Serum Hepcidin Levels Research Articles

The Relationship Between Hepcidin-Mediated Iron Dysmetabolism and COVID-19 Severity: A Meta-Analysis.

BackgroundsHepcidin has been identified as a systemic iron-regulatory hormone. Recent studies have suggested that iron metabolism disorders may be involved in the pathogenesis of acute respiratory distress syndrome and multiple organ dysfunction in coronavirus disease 2019 (COVID-19).ObjectivesTo re-evaluate the hepcidin-related iron metabolism parameters and explore the relationship between hepcidin-mediated iron dysmetabolism and COVID-19 severity.MethodsCOVID-19 is classified as mild and moderate as non-severe, severe and critical as severe. A meta-analysis was conducted. Four bibliographic databases were comprehensively searched up to December 31st 2021.ResultsSix unique studies with data from 477 COVID-19 patients were included. Compared to non-severe cases, severe cases had higher hepcidin (standardized mean difference (SMD), −0.39; 95% Confidence Interval (CI) [−0.76, −0.03]; P = 0.03) and ferritin (SMD, −0.84; 95% CI [−1.30, −0.38]; P = 0.0004). In five out of six studies, a total of 427 patients were tested for serum iron, and there were significant differences in their levels between severe and non-severe cases (SMD, 0.22; 95% CI [0.02, 0.41]; P = 0.03). A total of 320 patients from four out of six studies were tested for transferrin saturation, and the statistical difference was not significant (SMD, 0.06; 95% CI [−0.17, 0.28]; P = 0.64).ConclusionSevere COVID-19 cases had higher serum levels of hepcidin and ferritin, and lower serum iron, without significant differences in transferrin saturation. Further studies are needed to verify whether targeting the hepcidin-mediated iron metabolism axis may influence the outcome and treatment of COVID-19.

The correlation between hepcidin levels and iron parameters in patients with end-stage renal disease on regular hemodialysis successfully treated from hepatitis C virus by directly acting antiretrovirals

Background Hepcidin is a polypeptide secreted from the liver. It regulates iron metabolism by blocking further iron absorption when iron stores are high. Hepcidin levels are usually higher than the normal range in hemodialysis (HD) patients. Hepatitis C virus (HCV) infection leads to lowering of hepcidin levels, leading to more iron overload. The objectives were to determine whether there is a correlation between iron stores and hepcidin levels in HD patients after HCV treatment and to assess the level of hepcidin in those patients who were treated from HCV compared with those who have chronic HCV infection. Patients and methods In total, 60 patients on regular HD were recruited and 30 healthy controls. Group I: 30 patients who have been successfully treated from HCV by directly acting antiretroviral drugs with a persistently negative PCR for at least 3 months, group II: 30 patients with chronic HCV infection, and 30 healthy controls form group III. Serum hepcidin levels, iron profile, and complete blood count were compared in all groups. Results Hepcidin levels were significantly higher in the HCV-treated group versus the HCV-infected group (mean 226.77±144.13 and 87.77±40.77 ng/dl), respectively, significantly higher transferrin-binding capacity (TIBC), and mean levels 410.5±74.65 and 310.93±122.57 μg/dl. Ferritin levels were higher in the HCV-infected group (355.13±196, 899.5±1522 ng/dl) than in HCV-treated. There was a significant correlation between hepcidin and serum iron, TIBC, and transferrin saturation in the HCV-treated group. On regression analysis, only TIBC and transferrin saturation correlated significantly. Conclusions Post HCV treatment with directly acting antiretroviral drugs, hepcidin levels are higher than during HCV-infection state and correlate significantly to higher TIBC. Further studies are needed to establish the effect of iron supplementation on hepcidin level in this subgroup of patients.

