Is hepcidin-25 a predictor of atherosclerosis in hemodialysis patients?

Atherosclerotic cardiovascular disease is an important cause of mortality and morbidity in hemodialysis patients. Iron accumulation in arterial wall macrophages is increased in atherosclerotic lesions. Hepcidin is a key hepatic hormone regulating iron balance. It inhibits iron release from macrophages and iron absorption from enterocytes by binding and inactivating the cellular iron exporter ferroportin. The aim of this study is to investigate the relation of hepcidin-25, iron parameters, and atherosclerosis measured by carotid intima media thickness (CIMT) in hemodialysis patients. Eighty-two hemodialysis patients were enrolled in this cross-sectional study. Predialysis blood samples were centrifuged at 1500 g and 4°C for 10 minutes and stored at -80°C for the measurement of hepcidin-25. DRG hepcidin enzyme-linked immunosorbent assay kit was used for the measurement of hepcidin-25. Ultrasonographical B-mode imaging of bilateral carotid arteries was performed with a high-resolution real-time ultrasonography (Mindray DC7). Mean age of the study population was 57.90 ± 16.08 years and 43.9% were men. Total study population was grouped into two according to median value of hepcidin-25. There was no difference between groups with respect to age, dialysis vintage, and C-reactive protein. CIMT was found to be statistically significantly higher in low hepcidin-25 group. In correlation analysis, CIMT was found to be correlated with age (P < 0.01, R = 0.33) and hepcidin-25 (P < 0.01, R = 0.46). In linear regression analysis, age (ß = 0.31) and hepcidin-25 (ß = 0.44) were found to be the determinants of CIMT in hemodialysis patients. Our results implicate that hepcidin may take part in pathophysiology of atherosclerosis and cardiovascular disease in hemodialysis patients.

Effects of acute kidney injury on clinical outcomes in patients with upper gastrointestinal bleeding.

AIM: Upper gastrointestinal bleeding (UGIB) is a very frequently encountered condition that has a high morbidity and which increases treatment costs. Duration of hospital stay and mortality increases in patients with UGIB complicated by acute kidney injury (AKI). The aim of this study was to reveal risk factors in patients with UGIB developing AKI and to compare clinical outcomes and hospital costs between patients with UGIB developing AKI and those with UGIB not developing AKI. MATERIAL AND METHODS: This retrospective study included 245 patients admitted to the emergency unit and the intensive care unit for internal diseases at Ankara Numune Education and Research Hospital, Turkey. RESULTS: The difference in mortality rates between the patients with AKI and those without AKI was significant (p < 0.001). The mean duration of intensive care unit stay was 0.2 ± 1.1 days in the patients without AKI (n = 143) and 2.5 ± 5.6 days in the patients with AKI. It was significantly higher in the patients with AKI (p < 0.001). Hospital stay was significantly longer in the patients with AKI than those without AKI, and as severity of AKI increased, hospital stay became considerably longer (p < 0.001). Hospital costs were significantly higher in the patients with AKI than those without AKI, and as severity of AKI increased, hospital costs considerably rose (p < 0.001). CONCLUSION: AKI is a condition that lengthens hospital stay, increases hospital costs and creates a burden on health care systems. Detect kidney injury earlier and administering an appropriate treatment can improve clinical outcomes in patients with UGIB developing AKI.

Fibroblast growth factor is associated to left ventricular mass index, anemia and low values of transferrin saturation / El factor de crecimiento fibroblástico está asociado con el índice de masa ventricular izquierda, anemia y niveles bajos de saturación de la transferrina

