狼疮性肾炎患者外周血IL-18水平及其基因表达

为了探讨白细胞介素 18(IL 18)在狼疮性肾炎 (LN )发生、发展中的作用。我们采用逆转录多聚酶链反应 (RT PCR )及酶联免疫吸附 (ELISA )法测定 16例正常人及 18例LN患者外周血单个核细胞 (PBMC )IL 18mRNA表达量及其血浆水平。结果提示LN患者PBMCIL 18mRNA表达量及血浆IL 18水平均较正常对照组显著增高 [IL 18mRNA表达量为 :1 2 6 2± 0 189vs0 84 4± 0 15 5 ,P <0 0 0 1;IL 18血浆水平为 :(82 2 0 9± 5 32 77)pg/mlvs (2 39 5 7± 75 0 6 )pg/ml,P <0 0 0 1]。且WHOIV型LN增高较非IV型LN更为显著 [IL 18mRNA表达量为 :1 32 9± 0 2 1vs 1 138± 0 15 2 3,P <0 0 5 ;IL 18血浆水平为 :(1135 5 4± 5 15 34)pg/mlvs (5 0 8 6 5± 341 36 )pg/ml,P <0 0 1]。另外 ,血浆IL 18水平与肾组织活动指数 ,肾小管间质损害程度呈等级相关 (r分别为 :0 6 10和 0 4 99,P均 <0 0 5 ) ,也与血清肌酐 (Scr) ,血清内生肌酐清除率 (Ccr)及 2 4h尿蛋白排泄量 (2 4hUPQ )呈直线相关 (r分别为 :0 898、 0 6 2 8和 0 5 37,P均 <0 0 5 )。本研究认为循环IL 18表达和分泌增高可能参与LN的免疫发病过程 ,并与狼疮活动有一定的关系     

糖尿病患者外周血白细胞介素18分泌及基因表达

目的　探讨糖尿病 (DM)患者血浆白细胞介素 18(IL 18)水平及外周血单个核细胞 (PBMCs)IL 18mRNA表达量变化。方法　选取 10名健康志愿者及 30例DM患者 (Ⅱ型糖尿病 15例 ,Ⅰ型糖尿病 15例 )。应用IL 18特异的酶联免疫吸附法(ELISA)测定IL 18血浆水平 ,同时采用半定量逆转录多聚酶链反应 (RT PCR)技术 ,分析PBMCsIL 18mRNA表达量。结果　Ⅱ型糖尿病患者血浆IL 18水平及PBMCsIL 18mRNA表达量与正常对照组差异无统计学意义 [(2 73.1± 99.4 6 )vs (2 4 8.86± 82 .6 8)and(0 .731± 0 .12 9)vs (0 .715± 0 .116 ) ,P >0 .0 5 ];Ⅰ型糖尿病患者血浆IL 18水平及PBMCsIL 18mRNA表达量较正常对照组增高 ,差异有显著统计学意义 [(36 0 .17± 12 5 .4 8)vs (2 4 8.86± 82 .6 8)and (0 .935± 0 .132 )vs (0 .715± 0 .116 ) ,P <0 .0 5 ]。结论　Ⅰ型糖尿病患者外周血IL 18的高表达 ,提示其可能介导本病发病过程 ;IL 18可能不参与Ⅱ型糖尿病的发病过程     

原发性肾小球肾炎患者PBMC IL-18基因表达及其启动子区多态性分析

为进一步探明原发性肾小球肾炎 (PGN )的发病机制 ,我们对IL 18基因表达及IL 18基因启动子区单核苷酸多态性(SNP )与PGN发病的关系进行了探讨。首先 ,分离 30例PGN患者与 12名正常人外周血单个核细胞 (PBMC ) ,分别提取RNA和DNA ,半定量RT PCR检测PBMCIL 18mRNA表达水平 ;PCR扩增IL 18启动子区序列并作双向DNA测序 ,检测SNP。结果发现 ,PGN患者PBMCIL 18mRNA表达较对照组显著升高 (P <0 0 0 1) ;IL 18启动子区 6 5 6T/G和 6 0 7A/C等位基因频率在PGN患者和正常对照组间均存在显著性差异 (P <0 0 5 ) ,137G/C未发现有显著性差异 (P >0 0 5 )。结果提示 ,IL 18启动子区SNP可能与IL 18的产生有关 ,并参与PGN的发病机制     