Lactoferrin modulates increased liver DNA damage by reducing serum cytokine, hepcidin and iron levels in lipopolysaccharide-induced endotoxemia in rats

Lactoferrin modulates increased liver DNA damage by reducing serum cytokine, hepcidin and iron levels in lipopolysaccharide-induced endotoxemia in rats

Clinical interpretation of serum hepcidin-25 in inflammation and renal dysfunction

IntroductionHepcidin is a hormone that regulates systemic iron homeostasis. Serum hepcidin levels are under the influence of various stimuli, particularly inflammation and renal dysfunction. The measurement of hepcidin in circulation is a potentially useful clinical tool in the diagnosis, monitoring and treatment of iron metabolism disorder, although clinical interpretation of hepcidin level remains difficult. We evaluated he diagnostic potential and limitations of hepcidin-25 by investigating its relationship with iron and hematological indices, inflammation, and renal dysfunction. MethodsThis retrospective study included 220 adult patients not requiring dialysis. Variations of biologically active hepcidin-25 were examined using a mass spectrometry-based assay in various inflammatory and renal states. The log[hepcidin]:log[ferritin] ratio was calculated as an hepcidin index. ResultsIn 220 adult patients not requiring dialysis, variation in hepcidin-25 level was significantly larger once CRP exceeded 10 mg/l (p < 0.001). Inflammation was not a determinant of hepcidin-25 in the setting of renal dysfunction. Hepcidin-25 median (7.37 nM) and variance were significantly higher (p < 0.001), once estimated glomerular filtration rate (eGFR) dropped below 30 ml/min/1.73 m2. The log[hepcidin]:log[ferritin] index normalized hepcidin levels. Patients with iron deficiency have a notably lower index when compared to controls (-0.66 vs 0.3). ConclusionSevere renal dysfunction (eGFR < 30) affected hepcidin-25 expression and clearance to variable degree between individuals. Although, hepcidin-25 testing is not warranted in patients with infection, inflammatory autoimmune conditions (CRP > 10 mg/l) and/or severe renal dysfunction (eGFR < 30), the hepcidin index may serve as a potential biomarker for iron deficiency in complex cases.

Evaluation of serum hepcidin level in acne vulgaris patients

Background: Acne vulgaris is a pilosebaceous unit inflammatory condition. Although acne is not life-threatening, it can cause psychological issues such as low self-esteem and anxiety in people who suffer from it. Acne scarring is a common and unpleasant consequence of acne vulgaris. Predicting scarring liability can modify treatment protocol and aid in the prevention of such disfigurement. Methods: This study included 82 participants divided into 3 groups: 26 patients with acne vulgaris without scars, 36 patients with acne vulgaris with scars and 20 control. Serum hepcidin level was assessed by a commercially available double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) kit. Results: Serum hepcidin is significantly higher in patients suffering from acne without acne scars than patients suffering from acne with acne scars (p &lt; 0.05). serum hepcidin is significantly higher in the control group than patients with active acne with scars (p &lt; 0.05). There was a statistically significant difference between serum hepcidin level in control versus severe acne scars (p &lt; 0.05). Serum hepcidin level acts as a predictor of occurrence of acne scars and occurrence of severe acne scars. Serum hepcidin level can be used as an indication for beginning aggressive and specific acne treatment as systemic retinoid.

Levels of Serum Ferritin and Hepcidin in Patients with Uncomplicated Falciparum Malaria in Hodeidah, Yemen: Considerations for Assessing Iron Status

