scholarly journals Circulating Endothelial Cells and Chronic Kidney Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Kunying Zhang ◽  
Fang Yin ◽  
Lin Lin
Keyword(s):  
Chronic Kidney Disease ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Vascular Dysfunction ◽  
Endothelial Damage ◽  
Circulating Endothelial Cells ◽  
Response To Treatment ◽  
Term Outcome ◽  
Long Term Outcome

Endothelial dysfunction may play a crucial role in initiation of the pathogenesis of vascular disease and atherosclerosis. The identification and quantification of circulating endothelial cells (CEC) have been developed as a novel marker of endothelial function. We describe, in great detail, mechanisms of endothelial dysfunction and CEC detachment. We also review the relationship between numbers of CEC and disease severity and response to treatment. In addition, we describe the possible clinical use of CEC in chronic kidney disease (CKD) and kidney transplantation. In summary, CEC have been developed as a novel approach to assess the endothelial damage. Measurement of the CEC level would provide an important diagnostic and prognostic value on the endothelium status and the long-term outcome of vascular dysfunction.

scholarly journals Long-Term Outcome of Infants with Severe Chronic Kidney Disease

2009 ◽  
Vol 5 (1) ◽  
pp. 10-17 ◽  
Author(s):  
Djalila Mekahli ◽  
Vanessa Shaw ◽  
Sarah E. Ledermann ◽  
Lesley Rees
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Severe Chronic Kidney Disease

scholarly journals FGF23 impairs peripheral microvascular function in renal failure

2018 ◽  
Vol 315 (5) ◽  
pp. H1414-H1424 ◽  
Author(s):  
Melissa Verkaik ◽  
Rio P. Juni ◽  
Ellen P. M. van Loon ◽  
Erik M. van Poelgeest ◽  
Rick F. J. Kwekkeboom ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Asymmetric Dimethylarginine ◽  
Ex Vivo ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

Cardiovascular diseases account for ~50% of mortality in patients with chronic kidney disease (CKD). Fibroblast growth factor 23 (FGF23) is independently associated with endothelial dysfunction and cardiovascular mortality. We hypothesized that CKD impairs microvascular endothelial function and that this can be attributed to FGF23. Mice were subjected to partial nephrectomy (5/6Nx) or sham surgery. To evaluate the functional role of FGF23, non-CKD mice received FGF23 injections and CKD mice received FGF23-blocking antibodies after 5/6Nx surgery. To examine microvascular function, myocardial perfusion in vivo and vascular function of gracilis resistance arteries ex vivo were assessed in mice. 5/6Nx surgery blunted ex vivo vasodilator responses to acetylcholine, whereas responses to sodium nitroprusside or endothelin were normal. In vivo FGF23 injections in non-CKD mice mimicked this endothelial defect, and FGF23 antibodies in 5/6Nx mice prevented endothelial dysfunction. Stimulation of microvascular endothelial cells with FGF23 in vitro did not induce ERK phosphorylation. Increased plasma asymmetric dimethylarginine concentrations were increased by FGF23 and strongly correlated with endothelial dysfunction. Increased FGF23 concentration did not mimic impaired endothelial function in the myocardium of 5/6Nx mice. In conclusion, impaired peripheral endothelium-dependent vasodilatation in 5/6Nx mice is mediated by FGF23 and can be prevented by blocking FGF23. These data corroborate FGF23 as an important target to combat cardiovascular disease in CKD.NEW & NOTEWORTHY In the present study, we provide the first evidence that fibroblast growth factor 23 (FGF23) is a cause of peripheral endothelial dysfunction in a model of early chronic kidney disease (CKD) and that endothelial dysfunction in CKD can be prevented by blockade of FGF23. This pathological effect on endothelial cells was induced by long-term exposure of physiological levels of FGF23. Mechanistically, increased plasma asymmetric dimethylarginine concentrations were strongly associated with this endothelial dysfunction in CKD and were increased by FGF23.

scholarly journals Circulating argonaute-bound microRNA-126 reports vascular dysfunction & response to treatment in acute & chronic kidney disease