IL-18对SLE患者外周血淋巴细胞凋亡及相关基因表达的研究

本文研究SLE患者外周血淋巴细胞 (PBL )在IL 18刺激下细胞凋亡及凋亡相关基因表达情况。采用AnnexinV联合PI染色定量法及免疫荧光染色法。结果显示在IL 18刺激培养作用下 ,活动期SLE患者PBL凋亡发生率明显增高 (P <0 0 1) ,而静止期则无明显区别 (P >0 0 5 ) ,疾病活动性与PBL凋亡率呈正相关 (P <0 0 1)。Bcl 2表达活动期显著性升高 (P <0 0 5 ) ,静止期无明显著性差异 (P >0 0 5 )。Fas表达活动期显著升高 (P <0 0 0 1,静止期明显升高 (P <0 0 5 )。IL 18可引起SLE患者PBL凋亡率的增高 ,并导致调节紊乱 ,故在SLE发病机制中起作用     

白细胞介素18受体在人类外周血单个核细胞及肾组织表达的研究

目的 :进一步明确白细胞介素 (IL 18)在肾组织免疫性损伤中的作用。方法 :应用半定量逆转录 多聚酶链反应(RT PCR)技术检测 16例正常人 ,16例原发性系膜增生性肾小球肾炎 (MsPGN)患者以及 18例狼疮性肾炎 (LN)患者外周血单个核细胞 (PBMC)白细胞介素 18受体 (IL 18R)α链mRNA的表达量 ,并用免疫组化方法检测 6例正常肾组织 ,16例MsPGN)患者及 18例LN患者肾组织IL 18Rα链蛋白表达量。结果 :MsPGN患者PBMCIL 18RmRNA表达量较正常组有所增高 ,但未达统计学意义 (P >0 0 5 ) ,LN患者PBMCIL 18RmRNA表达量较正常人显著增高 (P <0 0 0 1) ;正常肾组织存在较弱的IL 18R表达 ,MsPGN患者肾组织IL 18R表达量较正常肾组织有所增强 ,但未达统计学差异 ,而LN患者肾组织IL 18R的表达量较正常肾组及MsPGN组均显著增强 (P <0 0 0 1) ,但Pearson相关分析发现LN患者PBMC及肾组织IL 18R表达量均不与血清肌酐 (Scr)水平及 2 4小时尿蛋白排泌量 (2 4h UPE)存在相关关系。结论 :IL 18信号在全身系统及肾组织局部的免疫调节中起一定的作用 ;IL 18在肾功能未严重损害MsPGN患者的发病过程中可能所起作用不大 ;LN患者不但存在IL 18的过量产生 ,而且存在着IL 18过度作用的问题 ,抑制过强的IL 18作用信号可能是LN治疗的新途径。     

初发SLE患者Th1/Th2及IL-10、IL-18基因的表达

探讨初发狼疮病人Th1/Th2分布及其调控细胞因子、细胞因子受体基因表达的差异。运用三色荧光标记法流式细胞术检测 35例未经药物治疗初发狼疮病人T细胞亚群分布 ,并以 10例正常人作对照 ;同时运用ABI770 0TagManRealTime定量PCR法检测其中 38例病人和 2 8例正常人IL 10、IL 18及其受体、IL 10 /IL 18mRNA表达的差异。结果 :(1)初发狼疮病人Th1较正常人明显减低 (P <0 0 5 ) ,但Th1/Th2无显著性改变 ;(2 )与正常组相比 ,SLE组病人IL 10mRNA表达无显著性差异 ,但IL 10R表达明显升高 (P <0 0 5 ) ;SLE组病人IL 18mRNA及其受体表达较正常人明显降低 (P值均 <0 0 5 ) ;(3)面部红斑组病人Th1/Th2较正常组降低 (P均 <0 0 5 ) ,IL 10R较正常组显著增高 (P <0 0 5 ) ;(4)RNP阳性组病人IL 10、较正常组升高 (P均 <0 0 5 ) ,IL 18降低 ;(5 )关节炎组病人IL 18R较无关节炎病人显著降低。SLE是一种以Th1细胞下降 ,Th2细胞相对占优势的免疫介导的自身免疫性疾病 ,源于诱导向Th1细胞分化的IL 18及其受体减少和细胞因子间失衡所致。     