Understanding the key regulator of iron homeostasis is critical to the improvement of iron supplementation practices in malaria-endemic areas. This study aimed to determine iron indices and hepcidin (HEPC) level in patients infected with Plasmodium falciparum compared to apparently healthy, malaria-negative subjects in Hodeidah, Yemen. The study included 70 Plasmodium falciparum-infected and 20 malaria-negative adults. Blood films were examined for detection and estimation of parasitemia. Hemoglobin (Hb) level was measured using an automated hematology analyzer. Serum iron and total iron binding capacity (TIBC) were determined by spectrophotometric methods. Levels of serum ferritin (FER) and HEPC were measured by enzyme-linked immunosorbent assays. Data were stratified by sex and age. Comparable Hb levels were found in P. falciparum-infected patients and malaria-negative subjects in each sex and age group (p > 0.05). Compared to their malaria-negative counterparts, disturbed iron homeostasis in patients was evidenced by the significantly lower serum iron levels in females (p = 0.007) and those aged <25 years (p = 0.02) and the significantly higher TIBC in males (p = 0.008). Levels of serum FER and HEPC were significantly elevated in P. falciparum-infected patients compared to the corresponding malaria-negative participants (p < 0.001). Serum FER correlated positively with parasite density (p = 0.004). In conclusion, patients with uncomplicated P. falciparum in Hodeidah display elevated levels of serum HEPC and FER. Hemoglobin level may not reflect the disturbed iron homeostasis in these patients. The combined measurement of iron indices and HEPC provides comprehensive information on the iron status so that the right intervention can be chosen.

Hepcidin-to-Ferritin Ratio as an Early Diagnostic Index of Iron Overload in β-Thalassemia Major Patients

Hepcidin (HEPC) hormone production is expected to be elevated in cases accompanying iron overload, but the opposite impact of ineffective erythropoiesis in β-thalassemia major (β-TM) patients overrides this effect. The role of the HEPC-to-ferritin (FER) ratio and its components in iron metabolism along with their diagnostic cutoff values, sensitivity, specificity, and accuracy in β-TM patients with iron overload, were examined in this study. This was a 1:1 case-control study with 120 participants, ages ranging from 2 to 30 years of both sexes, who were assigned into two groups: 60 β-TM patients with iron overload, and a control group, comprising 60 healthy individuals matched by gender and age. In the present study, we found slightly elevated serum HEPC concentration (21.9 ng/mL) compared to the controls (9.9 ng/mL), which was not statistically significant (p =0.1), and the median HEPC-to-FER ratio of the cases was significantly lower than the controls, with the median case-control difference of (–0.366; p < 0.001). Our results revealed a statistically significant impact (p < 0.001) of mean age on the serum HEPC level with the inverse linear correlation of (–0.487, p < 0.001). The area under the curve of the HEPC-to-FER ratio was 0.999 and the optimum cutoff value was 0.046 ng/mL (p < 0.001) with 100.0% sensitivity and 98.3% specificity. In conclusion, we found that serum HEPC-to-FER ratio, with an accuracy of 99.2%, may serve as an excellent index for the diagnosis of iron overload in β-TM patients differentiating them from nonthalassemic controls.

Evaluation of Iron Metabolism in Chronic Kidney Disease Patients by Serum Hepcidin level

Evaluation of Iron Metabolism in Chronic Kidney Disease Patients by Serum Hepcidin level

IRE-dependent Regulation of Intestinal Dmt1 Prevails During Chronic Dietary Iron Deficiency but is Dispensable in Conditions of Acute Erythropoietic Stress.

IRE-dependent Regulation of Intestinal Dmt1 Prevails During Chronic Dietary Iron Deficiency but is Dispensable in Conditions of Acute Erythropoietic Stress.

Hepcidin expression levels involve efficacy of pegylated interferon-α treatment in hepatitis B-infected liver

