SERUM LEVEL OF HEPCIDIN IN DIABETIC AND NON DIABETIC CHRONIC KIDNEY DISEASE STAGE 5 AND ITS APPLICATION IN ANEMIA
Hamdi Abdel-Azeim Mohammed;
Abstract
Chronic kidney disease is either kidney damage or a decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for 3 or more months. Whatever the underlying etiology, the destruction of renal mass with irreversible sclerosis and loss of nephrons leads to a progressive decline in GFR.
Chronic kidney disease (CKD) is characterized by an irreversible deterioration of renal function that gradually progresses to end-stage renal disease (ESRD).
Diabetes is the leading cause of CKD, and the rapidly increasing prevalence of diabetes worldwide virtually assures that the proportion of CKD attributable to diabetes will continue to rise.
Even when diabetes is controlled, the disease can lead to CKD and kidney failure. Most people with diabetes do not develop CKD that is severe enough to progress to kidney failure.
Anemia is a frequent complication of CKD, inadequate production of erythropoietin by the failing kidneys leads to decreased stimulation of the bone marrow to produce red blood cells. Anemia of CKD develops early and worsens with progressive renal insufficiency.
Hepcidin, a 25-amino-acid (aa) peptide, hormone is a key regulator of iron homeostasis, which controls dietary iron absorption, plasma iron concentrations, and tissue iron distribution. Hepcidin synthesis is physiologically increased by elevated plasma iron concentration decreased by erythropoietic activity and pathologically increased by inflammation. Increased Hepcidin concentrations lead to decreased iron absorption.
By contrast, a decreased level will cause increase iron release from the enterocytes and macrophages.
Aim: The aim of this study to spotlight serum level of hepcidin in CKD patient stage 5 and determine its impaction on renal anemia. By the same way the relationship between serum hepcidin and pathogenesis of DM also discussed in this study.
Material and methods: The study included 80 patients; divided into 40 diabetic patients and 40 non diabetic patients as well as 20 healthy control subjects.
Serum hepcidin, hs-CRP, serum ferritin, iron profiles, Hb concentration, Hct value, GFR, FBG, PPBG, GFR, serum creatinine and BUN were detected.Relationship between hepcidin and different parameters were analyzed in diabetic and non diabetic.
Result: serum hepcidin and ferritin were significantly higher in diabetic than non diabetic (p<0.001). A positive correlation between hepcidin and ferritin, as well as between hepcidin and hs-CRP levels was existed in diabetes and non diabetic groups (p < 0.001 respectively).
EPO was found to reduce level of hepcidin in both diabetic and non diabetic groups.
Conclusion: All of these data demonstrated that the higher hepcidin levels in diabetic patients may be due to that higher ferritin, the elevated hepcidin might have adaptive value through down-regulated iron absorb and play an important role in pathogenesis of DM.
Chronic kidney disease (CKD) is characterized by an irreversible deterioration of renal function that gradually progresses to end-stage renal disease (ESRD).
Diabetes is the leading cause of CKD, and the rapidly increasing prevalence of diabetes worldwide virtually assures that the proportion of CKD attributable to diabetes will continue to rise.
Even when diabetes is controlled, the disease can lead to CKD and kidney failure. Most people with diabetes do not develop CKD that is severe enough to progress to kidney failure.
Anemia is a frequent complication of CKD, inadequate production of erythropoietin by the failing kidneys leads to decreased stimulation of the bone marrow to produce red blood cells. Anemia of CKD develops early and worsens with progressive renal insufficiency.
Hepcidin, a 25-amino-acid (aa) peptide, hormone is a key regulator of iron homeostasis, which controls dietary iron absorption, plasma iron concentrations, and tissue iron distribution. Hepcidin synthesis is physiologically increased by elevated plasma iron concentration decreased by erythropoietic activity and pathologically increased by inflammation. Increased Hepcidin concentrations lead to decreased iron absorption.
By contrast, a decreased level will cause increase iron release from the enterocytes and macrophages.
Aim: The aim of this study to spotlight serum level of hepcidin in CKD patient stage 5 and determine its impaction on renal anemia. By the same way the relationship between serum hepcidin and pathogenesis of DM also discussed in this study.
Material and methods: The study included 80 patients; divided into 40 diabetic patients and 40 non diabetic patients as well as 20 healthy control subjects.
Serum hepcidin, hs-CRP, serum ferritin, iron profiles, Hb concentration, Hct value, GFR, FBG, PPBG, GFR, serum creatinine and BUN were detected.Relationship between hepcidin and different parameters were analyzed in diabetic and non diabetic.
Result: serum hepcidin and ferritin were significantly higher in diabetic than non diabetic (p<0.001). A positive correlation between hepcidin and ferritin, as well as between hepcidin and hs-CRP levels was existed in diabetes and non diabetic groups (p < 0.001 respectively).
EPO was found to reduce level of hepcidin in both diabetic and non diabetic groups.
Conclusion: All of these data demonstrated that the higher hepcidin levels in diabetic patients may be due to that higher ferritin, the elevated hepcidin might have adaptive value through down-regulated iron absorb and play an important role in pathogenesis of DM.
Other data
| Title | SERUM LEVEL OF HEPCIDIN IN DIABETIC AND NON DIABETIC CHRONIC KIDNEY DISEASE STAGE 5 AND ITS APPLICATION IN ANEMIA | Other Titles | قياس مستوى الهبسيدين في الدم لمرضي القصور الكلوى المزمن قبل الغسيل في مرضي السكري والغير سكري وتطبيقاته في مرض الانييميا | Authors | Hamdi Abdel-Azeim Mohammed | Issue Date | 2014 |
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