雌激素刺激活动性狼疮肾炎外周血单个核细胞的IL-10表达

探讨性激素对活动性狼疮肾炎外周血单个核细胞 (PBMC)Th2细胞活化的影响。采用ELISA、RT PCR等方法检测了雌激素对 19例活动性狼疮肾炎和 16例健康人外周血单个核细胞 (PBMC)IL 10表达的调节作用。活动期狼疮肾炎PBMCIL 10mRNA和蛋白含量明显高于正常人 (P <0 0 5 ) ;与正常对照相比 ,雌激素明显提高了活动性狼疮肾炎PBMCIL 10蛋白和mRNA水平 (P <0 0 5 ) ,雄激素的加入明显抑制了雌激素诱导的活动性狼疮肾炎PBMCIL 10蛋白和mRNA水平 (P <0 0 5 )。雌激素、雄激素比例失调可能参与了活动性狼疮肾炎IL 10的高效表达     

血液透析对转化生长因子β1及补体调节蛋白CD59基因表达的影响

目的　研究不同透析膜对维持性血液透析 (MHD)患者外周血转化生长因子 β1及补体调节蛋白CD5 9活性表达的影响。方法　通过流式细胞术和酶联免疫吸附法测定长期采用铜仿膜 (CU)与聚砜膜 (PSU)透析患者外周血TGF β1水平及CD5 9活性表达。结果　MHD患者血浆TGF β1水平明显增加 (P <0 .0 5 ) ,其中CU组为 (81.7± 8.7)ng mL ;PSU组为 (6 4 .3±8.3)ng mL ,与正常对照组 (49.3± 6 .1)ng mL相比均有显著差异 (P <0 .0 1,P <0 .0 5 ) ;而PSU组与CU组相比 ,外周血TGF β1水平明显下降 (P <0 .0 5 )。CD5 9在正常人外周血单个核细胞中无表达 ,而在尿毒症未透析组及血透组均有表达 ,其中未透析组表达较低 ,而血透组表达较高 ,CU膜血透组较PSU血透组表达要高 (P <0 .0 5 )。经相关分析结果显示 :CU组与PSU组内TGF β1水平与CD5 9表达均呈现良好的相关性 (r=0 .6 4 0 9与 0 .5 83,P <0 .0 5 )。 结论　血液透析通过血液 透析膜间相互反应可活化补体 ,诱导外周血单个核细胞 (PBMC)合成TGF β1增多 ,而增高的TGF β1水平可上调CD5 9基因表达 ,抑制补体异常活化造成的细胞破坏 ,对机体具有代偿性保护意义。然而不同透析膜如CU和PSU对MHD患者TGF β1与CD5 9的影响有所不同 ,这些变化与透析膜的生物相容性有关     

川芎嗪和地塞米松对狼疮肾炎患者PBMC IL-12表达及合成Ig的影响

应用细胞培养技术 ,采用半定量RT PCR法和ELISA检测等方法 ,以正常人为对照 ,观察川芎嗪 (33μg/ml)和地塞米松 (10 5mol/L )对培养的狼疮肾炎 (LN )活动期、静止期外周血单个核细胞 (PBMC )表达IL 12和产生免疫球蛋白 (Ig)的影响。结果表明 ,LN活动期、静止期较正常对照组IL 12蛋白、基因水平明显增高 (P <0 0 1) ,川芎嗪仅对活动期狼疮肾炎PBMCIL 12表达明显抑制 ,而地塞米松明显抑制狼疮肾炎PBMCIL 12表达 (P <0 0 1) ,两种药物对正常人对照IL 12表达及合成Ig无明显抑制作用 (P >0 0 5 ) ,川芎嗪和地塞米松均明显抑制狼疮肾炎活动期及静止期Ig合成 (P <0 0 1或 <0 0 5 )。提示 :狼疮肾炎患者有高水平的IL 12 ,川芎嗪、地塞米松通过下调狼疮肾炎IL 12表达及Ig的合成 ,减轻狼疮肾炎的发生和发展。     

