missense mutation using our established paradigm to study brain structure and function. As the protein encoded by PROM1, known as CD133, is used to identify stem/progenitor cells that can be found in peripheral blood and reflect endothelial reparatory mechanisms, other parameters were subsequently examined that included measures of vascular function, endothelial function and angiogenic capacity. We found that aspects of endothelial function assayed ex vivo were abnormal in patients with the R373C PROM1 mutation, with impaired adhesion capacity and higher levels of cellular damage. We also noted renal infections, haematuria and recurrent miscarriages possibly reflecting consequences of abnormal tubular modelling. Further studies are needed to confirm these findings.

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“…Indeed, low levels of EPC predicted the occurrence of cardiovascular events and death in coronary artery disease patients (104). An imbalance between the expression of circulating endothelial cells (reflecting inflammatory endothelial damage) and EPC (reflecting endothelial repair capacity) seems to exist in CKD (105,106). This imbalance may contribute to the pathogenesis and progression of the atherosclerosis process in CKD patients and may be linked to the ability of circulating inflammatory endothelial cells to interfere with the functional capacity for vessel wall repair by EPCs (107).…”

Section: Endothelial Dysfunction-a Common Feature Of Ckd Linked To Admentioning

confidence: 99%

Emerging Biomarkers for Evaluating Cardiovascular Risk in the Chronic Kidney Disease Patient

Stenvinkel¹,

Carrero²,

Axelsson³

et al. 2008

Clinical Journal of the American Society of Nephrology

491

373

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Premature cardiovascular disease (CVD), including stroke, peripheral vascular disease, sudden death, coronary artery disease, and congestive heart failure, is a notorious problem in patients with chronic kidney disease (CKD). Because the presence of CVD is independently associated with kidney function decline, it appears that the relationship between CKD and CVD is reciprocal or bidirectional, and that it is this association that leads to the vicious circle contributing to premature death. As randomized, placebo-controlled trials have so far been disappointing and unable to show a survival benefit of various treatment strategies, such a lipid-lowering, increased dialysis dose and normalization of hemoglobin, the risk factor profile seems to be different in CKD compared with the general population. Indeed, seemingly paradoxical associations between traditional risk factors and cardiovascular outcome in patients with advanced CKD have complicated our efforts to identify the real cardiovascular culprits. This review focuses on the many new pieces that need to be fit into the complicated puzzle of uremic vascular disease, including persistent inflammation, endothelial dysfunction, oxidative stress, and vascular ossification. Each of these is not only highly prevalent in CKD but also more strongly linked to CVD in these patients than in the general population. However, a causal relationship between these new markers and CVD in CKD patients remains to be established. Finally, two novel disciplines, proteomics and epigenetics, will be discussed, because these tools may be helpful in the understanding of the discussed vascular risk factors.

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End-stage renal disease causes an imbalance between endothelial and smooth muscle progenitor cells

Cited by 78 publications

References 44 publications

Endothelial progenitor cell dysfunction in patients with progressive chronic kidney disease

Endothelial progenitor cell dysfunction in patients with progressive chronic kidney disease

Extended extraocular phenotype of PROM1 mutation in kindreds with known autosomal dominant macular dystrophy

Emerging Biomarkers for Evaluating Cardiovascular Risk in the Chronic Kidney Disease Patient

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