BackgroundHepcidin is the master iron regulator hormone produced by the liver. The association of serum hepcidin with pegylated interferon therapy in patients with chronic hepatitis C infection has been studied. However, the role of serum hepcidin level in predicting the effect of pegylated interferon treatment in patients with chronic hepatitis B (CHB) infection is yet to be elucidated. Our study aims to investigate the correlation between hepcidin expression levels and the curative effect of interferon-alpha therapy in patients with CHB. MethodsA total of 47 patients with CHB who accepted pegylated interferon-α (PEG-IFN- α) treatment were recruited. The serum level of hepcidin was estimated by ELISA. The alternation in the gene expression level of hepcidin was detected by RT-PCR, and immunofluorescence cell staining was performed to detect hepcidin peptide. The induction of antiviral proteins was analyzed by Western blotting. The predictive value of early on-treatment variation in serum hepcidin during treatment progress was assessed by receiver operating characteristic analysis. ResultsHigh levels of early on-treatment serum hepcidin were observed in patients who achieved a decline in HBsAg > 1 log10 IU/mL or HBV DNA > 1 log10 IU/mL. In vitro, an elevation of the hepcidin expression in HepG2.2.15 cells induced by PEG-IFN-α treatment was noted. Furthermore, combined treatment with hepcidin and PEG-IFN-α increased the levels of antiviral proteins. The predictive cut-off value of hepcidin for HBsAg decline > 1 log10 IU/mL was 239 pg/mL, and the sensitivity and specificity were 72.73% and 70.97%, respectively. The predictive cut-off value of hepcidin for the decline in HBV DNA > 1 log10 IU/mL was 190.4 pg/mL, and the sensitivity and specificity were 72.73% and 61.11%, respectively. Early-on treatment changes in the hepcidin level signified the predictive value of the PEG-IFN-α curative effect. ConclusionsA higher early-on treatment hepcidin level indicates a higher possibility of HBsAg and HBV DNA decline in patients with CHB during PEG-IFN-α treatment. A high early-on treatment serum hepcidin level is significant in predicting the PEG-IFN-α therapeutic effect in patients with CHB.

The Effect of Oral and Intravenous Iron Supplementation on Serum Hepcidin and Ferritin Levels in Rattus Norvegicus Pregnant Strain Wistar with Anemia

Background: Anemia is an indirect cause of high maternal mortality rates worldwide characterized by low levels of hemoglobin, hepcidin, and serum ferritin. Hepcidin is a biomarker of iron metabolism in the body while ferritin acts as a store of iron. Hepcidin and ferritin levels during pregnancy will decrease. To restore the levels, supplementation is required either orally or intravenously. This study aimed to determine the effect of oral and intravenous iron supplementation on hepcidin and ferritin levels. Methods: This was an experimental laboratory study using Posttest Only Control Group Design. The sample was 24 Rattus Norvegicus divided into 4 groups: the negative control group without treatment, the positive control group given NaNo, the, P1 given oral iron supplementation, and the P2 given intravenous iron. The maintenance of the test animals in this study was carried out at the Pharmacy laboratory of Universitas Andalas Padang in June-August 2021. The experimental animals were Rattus Norvegicus Wistar females weighing 200-250 grams, aged between 3-4 months conditioned to be pregnant. The serum examination of hepcidin and ferritin levels used the ELISA method and the normality test used Shapiro Wilk. Then, the significance test used One-Way ANNOVA followed by multiple comparisons of Bonferroni types. Results: The results showed that there were significant differences (p&lt;0.05) in hepcidin levels in the positive control group, treatment group 1, treatment 2 that were 219.52 ng/ml, 220.27 ng/ml, and 221.49 ng/ml. Likewise, the ferritin levels in the positive control group, treatment 1, and treatment 2 were 5.91 ng/ml, 6.81 ng/ml and 7.72 ng/ml. Conclusion: Based on the findings, it can be concluded that oral and intravenous iron supplementation had an effect on increasing serum hepcidin and ferritin levels in Rattus norvegicus pregnant strain Wistar with anemia. Keywords: Oral iron supplementation, intravenous supplementation, hepcidin and ferritin

Serum Hepcidin Level among Chronic Kidney Disease Subjects Accessing Healthcare in Braithwaite Memorial Specialist Hospital Port Harcourt

Hepcidin is the major controller of systemic iron homeostasis and the role of the kidney in regulating hepcidin level is vital in the whole process of iron and hepcidin relationship. This study was aimed at evaluating serum Hepcidin level among Chronic Kidney Disease subjects accessing Healthcare in BMSH Port Harcourt Metropolis. The study was conducted in Port Harcourt at Braithwaite Memorial Specialist Hospital among 55 CKD subjects and 33 normal individuals making up the control group. Subjects were selected randomly and 5mls of blood was collected in plain bottle using venipuncture technique for laboratory assessment of hepcidin. Hepcidin was assayed using competitive ELISA method. T-test was used to compare the mean difference oh hepcidin between both groups. Result showed that there was a significant difference in hepcidin level between CKD and control groups; 52.00±36.00ng/ml for CKD group and 16.00±13.00ng/ml for control group, p&lt;0.05. This study has shown that CKD has a significant impact in hepcidin level blood and consequently on iron regulation.