IL-18在实验性暴发型肝衰竭发病机制中的作用

为探讨IL 18在暴发型肝衰竭发生中的表达变化及对其他细胞因子的调控作用。采用D 氨基半乳糖 (D Gal) 90 0mg/kg与脂多糖 (LPS ) 10 μg/kg诱导BALB/c小鼠暴发型肝衰竭 ,检测不同时间点血清转氨酶 (ALT、AST )和肝组织病理、DNA梯形条带 ,评估肝损伤情况 ;用半定量RT PCR和相应的分析软件分析不同时间点肝组织中IL 18mRNA、TNF αmRNA和IFN γmRNA表达及ELISA方法检测血浆IL 18、TNF α和IFN γ的蛋白表达。结果 :D Gal/LPS给予后 4h血清转氨酶明显升高 ,7h小鼠开始死亡 ,10h死亡率达 80 %。肝组织病理学检查发现 ,5h肝窦扩张、炎性细胞浸润、枯否细胞增生 ;7h肝细胞大量凋亡、坏死或肝组织出现大量出血性坏死 ;5h电镜示肝细胞核仁碎裂、线粒体肿胀或空泡变性 ;7h核仁边聚 ,呈半月型 ,表现为典型的凋亡形态学变化 ,线粒体大部分空泡变性。DNA电泳显示 5h始出现梯形条带。正常小鼠肝组织IL 18mRNA有少量表达 ,TNF αmRNA、IFN γmRNA微量表达。给药后 ,三者的mRNA分别在 1h、 2h、 3h达高峰 ,血浆中TNF α、IFN γ水平与其mRNA变化显著正相关 (rTNF α=0 4 3,P =0 0 1;rIFN γ=0 6 9,P <0 0 0 1) ,而血浆IL 18与其mRNA表达无明显相关 (r= 0 12 ,P =0 2 5 )。本实验诱导的暴发型肝衰竭模型中 ,肝细?     

原发性肾小球肾炎患者外周血IL—18 mRNA表达的研究

目的 探讨白细胞介素18（IL-18）在原发性肾小球肾炎（PGN）中的作用。方法 采用反转录多聚酶链反应（RT-PCR）及酶联免疫吸附法（ELISA）测定11例正常人及46例不同病程PGN患者外周血单核细胞（PBMC）IL-18 mRNA表达量及血浆中IL-18分泌水平。结果 肾功能代偿期原发性肾小球肾炎患者PBMC IL-18 mRNA表达量及血浆中IL-18的水平与正常对照组无统计学差异,而伴有肾功能损害的PGN患者则显著增高,且与肾功能损害相平行;直线相关分析显示;血浆内IL-18水平与Scr呈正相关、与Ccr呈负相关、与24h尿蛋白排泄量不相关。结论 外周血IL-18不参与PGN早期的发病过程,但当疾病进一步发展至伴有肾功能不全时,IL-18分泌水平相对升高可能在本病的进一步发展中发挥一定的作用。     

IL-6 mRNA synthesis by peripheral blood mononuclear cells (PBMC) in patients with chronic renal failure

We measured levels of IL-6 mRNA in PBMC obtained from patients with chronic renal failure, using polymerase chain reaction (PCR), PBMC were isolated from 45 patients on haemodialysis (HD) at the start of HD. PBMC were also isolated from 35 patients on HD at the end of HD, 23 patients on continuous ambulatory peritoneal dialysis (CAPD), 24 undialysed patients with chronic renal failure (CRF), and 19 healthy controls. Total RNA was extracted from PBMC with RNA zol and reverse transcribed into cDNA. To prepare samples containing identical amounts of β-actin cDNA, we performed competitive PCR by co-amplifying serial dilutions of mutant templates containing a single point mutation which generated a unique Eco RI site. Next, to measure IL-6 cDNA semiquantitatively in the samples containing identical amounts of β-actin (100 pg), we performed PCR amplification using 2 fg of the IL-6 mutant template containing a unique Eco RI site. Higher levels of IL-6 mRNA in the PBMC were observed in the HD patients than in the CAPD patients and healthy controls. The levels of IL-6 mRNA in the PBMC at the end of HD were not significantly higher than those at the start of HD. These results suggest that the dialysis session itself did not significantly affect IL-6 mRNA levels in the PBMC, but that chronic stimulation by maintenance HD may be associated with higher levels of IL-6 mRNA observed in HD patients.     

