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作 者:张熔[1] 李丰益[1] 高举[1] 廖清奎[1] 刘先蓉[2] 王莉[3]
机构地区:[1]四川大学华西第二医院儿童血液肿瘤研究室 [2]四川大学华西医院肾脏内科 [3]四川省人民医院肾脏内科,四川成都610041
出 处:《华西医学》2008年第2期286-288,共3页West China Medical Journal
基 金:2004年杨森科学研究基金资助项目
摘 要:目的:探讨铁稳态调节信号分子hepcidin在慢性肾功衰(CRF)肾性贫血发病机制中的作用,为临床诊治铁紊乱相关的肾性贫血寻找理论依据。方法:采用酶联免疫吸附试验(ELISA)、放射免疫法、比色法等分别测定30例初治CRF贫血患者(其中11例患者同时检测尿液pro-hepcidin水平)、30例健康对照者血清hepcidin的前体肽pro-hepcidin、促红细胞生成素(EPO)以及相关铁和血液学参数水平。结果:初治CRF贫血组血清pro-hepcidin水平(242.13±96.65ng/ml)显著低于正常对照组(1019.68±388.31 ng/mL)水平(P<0.001)。初治CRF贫血组内尿毒症者血清pro-hepcidin水平显著高于氮质血症者(P<0.05)。初治CRF贫血患者血清Pro-hepcidin与铁蛋白、Urea、Crea、MCHC呈显著正相关(P<0.01),与EPO的自然对数、Hct呈负相关(P<0.05);尿pro-hepcidin和血Urea呈负相关(P<0.05),血尿pro-hepcidin水平无统计学相关性(P>0.05)。结论:慢性肾功衰肾性贫血时,贫血和缺氧等对hepcidin的下调作用较强,这可能是机体代偿保护性机制的一种反映,但此时相对缺乏的EPO、肾功能损害和炎症等因素削弱了对hepcidin的下调作用,推测hepcidin水平仍是相对升高的,并参与了慢性肾功衰肾性贫血的发病。Objective:To explore the recently detected hepcidin,a central regulator of iron homeostasis,whether plays a role in the pathogenesis of the anemia of chronic renal failure(CRF)in order to give some clues to clinic diagnosis and treatment for the anemia of CRF relevant to perturbation of iron metabolism by determining its pro-hepcidin concentration.Methods:Thirty untreated patients with anemia of CRF and 30 normal individuals were studied.ELISA,radioimmunoassay,colorimetric methods etc were used for serum pro-hepcidin(including urinary pro-hepcidin of 11 patients in CRF),EPO,ferritin,serum iron,TIBC and other parameters concentration,respectively.Results:Serum pro-hepcidin concentration was statistically significantly different between the CRF and control group(P〈0.001),and CRF group(242.13±96.65 ng/mL)was greatly lower than control group(1019.68±388.31 ng/mL).Serum pro-hepcidin concentration in the patients with uremia was higher than that of azotemia.Serum pro-hepcidin concentration exhibited a statistically significant positive correlation with serum ferritin,MCHC,Urea,Crea concentration(P〈0.01),negative correlation with natural logarithm of EPO,Hct concentration(P〈0.05).Urine pro-hepcidin concentration showed no correlation as well with that of serum(P〉0.05).Conclusion:Hepcidin plays a pathogenic role in the anemia of CRF.Down-regulation of hepcidin by anemia or hypoxia is stronger than up-regulation of it,this is the body's protective response.But the failure of renal function,inflammation,relative insufficient EPO weaken down regulation of hepcidin,it is possibility that hepcidin concentration is still relatively higher in CRF.
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