2020 ◽  
Author(s):  
Kathleen M Scullion ◽  
A D Bastiaan Vliegenthart ◽  
Laura Rivoli ◽  
Wilna Oosthuyzen ◽  
Tariq E Farrah ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Function ◽  
Clinical Decision Making ◽  
Vascular Dysfunction ◽  
Unmet Need ◽  
Post Treatment ◽  
Response To Treatment ◽  
Serum Samples ◽  
Anca Vasculitis

Background: Vascular and kidney dysfunction commonly co-exist. There is an unmet need for biomarkers of vascular health. Circulating microRNAs (miRs) are disease biomarkers; miR-126 is endothelial cell-enriched. We measured circulating miR-126 in rats with nephrotoxic nephritis (NTN) and humans with acute endothelial and renal injury (vasculitis associated with autoantibodies to neutrophil cytoplasm antigens (ANCA)). We then compared these findings to those from patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD), and explored the relationship between miR-126 and markers of vascular dysfunction. Methods: In rats, NTN was induced with nephrotoxic serum. Samples were prospectively collected from 70 patients with ANCA vasculitis (at presentation and once in treatment-induced remission), healthy subjects (n=60), patients with CKD (n=30) and ESRD before and after dialysis (n=15). In humans and rats, miR-126 and miR-122 (liver-specific control) were measured and correlated with vascular function. Results: In NTN rats, miR-126 was selectively reduced. In ANCA vasculitis, pre-treatment circulating miR-126 was reduced compared to health (88-fold reduction, ROC-AUC 0.87 (0.80-0.94)). miR-126 increased 3.4-fold post-treatment but remained lower than in health (~26-fold). There was no change in miR-122. Plasma fractionation demonstrated that argonaute 2-bound miR-126 increased with treatment of ANCA vasculitis. Urinary miR-126 decreased post-treatment. miR-126 did not differ between CKD and health but its concentration significantly correlated with measures of endothelial dysfunction. miR-126 was substantially reduced in ESRD (~350 fold compared to health and CKD). Conclusions: miR-126 may be a marker of vascular inflammation and has the potential to aid in clinical decision-making.

scholarly journals Perinephric pseudocyst in a cat: management by ultrasound-guided drainage

2018 ◽  
Vol 68 (2) ◽  
pp. 245
Author(s):  
K. K. ADAMAMA-MORAITOU ◽  
D. PARDALI ◽  
I. VAFIADIS ◽  
M. N. PATSIKAS ◽  
N. N. PRASSINOS
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Abdominal Distension ◽  
Sudden Onset ◽  
Ultrasound Guided ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Mild Anemia ◽  
Biochemical Testing ◽  
Moderate Chronic Kidney Disease

A 15-year-old castrated DSH cat was presented with a sudden onset of abdominal distension of 10 days duration. Polyuria/polydipsia, sporadic vomiting and weight loss were also mentioned by the owners. Distension of the cranial abdomen was observed on admission, and two smooth masses were palpated in the abdomen. Mild anemia and azotemia were detected on hematological and biochemical testing. Plain lateral and dorsoventral radiographic views of the abdomen were compatible with renomegaly. Ultrasonography revealed the presence of fluid surrounding both kidneys, and analysis of the accumulated fluid confirmed the diagnosis of bilateral subcapsular transudative perinephric (perirenal) pseudocysts. The precise etiology of pseudocysts formation in our cat could not be identified. Emphasis is placed on their development, due to the coexisting chronic kidney disease, but also to other causes. Although surgical or laparoscopical resection of the cyst wall is generally recommended, owners of this cat elected periodical ultrasound-guided drainage of the perinephric fluid. This might be a reasonable decision, due to its advanced age and the macroconcurrent moderate chronic kidney disease. The long term outcome was favorable, with permanent remission of the perinephric pseudocysts after only three evacuations. The cat died, approximately 20 months after the initial presentation, due to deterioration of chronic kidney disease, and perinephric pseudocysts could not be detected clinically at that time.