Children with chronic renal failure have reduced numbers of memory B cells

Reduced serum IgG and subclass levels have been demonstrated in children with chronic renal failure. To study possible causes of this reduction, we analysed B cell subset composition, T helper cell frequencies and immunoglobulin (Ig) production capacity in vitro in children with chronic renal failure, with or without dialysis treatment. B cell subsets were characterized by determining CD27, IgM, IgD and CD5 expression within the CD19(+) population. Intracellular expression of interferon (IFN)-gamma, interleukin (IL)-2 and IL-4 in PMA/ionomycin-stimulated peripheral blood mononuclear cells (PBMC) was used to evaluate T helper frequencies. The capacity of B cells to secrete Ig in vitro was determined by measuring IgG(1), IgG(2) and IgM in culture supernatants of anti-CD2/CD28 monoclonal antibody (MoAb)- or SAC/IL-2-stimulated PBMC. Memory B cell numbers (identified as percentage or absolute number of CD19(+) IgM-IgD- or CD19(+)CD27(+) lymphocytes) were lower in children treated with haemodialysis (HD), peritoneal dialysis (PD) and children with chronic renal failure before starting dialysis treatment (CRF) compared to healthy controls (HC) (P < 0.05). Compared with HC, CD5(+) (naive) B cells were reduced in HD-treated patients but not for PD or for children with chronic renal failure before starting dialysis treatment (CRF). No significant differences in CD4(+) T helper cell subsets were found between the groups. However, CRF children had a higher percentage of IFN-gamma producing CD8(+) T lymphocytes compared to HC (P = 0.02). Finally, IgG(1), IgG(2) and IgM production in vitro was similar in the four groups. In conclusion, significantly lower numbers of memory type B cells were found in children with chronic renal failure compared to healthy controls. This reduction may contribute to the low Ig levels found in these children.     

Disturbance of the autonomic nerve system in patients with chronic renal failure--represented by variation coefficient of R-R intervals in the ECG as a parameter

Autonomic nerve dysfunction in patients with chronic renal failure has of late become an issue to be investigated. R-R intervals in resting electrocardiograms were measured to evaluate activities of the cardiac parasympathetic nerve system. A total of 140 patients with chronic renal failure were studied to be compared with 20 normal controls (cont.) and 39 with diabetes mellitus (DM). Of these patients 15 were subjected to conservative treatment (CRF), while 125 patients were undergoing hemodialysis due to chronic renal failure-100 of them derived from chronic glomerulonephritis (HD) and 25 from diabetes mellitus (DM.HD). The variation coefficient of the R-R interval (CVRR) was measured after the subject patients had rested for over 15 minutes before a dialysis session. The mean CVRR were 2.15 +/- 1.25% in CRF group, 2.36 +/- 1.37% in HD and 1.37 +/- 0.99% in DM.HD. These values were significantly lower than in control group (4.70 +/- 2.64%). On the other hand, the value in DM.HD group, as shown above, was significantly lower than in HD. In CRF group the CVRR values lowered as residual renal functions decreased. No significant correlations between CVRR S and the duration of hemodialysis treatment were noted among the groups. In HD group the CVRR S were significantly lower in patients with hypotensive tendency during hemodialysis than in those who enjoyed good control of blood pressure. These results suggest that the measurement of CVRR S can be of help in evaluating autonomic nerve dysfunction in patients with chronic renal failure.     