Interleukin-6 triggers toxic neuronal iron sequestration in response to pathological α-synuclein.

SUMMARYα-synuclein (α-syn) aggregation and accumulation drive neurodegeneration in Parkinson’s disease (PD). The substantia nigra of patients with PD contains excess iron, yet the underlying mechanism accounting for this iron accumulation is unclear. Here, we show that misfolded α-syn activates microglia, which release interleukin 6 (IL-6). IL-6, via its trans-signaling pathway, induces changes in the neuronal iron transcriptome that promote ferrous iron uptake and decrease cellular iron export via a pathway we term the cellular iron sequestration response, or CISR. The brains of patients with PD exhibit molecular signatures of the IL-6-mediated CISR. Genetic deletion of IL-6, or treatment with the iron chelator deferiprone, reduces pathological α-syn toxicity in a mouse model of sporadic PD. These data suggest that IL-6-induced CISR leads to toxic neuronal iron accumulation, contributing to synuclein-induced neurodegeneration.

Genetic variants in promoter region of TFR2 is associated with the risk of non-alcoholic fatty liver disease in a Chinese Han population: a case-control study.

Iron overload is frequently observed in non-alcoholic fatty liver disease (NAFLD). Transferrin receptor 2 (TFR2) is an important key factor in iron regulation. We aimed to investigate whether TFR2 single nucleotide polymorphisms (SNPs) contribute to susceptibility to NAFLD in a Chinese Han population. Five tag SNPs (rs10247962, rs4434553, rs2075672, rs1052897, and rs3757859) in the TFR2 gene were selected and genotyped in a case-control study on participants who visited two affiliated hospitals of Fujian Medical University between June 2011 and August 2017. Propensity score matching and inverse probability of treatment weighting analyses were used to verify the risk associated with TFR2 SNPs. Logistic regression analyses suggested that subjects with the rs4434553 GA or GG genotype had a lower risk of NAFLD than those carrying the AA genotype (odds ratio = 0.630, 95% confidence interval = 0.504-0.788). Moreover, the rs4434553 GA or GG genotype was negatively correlated with body mass index, hepatic steatosis index, and serum ferritin (b = -0.363, P = 0.008; b = -1.040, P = 0.009; b = -35.258, P = 0.015, respectively), and positively associated with serum hepcidin level (b = 35.308, P < 0.001). Moreover, rs10247962 and rs1052897 had multiplicative interactions with age in relation to the risk of NAFLD (P for interactions, 0.041 and 0.034, respectively). The cumulative effects of the rs10247962, rs1052897, and rs4434553 SNPs were positively associated with the risk of NAFLD (adjusted P trend = 0.012). In this Chinese Han population, the rs4434553 polymorphism in TFR2 may be an independent influencing factor associated with the susceptibility to NAFLD. The ageing effect on the development of NAFLD may be inhibited by SNPs rs10247962 and rs1052897.

Acute phase reactant proteins in Buerger's disease: Is it a systemic disease?