Background: Fibroblast growth factor 23 (FGF-23) is a phosphorus-regulating hormone. In chronic kidney disease (CKD), circulating FGF-23 levels are markedly elevated and independently associated with mortality. Left ventricular hypertrophy (LVH) is a potent risk factor for mortality in CKD, and FGFs have been implicated in the pathogenesis of myocardial hypertrophy. In addition, the effect of anemia on CV disease and LVH is well known in CKD. A relation between iron and FGF-23 metabolism is mentioned in a few studies. The aim of this study was to test the association of FGF-23 levels with echocardiographic (ECHO) and iron parameters in peritoneal dialysis patients (PD). Methods: In this cross-sectional study, 61 subjects with PD (29 women and 32 men, mean age: 46.9±13.3 years, mean PD vintage: 69.5±39 months) underwent echocardiograms to assess left ventricular mass index (LVMI). Medical treatments and average values of the basic laboratory results of the last 6 months for all patients were recorded. Serum FGF- 23 concentrations were measured using intact FGF-23 (iFGF-23) human enzyme-linked immunosorbent assay (ELÿISA) kit. According to the median levels of serum FGF-23 the patients were grouped into two (FGF-23 high and low groups). Results: Significant positive correlation was recorded between serum FGF-23 levels and LVMI (P = 0.023). There was also significant difference in terms of hemoglobin (12.1±2 versus 11.0±2, P = 0.017), transferrin saturation (TSAT) (24.9±16.8 versus 19.5±10.8, P = 0.042) between low and high FGF-23 group. Also in linear regression analysis the negative relation between FGF-23 and hemoglobin is persisted (r = 0.199, P = 0.045). Conclusions: FGF-23 is associated with LVMI, anemia and low TSAT in patients with PD. Whether increased FGF-23 is a marker or a potential mechanism of myocardial hypertrophy and anemia in patients with end-stage renal disease (ESRD) requires further study (AU)

Introducción: El factor de crecimiento fibroblástico 23 (FGF-23) es una hormona reguladora del fósforo. En la enfermedad renal crónica (ERC), los niveles de FGF-23 son especialmente elevados y se relacionan de manera independiente con mortalidad. La hipertrofia ventricular izquierda (HVI) es un importante factor de riesgo de mortalidad en la ERC y se ha implicado a los FGF en la patogenia de la hipertrofia del miocardio. Además, se conoce el efecto de la anemia en la enfermedad cardiovascular y la HVI en la ERC. En algunos estudios se menciona una relación entre el hierro y el metabolismo del FGF-23. El objetivo de este estudio fue comprobar la asociación de los niveles de FGF-23 con parámetros ecocardiográficos y de hierro en pacientes con diálisis peritoneal (DP). Metodología: En este estudio transversal se procedió a realizar un ecocardiograma a 61individuos con DP (29mujeres y 32 hombres; media de edad: 46,9±13,3 años; DP clásica media: 69,5±39 meses) para evaluar el índice de masa ventricular izquierda (IMVI). Se registraron los tratamientos médicos y los valores promedio de los resultados básicos de laboratorio de los últimos 6 meses de todos los pacientes. Las concentraciones en suero del FGF-23 se midieron con el kit ELISA (enzyme-linked immunosorbent assay) de FGF-23 humano intacto (iFGF-23). Según los niveles promedio de FGF-23 en suero, los pacientes se distribuyeron en dos grupos (FGF-23 alto y bajo). Resultados: Se registró una correlación positiva significativa entre los niveles de FGF-23 en suero e IMVI (P = 0,023). También hubo diferencias significativas en cuanto a la hemoglobina (12,1±2 frente a 11,0±2, P = 0,017) y saturación de la transferrina (TSAT; 24,9±16,8 frente a 19,5±10,8, P = 0,042) entre los grupos de FGF-23 bajo y alto. También en el análisis de regresión lineal se mantuvo la relación negativa entre el FGF-23 y la hemoglobina (r = 0,199, P = 0,045). Conclusiones: El FGF-23 se asocia con IMVI, anemia y TSAT baja en pacientes con DP. Saber si el aumento del FGF-23 es un marcador o un mecanismo potencial de la hipertrofia miocárdica y la anemia en pacientes con insuficiencia renal terminal exige un estudio en mayor detalle (AU)

Fibroblast growth factor is associated to left ventricular mass index, anemia and low values of transferrin saturation.

