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HEPCIDIN AND IRON BIOMARKERS MODULATED IN HEMODIALYSIS PATIENTS
M Mohammed1, E Sarhat2, M Marbut2
11Kirkuk Health Directorate, Iraq.
Insights
Serum hepcidin and ferritin levels are significantly elevated in hemodialysis patients with chronic kidney disease (CKD), indicating potential inflammation and iron dysregulation. These levels decrease after dialysis, suggesting its role in CKD-related complications.
Area of Science:
- Nephrology
- Hematology
- Biochemistry
Background:
- Chronic kidney disease (CKD) is a prevalent condition affecting kidney function and structure, often co-occurring with other health issues.
- Inflammation and iron metabolism dysregulation are common complications in CKD patients undergoing hemodialysis (HD).
- Serum hepcidin, a key regulator of iron homeostasis, is implicated in inflammatory processes.
Purpose of the Study:
- To investigate the role of serum hepcidin in inflammation among hemodialysis patients with chronic kidney disease (CKD).
- To compare serum hepcidin levels in CKD patients undergoing hemodialysis with healthy controls.
- To explore correlations between serum hepcidin and other biochemical markers in CKD patients.
Main Methods:
- A prospective hospital-based study involving 30 CKD patients on regular hemodialysis and 30 healthy controls.
- Serum hepcidin levels were measured using Enzyme-Linked Immunosorbent Assay (ELISA).
- Serum iron and total iron-binding capacity (TIBC) were also analyzed.
Main Results:
- Hemodialysis patients exhibited significantly higher serum hepcidin and ferritin levels compared to controls.
- Serum iron and TIBC were lower in HD patients than in the control group.
- Serum hepcidin levels decreased after hemodialysis and positively correlated with ferritin, urea, and creatinine, while negatively correlating with serum iron and hemoglobin.
Conclusions:
- Elevated serum hepcidin and ferritin in hemodialysis patients suggest their involvement in inflammation and iron metabolism dysregulation in CKD.
- Hepcidin levels appear to be influenced by hemodialysis treatment.
- Further research is warranted to elucidate the precise mechanisms and clinical implications of hepcidin in CKD-related inflammation.
Abstract:
Chronic kidney disease (CKD) describes abnormal kidney function and/or structure. It is common, frequently unrecognized, and often exists together with other conditions.Aim - to investigate the role of serum hepcidin in inflammation among hemodialysis patients with chronic kidney disease (CKD).This prospective hospital-based study conducted in Kirkuk city included 30 CKD patients undergoing regular hemodialysis at Kirkuk General Hospital, along with 30 healthy individuals as controls. Blood samples were collected before and after hemodialysis, as well as from the control group, and analyzed for various parameters. The blood samples were collected for determination of hepcidin levels were determined using Enzyme-Linked Immunosorbent Assay, while S. iron, total iron-binding capacity (TIBC).The study found that HD patients had significantly higher levels of serum hepcidin compared to the control group. The mean serum hepcidin level in HD patients was 246.1±72.4 ng/ml, while in the control group, it was 105.7±20.2 ng/ml. Serum ferritin levels were also found to be significantly higher in HD patients compared to the control group (430.5±148.3 ng/ml vs. 153.8±60.6 ng/ml). HD patients had lower serum iron and total iron-binding capacity (TIBC) levels compared to the control group (63.10±15.62 µg/dl vs. 92.98±26.68 µg/dl and 265.4±61.1 µg/dl vs. 273.3±65.9 µg/dl, respectively). After dialysis, both serum hepcidin levels decreased, with the mean serum hepcidin decreasing from 246.1±72.4 ng/ml to 206.3±61.8 ng/ml The study also demonstrated a positive correlation between hepcidin levels serum ferritin, urea, and creatinine, and a negative correlation with serum iron and hemoglobin levels in patients before hemodialysis.HD patients have higher levels of serum hepcidin, ferritin, iron and TIBC, suggesting potential involvement in inflammation and iron metabolism dysregulation.
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