Aim: The aim of this study was evaluating acute phase reactant (APR) proteins including high sensitivity C-reactive protein (hsCRP), pentraxin 3 (PTX3), fibrinogen, complement C3, hepcidin, and albumin in patients suffering from Buerger's disease (BD) compared to controls.Methods: The APRs were evaluated in 92 cases of BD patients and 90 healthy age and sex matched controls of blood from Iran and Turkey. The diagnosis was done according to Shionoya's criteria. However, patients with age less than 40 were included, instead of those less than 50. The diagnosis was confirmed by angiography or CT angiography. The patients were categorized into active and quiescent phases of the disease according to clinical manifestation. Patients with rest pain, non-healing ulcer, and gangrene were categorized in the active phase of the disease and the patients with unchanged claudication for more than 6months without trophic lesions or gangrene were categorized in the quiescent phase of the disease.Results: The serum level of PTX3, hsCRP, fibrinogen, C3, and hepcidin in BD was significantly higher than controls (p < 0.004). Also, albumin in the BD group was significantly lower than controls (p < 0.001). In patients that categorized in the active phase, fibrinogen, C3, and hsCRP were significantly higher and albumin was significantly lower compared to patients in the quiescent phase. No significant difference was found between the level of PTX3 and hepcidin in the patients in active and quiescent phases of the disease.Conclusion: The pattern of the level of APRs in BD seems more likely systemic inflammatory disorder than atherosclerosis obliterans. More clinical trials for evaluating the efficacy of anti-inflammatory medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids as a part of management of BD are required. Also, according to low level of albumin in TAO, a protein rich diet might be beneficial for BD patients in the active phase of their disease.

Crosstalk between Acidosis and Iron Metabolism: Data from In Vivo Studies.

Iron absorption requires an acidic environment that is generated by the activity of the proton pump gastric H(+)/K(+)ATPase (ATP4), expressed in gastric parietal cells. However, hepcidin, the iron regulatory peptide that inhibits iron absorption, unexpectedly upregulates ATP4 and increases gastric acidity. Thus, a concept of link between acidosis and alterations in iron metabolism, needs to be explored. We investigated this aspect in-vivo using experimental models of NH4Cl-induced acidosis and of an iron-rich diet. Under acidosis, gastric ATP4 was augmented. Serum hepcidin was induced and its mRNA level was increased in the liver but not in the stomach, a tissue where hepcidin is also expressed. mRNA and protein levels of intestinal DMT1(Divalent Metal Transporter 1) and ferroportin were downregulated. Serum iron level and transferrin saturation remained unchanged, but serum ferritin was significantly increased. Under iron-rich diet, the protein expression of ATP4A was increased and serum, hepatic and gastric hepcidin were all induced. Taken together, these results provide evidence of in-vivo relationship between iron metabolism and acidosis. For clinical importance, we speculate that metabolic acidosis may contribute in part to the pathologic elevation of serum hepcidin levels seen in patients with chronic kidney disease. The regulation of ATP4 by iron metabolism may also be of interest for patients with hemochromatosis.

Caffeine and alcohol – Friends or foes of human iron stores?

Background & AimsThere is clear evidence that lifestyle factors affect iron bioavailability. However, information regarding the effect of alcohol and caffeine consumption on iron metabolism is limited. The aim of the current study was to evaluate the effect of caffeine and alcohol consumption on iron metabolism in healthy men, regarding their everyday physical activity level. MethodsThe study enrolled 83 men (59 physically active and 24 sedentary men) aged 18–32 years. Fasting blood samples were collected. ELISA kits were used to determine levels of ferritin, soluble transferrin receptor, hepcidin, hemojuvelin, and C-reactive protein (hsCRP). Level of physical activity was assessed using the International Physical Activity Questionnaire (IPAQ). Caffeine and alcohol intake was assessed using a food frequency questionnaire. A general linear model was performed to evaluate the relationship between caffeine intake and levels of serum ferritin, ferritin, soluble transferrin receptor, hepcidin, hemojuvelin, and hsCRP. ResultsPhysically active men (but not sedentary men) who consumed alcohol in excess presented higher ferritin levels when compared to moderate drinkers and abstainers (R2 = 0.35, p = 0.0001). Heavy drinkers presented the highest hepcidin levels when compared to both abstainers and moderate drinkers (p < 0.0001 for physically active, and p = 0.0267 for sedentary men). However, moderate drinkers showed significantly lower hsCRP levels when compared to heavy drinkers and abstainers drinkers (p < 0.0001 for physically active, and p = 0.0116 for sedentary men). Greater caffeine intake was generally associated with greater serum hepcidin levels, with the strongest effect on moderate drinkers. A significant influence of caffeine intake on hsCRP was shown for physically active men but not for sedentary men - greater caffeine intake was connected with higher hsCRP levels for participants who drank alcohol. ConclusionBased on the presented results it can be assumed that high caffeine consumption may lead to suppression of iron bioavailability through increased inflammation. Furthermore, physical activity and moderate alcohol consumption seemed to benefit reduction of inflammatory response, at least as represented by hsCRP levels.