Abstract 3: HDL-MicroRNA-92a and Interleukin-33 Axis Underlies Endothelial Dysfunction Associated With Atherosclerosis and Chronic Kidney Disease

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Carrie B Wiese ◽  
Cynthia L Toth ◽  
Fatiha Tabet ◽  
Robert C Taylor ◽  
Stuart R Landstreet ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Locked Nucleic Acid ◽  
High Density Lipoproteins ◽  
Mrna Levels ◽  
Interleukin 33 ◽  
General Cargo ◽  
Aortic Endothelial

Chronic kidney disease (CKD) is associated with endothelial dysfunction and atherosclerosis. High-density lipoproteins (HDL) serve as a general cargo carrier for a wide-variety of proteins, nucleic acids, and small molecules which likely confer many of HDL’s alternative functions. Human coronary artery endothelial cells (HCAEC) treated with native HDL were found to have increased intracellular levels of miR-92a, a miRNA recently found to protect against endothelial dysfunction and atherosclerosis. Moreover, HDL delivery of miR-92a was inhibited using SR-BI blocking antibodies in endothelial cells. Likewise, aortic endothelial miR-92a levels were found to be significantly decreased (50%) in Apoe-/- mice compared to wild-type controls, which may be a function of the absence of HDL in these mice. Using photoactivatable-ribonucleoside-crosslinked-immunoprecipitation-high-throughput-sequencing, we found that HDL transfer multiple miR-92a isomiR variants from macrophages to HCAECs, which were found in association with Argonaute2 RNA-induced silencing complexes. Using whole-genome arrays, we found that HDL alters the expression of many genes in HCAECs, including the significant down-regulation of 18 putative miR-92a targets. Strikingly, miR-92a was found to be significantly increased 8.5-fold on HDL from CKD subjects. Interleukin-33 (IL-33) is a cytokine and nuclear transcription factor largely expressed in endothelial cells. HDL from both normal and CKD subjects significantly decreased IL-33 expression in HCAECs, as determined by real-time PCR and microarrays. In a mouse model of CKD (Apoe-/-; 5/6 nephrectomy), IL-33 expression was increased in aortic endothelial cells; however, a single HDL injection (4mg) reduced IL-33 mRNA back to sham levels at 7d post-injection. Most interestingly, HDL loaded with locked-nucleic acid miR-92a inhibitors blocked HDL’s ability to suppress CKD induced IL-33 expression in the aortic endothelium. IL-33 may represent a novel marker of endothelial dysfunction, as IL-33 mRNA levels were also found to be increased in HCAECs under disturbed flow conditions. Results from this study suggest that HDL suppression of IL-33 in CKD requires miR-92a, which is also transferred to endothelial cells by HDL.

scholarly journals Using CHADS2 and CHA2DS2-VASc scores for mortality prediction in patients with chronic kidney disease

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Po-Chao Hsu ◽  
Wen-Hsien Lee ◽  
Szu-Chia Chen ◽  
Yi-Chun Tsai ◽  
Ying-Chih Chen ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
High Risk ◽  
Kidney Disease ◽  
Mortality Prediction ◽  
Multivariate Model ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Basic Model ◽  
All Cause Mortality

Abstract Chronic kidney disease (CKD) is a public health issue and is associated with high morbidity and mortality. How to identify the high-risk CKD patients is very important to improve the long-term outcome. CHADS2 and CHA2DS2-VASc scores are clinically useful scores to evaluate the risk of stroke in patients with atrial fibrillation. However, there was no literature discussing about the usefulness of CHADS2 and CHA2DS2-VASc scores for cardiovascular (CV) and all-cause mortality prediction in CKD patients. This longitudinal study enrolled 437 patients with CKD. CHADS2 and CHA2DS2-VASc scores were calculated for each patient. CV and all-cause mortality data were collected for long-term outcome prediction. The median follow-up to mortality was 91 (25th–75th percentile: 59–101) months. There were 66 CV mortality and 165 all-cause mortality. In addition to age and heart rate, CHADS2 and CHA2DS2-VASc scores (both P value < 0.001) were significant predictors of CV and all-cause mortality in the multivariate analysis. Besides, in direct comparison of multivariate model, basic model + CHA2DS2-VASc score had a better additive predictive value for all-cause mortality than basic model + CHADS2 score (P = 0.031). In conclusion, our study showed both of CHADS2 and CHA2DS2-VASc scores were significant predictors for long-term CV and all-cause mortality in CKD patients and CHA2DS2-VASc score had a better predictive value than CHADS2 score for all-cause mortality in direct comparison of multivariate model. Therefore, using CHADS2 and CHA2DS2-VASc scores to screen CKD patients may be helpful in identifying the high-risk group with increased mortality.

