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Exploring anemia in Lupus Nephritis Hepcidin and erythropoietin Connection

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Abstract Background: Hematological abnormalities are common in systemic lupus erythematosus (SLE), including anemia, which is often attributed to chronic disease. Hepcidin, an iron-regulatory protein influenced by inflammatory cytokines, plays a role in the anemia pathophysiology. This study aimed to investigate the role of hepcidin in the serum profiles of lupus nephritis patients with anemia. Methods: A prospective cohort study was conducted on 100 lupus nephritis patients at Mansoura University, Egypt. Two groups were identified based on hemoglobin levels: anemia (Hb < 12 g/dl) and non-anemia (Hb ≥ 12 g/dl). Demographic and clinical data were analyzed using appropriate statistical tests, including t-tests, chi-square, and Fisher's exact test. Results: Both groups had similar ages but differed significantly in gender distribution, with more females in the anemia group. BMI, diabetes mellitus, and hypertension rates were comparable between groups. The duration of lupus nephritis and management approaches did not differ. Biopsy results indicated differences in the class of lupus nephritis, with the majority in the anemia group having class 4 and class 3. Serum chemistry, including serum creatinine, was similar between groups. The anemia group had lower hematocrit, MCH, and transferrin saturation, indicating microcytic hypochromic anemia with low transferrin saturation. Hepcidin levels were high in both groups, with a slightly higher level in the anemia group. Conclusion: Anemia in lupus nephritis patients is primarily due to iron deficiency, associated with elevated hepcidin levels. Further research is needed to explore these patients' underlying causes of anemia.
Title: Exploring anemia in Lupus Nephritis Hepcidin and erythropoietin Connection
Description:
Abstract Background: Hematological abnormalities are common in systemic lupus erythematosus (SLE), including anemia, which is often attributed to chronic disease.
Hepcidin, an iron-regulatory protein influenced by inflammatory cytokines, plays a role in the anemia pathophysiology.
This study aimed to investigate the role of hepcidin in the serum profiles of lupus nephritis patients with anemia.
Methods: A prospective cohort study was conducted on 100 lupus nephritis patients at Mansoura University, Egypt.
Two groups were identified based on hemoglobin levels: anemia (Hb < 12 g/dl) and non-anemia (Hb ≥ 12 g/dl).
Demographic and clinical data were analyzed using appropriate statistical tests, including t-tests, chi-square, and Fisher's exact test.
Results: Both groups had similar ages but differed significantly in gender distribution, with more females in the anemia group.
BMI, diabetes mellitus, and hypertension rates were comparable between groups.
The duration of lupus nephritis and management approaches did not differ.
Biopsy results indicated differences in the class of lupus nephritis, with the majority in the anemia group having class 4 and class 3.
Serum chemistry, including serum creatinine, was similar between groups.
The anemia group had lower hematocrit, MCH, and transferrin saturation, indicating microcytic hypochromic anemia with low transferrin saturation.
Hepcidin levels were high in both groups, with a slightly higher level in the anemia group.
Conclusion: Anemia in lupus nephritis patients is primarily due to iron deficiency, associated with elevated hepcidin levels.
Further research is needed to explore these patients' underlying causes of anemia.

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