The effects of hypoxia-inducible factors-1α and -2α and erythroferrone on hepcidin in patients with chronic kidney disease stages 3–5 and renal anemia

Objective This study aimed to investigate the effects of hypoxia-inducible factor-1α (HIF-1α), hypoxia-inducible factor-2α (HIF-2α), and erythroferrone (ERFE) on hepcidin in patients with chronic kidney disease (CKD) stages 3–5 and renal anemia. Methods A total of 90 patients with CKD stages 3–5 and renal anemia were selected for the study at the Nephrology Department of Fujian Provincial People’s Hospital and divided into three groups, according to CKD stage, while another 30 healthy subjects who underwent a physical examination at the hospital during the same period were selected as the normal group. The serum levels of hepcidin, HIF-1α, HIF-2α, ERFE, and furin were measured using an avidin biotin peroxidase complex enzyme-linked immunosorbent assay to compare the differences between the groups in the related indicators. Results ① Serum HIF-2α, HIF-1α, ERFE, and furin levels increased gradually in the patients with CKD stages 3–5 ( p &lt; 0.05, p &lt; 0.01). ②Simple correlation analysis:Serum hepcidin was positively correlated with HIF-2α, ERFE, and HIF-1α in the CKD patients ( p &lt; 0.01). ③Serum hepcidin was positively correlated with HIF-2α, HIF-1α, and ERFE in the CKD patients injected with erythropoietin (EPO) ( p &lt; 0.01), while serum hepcidin was positively correlated with HIF-2α and HIF-1α ( p &lt; 0.01) in the patients not injected with EPO. ④ Multivariate linear regression analysis showed that HIF-1α, (β = 4.36, p &lt; 0.01), serum ferritin(SF) (β = 0.13, p &lt; 0.01), and HIF-2α (β = 0.66, p &lt; 0.01) were significantly correlated with hepcidin. Conclusion HIF-1α, HIF-2α, and SF are factors which have an effect on hepcidin in patients with CKD stages 3–5 and renal anemia. The increase of HIF-1α, HIF-2α, and ERFE does not seem to inhibit the increase of hepcidin.

Early diagnosis of acute kidney injury by measurement of Interleukin-6 (IL-6) and Hepcidin levels in patients following cardiac catheterization

Acute kidney damage is a severe condition common in patients who have undergone heart surgery (catheterization) and secondary injury is also referred to as being synonymous with surgery. The goal of this research is to determine the rate of serum urea, Interleukin-6 (IL-6) and Hepcidin levels in patients with acute renal injury (AKI) following cardiac catheterization. The study included 81 patients (64 males and 17 females) ranging in age from 40 to 75 years. Data from most patients is reported in the form of an age, gender and smoking background questionnaire. The results indicate a significant increase in serum urea, Interleukin-6 (IL-6) and Hepcidin levels in patients with severe renal insufficiency after cardiac catheterization in (79%) males versus (21%) females. According to the outcomes of this study, improved risk prediction could improve patient monitoring and treatment after surgery, as well as direct patient treatment and decision making. Also, the findings show that they enhance participation in AKI interventional trials.

Serum hepcidin levels related to interlukin-6 in patients with acute myeloid leukemia before and after treatment

Serum hepcidin levels related to interlukin-6 in patients with acute myeloid leukemia before and after treatment