BACKGROUND: Fibroblast growth factor 23 (FGF-23) is a phosphorus-regulating hormone. In chronic kidney disease (CKD), circulating FGF-23 levels are markedly elevated and independently associated with mortality. Left ventricular hypertrophy (LVH) is a potent risk factor for mortality in CKD, and FGFs have been implicated in the pathogenesis of myocardial hypertrophy. In addition, the effect of anemia on CV disease and LVH is well known in CKD. A relation between iron and FGF-23 metabolism is mentioned in a few studies. The aim of this study was to test the association of FGF-23 levels with echocardiographic (ECHO) and iron parameters in peritoneal dialysis patients (PD). METHODS: In this cross-sectional study, 61 subjects with PD (29 women and 32 men, mean age: 46.9±13.3 years, mean PD vintage: 69.5±39 months) underwent echocardiograms to assess left ventricular mass index (LVMI). Medical treatments and average values of the basic laboratory results of the last 6 months for all patients were recorded. Serum FGF-23 concentrations were measured using intact FGF-23 (iFGF-23) human enzyme-linked immunosorbent assay (ELISA) kit. According to the median levels of serum FGF-23 the patients were grouped into two (FGF-23 high and low groups). RESULTS: Significant positive correlation was recorded between serum FGF-23 levels and LVMI (P=0.023). There was also significant difference in terms of hemoglobin (12.1±2 versus 11.0±2, P=0.017), transferrin saturation (TSAT) (24.9±16.8 versus 19.5±10.8, P=0.042) between low and high FGF-23 group. Also in linear regression analysis the negative relation between FGF-23 and hemoglobin is persisted (r=0.199, P=0.045). CONCLUSIONS: FGF-23 is associated with LVMI, anemia and low TSAT in patients with PD. Whether increased FGF-23 is a marker or a potential mechanism of myocardial hypertrophy and anemia in patients with end-stage renal disease (ESRD) requires further study.

Do elevated plasma S100A12 levels predict atherosclerosis in peritoneal dialysis patients?

AIM: Atherosclerotic cardiovascular disease is one of the major causes of mortality and morbidity in peritoneal dialysis (PD) patients. S100A12 is an endogenous receptor ligand of advanced glycation end-products. It was shown to contribute to the development of atherosclerosis in animal models. The aim of this study was to evaluate the relationship between S100A12 levels and carotid atherosclerosis in PD patients. METHODS: A cross-sectional study was performed in 56 PD patients and 20 control subjects. Plasma S100A12 levels were measured from all participants beside routine laboratory evaluation. All subjects underwent high-resolution B-mode ultrasonography to determine carotid intima media thickness (CIMT). S100A12 levels were compared between patient and control groups. Correlation analyses of S100A12 with other laboratory values and CIMT were also performed. RESULTS: Plasma S100A12 levels were higher in PD patients compared with control subjects (129.5 ± 167.2 ng/mL vs. 48.5 ± 30.3 ng/mL, respectively, p < 0.001). In the patient group, CIMT was found to be positively correlated with age (r = 0.354; p = 0.007), CRP level (r = 0.269; p = 0.045), and S100A12 (r = 0.293; p = 0.028) level while it was found to be negatively correlated with hemoglobin concentration (r = -0.264; p = 0.049). In the linear regression analysis, the model, including CRP, S100A12, age, and Hgb, was found to be significant (F: 4.177, p: 0.005). When the parameters are analyzed age and S100A12 were found to be independent determinants of CIMT (ß = 0.308, p = 0.018 and ß = 0.248, p = 0.049, respectively). CONCLUSIONS: This study suggests that an elevated plasma S100A12 level was closely associated with atherosclerosis. With aging elevated plasma S100A12 may show a powerful proatherogenic potential in patients undergoing PD.

The relation between apelin levels, echocardiographic findings and carotid intima media thickness in peritoneal dialysis patients.

BACKGROUND: Cardiovascular disease (CVD) is the most important cause of morbidity and mortality in patients with end stage renal disease (ESRD). Apelin expressed in endothelial and other tissues including brain and kidney is an adipocytokine defined recently and is emerging an important mediator of cardiovascular homeostasis. The aim of this study was to test whether apelin levels might be associated with carotid artery atherosclerosis and left ventricular mass index (LVMI) in peritoneal dialysis patients. PATIENTS AND METHODS: Fifty peritoneal dialysis patients (25 female, mean age 41.4 ± 11.9 years, mean dialysis vintage 65.0 ± 35.4 months) and 18 healthy individuals (9 female, mean age 41.7 ± 6.8 years) were included in this cross-sectional study. Serum apelin 12 levels, echocardiographic findings and carotid intima media thickness (CIMT) were recorded as well as clinical and laboratory data. RESULTS: There were no differences between the patient and the control groups with regard to demographic characteristics. In patient group, LVMI, CIMT, CRP and apelin levels were elevated compared to control group. However there was no association between apelin, LVMI and CIMT. There was a positive correlation between apelin and CRP, which was not statistically significant. When patients were divided into two groups according to the mean serum apelin levels, LVMI, CIMT and CRP were higher in the high apelin group but this difference did not reach statistical significance. CONCLUSION: We observed an increased inflammation and CVD risk in peritoneal dialysis patients. However, serum apelin levels seem not to be associated with cardiovascular risk in this group of patients.