Endostatin in chronic kidney disease: Associations with inflammation, vascular abnormalities, cardiovascular events and survival

Kanbay, Mehmet; Afsar, Barış; Siriopol, Dimitrie; Ünal, Hilmi Umut; Karaman, Murat; Sağlam, Mutlu; Gezer, Mustafa; Taş, Ahmet; Eyıleten, Tayfun; Güler, Ahmet; Aydın, İbrahim; Oğuz, Yusuf; Tarim, Kayhan; Covic, Adrian; Yılmaz, Mahmut İlker

doi:10.1016/j.ejim.2016.06.033

Cited by 31 publications

(20 citation statements)

References 39 publications

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“…Elevated inflammatory response and increased proteinuria are considered among the important causes of this increased risk 12 . Our previous studies also revealed that vascular inflammation and endothelial dysfunction are the main contributors for CVD events in this patient populations 7 , 13 – 15 .…”

Section: Introductionsupporting

confidence: 57%

Cardiovascular disease risk assessment in patients with familial Mediterranean fever related renal amyloidosis

Romano

Piskin

Berard

et al. 2020

Sci Rep

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Chronic inflammation and proteinuria is a risk factor for cardiovascular disease (CVD) in patients with chronic kidney diseases and rheumatologic disorders. Our aim was to investigate the CVD events (CVDEs) and survival between the patients with FMF-related AA amyloidosis and glomerulonephropathies (GN) to define possible predictors for CVDEs. A prospective follow-up study with FMF-amyloidosis and glomerulonephropathy (GN) was performed and patients were followed for CVDEs. Flow-mediated dilatation (FMD), FGF-23, serum lipid, hsCRP levels, BMI and HOMA were assessed. A Cox regression analysis was performed to evaluate the risk factors for CVDEs. There were 107 patients in the FMF-amyloidosis group and 126 patients with GN group. Forty-seven CVDEs were observed during the 4.2-years follow up; all 28 patients in the FMF-amyloidosis group and 14/19 patients with GN developed CVDEs before the age of 40 (p = 0.002). CVD mortality was 2.8 times higher (95% CI 1.02–7.76) in patients with FMF-amyloidosis. Across both groups, FMD and FGF23 (p < 0.001) levels were independently associated with the risk of CVDEs. Patients with FMF-amyloidosis are at increased risk of early CVDEs with premature mortality age. FGF 23, FMD and hsCRP can stratify the risk of early CVD in patients with FMF-related AA amyloidosis.

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Section: Introductionsupporting

confidence: 57%

Cardiovascular disease risk assessment in patients with familial Mediterranean fever related renal amyloidosis

Romano

Piskin

Berard

et al. 2020

Sci Rep

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“…The association between baseline endostatin concentrations and graft loss is stable, robust, and strong. This study confirms earlier findings that endostatin concentration was correlated with kidney function and age [24][25][26][27]. To further address whether the effect of endostatin is independent of kidney function, age and other risk factors, we applied multiple regression models (Table 3), all models demonstrated the same: endostatin is an independent risk of graft loss after kidney transplantation.…”

Section: Discussionsupporting

confidence: 85%

Endostatin Is an Independent Risk Factor of Graft Loss after Kidney Transplant

Chu¹,

Hasan²,

Gaballa³

et al. 2020

Am J Nephrol

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Background: Endostatin is a 20-kDa C-terminal fragment of collagen XVIII, known for its ability to inhibit the proliferation of capillary endothelial cells. Previous studies suggested that circulating endostatin independently predicts incident chronic kidney disease. However, the impact of endostatin on graft loss level in kidney transplant recipients (KTRs) remains unknown. Methods: We conducted a prospective observational cohort study in 574 maintenance KTRs. Patients were followed for kidney graft loss and allcause mortality during a median follow-up of 48 months. Serum-, and urine-samples and clinical data were collected at baseline. Serum Endostatin concentration was analyzed by an ELISA. Results: Among 574 patients, 37 patients had graft loss and 62 patients died. For graft loss, the optimal cut-off value based on receiver operating characteristics analysis (area under the curve 0.79, 95% CI 0.71-0.86, p < 0.001) of endostatin was 147.3 pmol/L. Kaplan-Meier curves revealed that higher serum endostatin concentrations positively correlated with graft loss (p < 0.001). Multivariable Cox regression analyses showed that baseline endostatin concentrations were significantly associated with graft loss after adjusting for graft loss risk factors (adjusted hazard ratio [HR] 8.34; 95% CI 2.19-31.72; p = 0.002). The adjusted HRs for classical graft loss risk factors such as baseline estimated glomerular filtration rate and urinary protein excretion were lower (1.91 and 5.44, respectively). In contrast to graft loss, baseline endostatin concentrations were not associated with all-cause mortality. Conclusion: Increased serum endostatin at baseline is independently associated with the risk of graft loss in KTRs.

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“…In addition to traditional risk factors for CVD such as older age, male gender, smoking, hypertension, diabetes, and hyperlipidemia, nontraditional risk factors such as anemia, inflammation and oxidative stress, and mineral and bone abnormalities in CKD [3-8] have an undeniable influence on the increased prevalence of CVD observed in CKD. One of the most important pathophysiological mechanisms for CVD in patients with CKD is the widespread and possibly accelerated formation of atherosclerotic plaques due to hyperlipidemia, uremic toxins, inflammation, oxidative stress, and endothelial dysfunction [9, 10]. Recent studies showed that the level of oxidized low-density lipoprotein (LDL) cholesterol increases and high density lipoprotein (HDL) cholesterol dysfunction occurs as kidney function declines and inflammation becomes more pronounced [9, 11] (Fig.…”

Section: Introductionmentioning

confidence: 99%

Disorders of Lipid Metabolism in Chronic Kidney Disease

et al. 2018

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Cardiovascular disease (CVD) is the leading cause of death in chronic kidney disease (CKD). One of the most important pathophysiological mechanisms for CVD in patients with CKD is the widespread and possibly accelerated formation of atherosclerotic plaques due to hyperlipidemia, uremic toxins, inflammation, oxidative stress, and endothelial dysfunction. Recent studies showed that the level of oxidized low-density lipoprotein cholesterol increases, and that high-density lipoprotein cholesterol dysfunction occurs as kidney function declines and inflammation becomes more prevalent. In this review, we aimed to discuss the effect of kidney dysfunction, oxidative stress, and inflammation on lipid profile.

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Endostatin in chronic kidney disease: Associations with inflammation, vascular abnormalities, cardiovascular events and survival

Cited by 31 publications

References 39 publications

Cardiovascular disease risk assessment in patients with familial Mediterranean fever related renal amyloidosis

Cardiovascular disease risk assessment in patients with familial Mediterranean fever related renal amyloidosis

Endostatin Is an Independent Risk Factor of Graft Loss after Kidney Transplant

Disorders of Lipid Metabolism in Chronic Kidney Disease

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