Imbalance between Detached Circulating Endothelial Cells and Endothelial Progenitor Cells in Chronic Kidney Disease

2006 ◽  
Vol 24 (2) ◽  
pp. 196-202 ◽  
Author(s):  
Ernesto Rodríguez-Ayala ◽  
Qiang Yao ◽  
Carolina Holmén ◽  
Bengt Lindholm ◽  
Suchitra Sumitran-Holgersson ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Endothelial Cells ◽  
Kidney Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Circulating Endothelial Cells ◽  
Endothelial Progenitor

scholarly journals MO474PCSK9 LEVELS AND MARKERS OF INFLAMMATION, OXIDATIVE STRESS AND ENDOTHELIAL DYSFUNCTION IN A POPULATION OF NON-DIALYSIS CHRONIC KIDNEY DISEASE PATIENTS: IS THERE AN ASSOCIATION?

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Evangelia Ntounousi ◽  
Konstantinos Tellis ◽  
Paraskevi Pavlakou ◽  
Anila Duni ◽  
Vassilios Liakopoulos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Renal Function ◽  
Lipid Metabolism ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Endothelial Damage ◽  
Apo B ◽  
Markers Of Inflammation ◽  
Ckd Stage

Abstract Background and Aims Proprotein convertase subtilisin / kexin 9 (PCSK9) plays an important role in lipid metabolism while available literature regarding its involvement in the pathogenesis of atherosclerosis and in the expression of genes associated with apoptosis and inflammation is constantly increasing. Patients with chronic kidney disease (CKD) experience disproportionately increased cardiovascular morbidity and mortality due to dyslipidemia, accelerated atherosclerosis, inflammation, oxidative stress and other risk factors. In the present cross-sectional study, we investigated the possible association of serum PCSK9 levels with markers of inflammation, oxidative stress and endothelial damage in patients with CKD. Method Ninety-two patients with CKD stage II-ΙV (eGRF CKD-EPI 47.3 ±25.7ml/min/1,73m2, mean age 66 years, 51 men) were included. Plasma PCSK9 levels were correlated with comorbidities (arterial hypertension; diabetes mellitus, history of cardiovascular disease), renal function indices (eGFR, proteinuria – UPR/24h), lipid parameters (LDL-cholesterol, HDL-cholesterol, triglycerides, Lp (a), APO-A1, APO-B), as well as soluble biomarkers of inflammation, oxidative stress and endothelial damage (hs-CRP, fibrinogen, 8-epiPGF2a, ox-LDL, IL-6, TNF-α, sICAM-1, sVCAM-1). Results The mean plasma value of PCSK9 was 278.1ng/ml. PCSK9 levels showed direct correlation with serum triglycerides (p = 0.03), Lp(a) (p = 0.01), and sICAM-1 levels (p = 0.03). There was no significant correlation between PCSK9 levels and indices of renal function, other lipid profile parameters, inflammatory markers or co-morbidities. Multiple regression analysis showed a significant effect of the Lp(a) on PCSK9 levels, for each unit of higher Lp(a), an increase by 3.082 is expected (95% CI: 0.935 - 5.228, p=0.006). At the same time, patients receiving statins are expected to have on average 63.8ng/ml higher PCSK9 values compared to patients not receiving statins (95% CI: 14.6 - 113.5 p=0.012). Conclusion Plasma levels of PCSK9 in non-dialysis CKD patients are correlated with endothelial dysfunction and lipid metabolism parameters. Statin intake increases PCSK9 levels significantly in this patient population. PCSK9 levels are not correlated with the severity of kidney disease. Major prospective studies are necessary to investigate the role of PCSK9 in the atherosclerotic cardiovascular outcome in CKD

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