A new role of uric acid as an antioxidant in human plasma

Free radical attack upon uric acid (UA) nonenzymatically generates allantoin (ALT), and the presence of ALT in human plasma suggests free radical intervention within the body. To assess this possibility, we determined plasma ALT in patients with chronic renal failure (CRF) and some other diseases by high-performance liquid-chromatography (HPLC). Heparinized blood samples were obtained from 15 healthy controls, CRF patients under conservative management (n = 13) or hemodialysis (HD) treatment (n = 8) and patients with gout (n = 11) or rheumatoid arthritis (RA, n = 13). Although not seen in normal plasma samples, ALT was detected in 63% and 31% of patients receiving HD and conservative treatment, respectively. The plasma ALT level decreased after each HD session. ALT was also detected in 18% and 23% of the patients with gout and RA, respectively. ALT was found to be generated by ultraviolet radiation or by the addition of H2O2 to a normal pool-plasma. Addition of Fe(2+) and H2O2 increased the ALT level to about twice that of only H2O2. Addition of either catalase, desferal, EDTA, DMTU, DMSO or mannitol to the plasma decreased ALT generation. These findings suggest that ALT is generated from UA attacked by free radicals, especially by the hydroxyl radical, and that UA plays a role as an antioxidant in the plasma of patients with CRF and some other diseases.     

Elevation of pro-inflammatory cytokines, C-reactive protein and cardiac troponin T in chronic renal failure patients on dialysis

Chronic renal failure (CRF) patients suffer from a chronic inflammation. They are at increased risk of cardiovascular disease. In order to investigate this inflammatory process and cardiovascular risk factors associated with haemodialysis (HD) and peritoneal dialysis (PD), we compared serum/plasma pro-inflammatory cytokines, C-reactive protein (CRP), and cardiac troponin T (cTnT) of 146 CRF patients treated or not treated with PD or HD. Serum cytokines and CRP as well as plasma cTnT were measured by enzyme-linked immunosorbent assay, chemiluminescence immunoassay, and electrochemiluminescence immunoassay, respectively. Results indicated that serum interleukin (IL)-18 concentrations were significantly higher in PD and low creatinine clearance pre-dialysis CRF (LCC) patients than HD patients (both p < 0.05). IL-6 and tumour necrosis factor (TNF)-alpha concentrations were significantly higher in PD patients than LCC patients (both p < 0.01). Serum hsCRP and plasma cTnT in HD were significantly higher than LCC (both p < 0.01). The elevation of pro-inflammatory cytokines should play an important role in the chronic inflammation and increased cardiovascular risk of CRF patients on dialysis. We are evaluating further the diagnostic and prognostic applications of pro-inflammatory cytokines and biochemical inflammatory markers for these patients.     

Leukocyte tissue-type plasminogen activator activity in dialysis patients

Plasma fibrinopeptide B beta 15-42 was significantly high in undialyzed and hemodialyzed chronic renal failure (CRF) patients, indicating that the fibrinolytic system as well as the coagulation system is stimulated. There are two kinds of plasminogen activators (PA) for the fibrinolytic system: urokinase (UK) and tissue-type PA (t-PA). PA activity of peripheral leukocytes from healthy volunteers, continuous ambulatory peritoneal dialysis (CAPD) patients and hemodialysis (HD) patients was measured and compared. Peripheral leukocyte PA in the euglobulin fraction was purified using zinc-chelate-Sepharose 6B column and Concanavalin A-Sepharose column chromatography. The different PA activity was quantitatively identified by electrophoretic enzymography and was confirmed using antibody against UK and t-PA. PA activity of peripheral leukocytes was significantly higher in HD patients on the cupro-ammonium processing membrane dialyzer than in CAPD patients and healthy volunteers. All PA activity in the three groups was UK, and t-PA was not detected. This suggested that the inflammatory response was continuously induced in HD patients, resulting in the induction of PA activity of the leukocytes and plasma, and that different mechanisms were involved for the synthesis or secretion of UK and t-PA.     

Mechanisms of neutrophil apoptosis in uremia and relevance of the Fas (APO-1, CD95)/Fas ligand system

The regulation of neutrophil apoptosis in chronic renal failure (CRF) has not been clearly defined. The Fas/FasL system is an important apoptotic regulatory pathway in a wide variety of cells. Fas is a widely expressed cell surface protein that transduces an apoptotic signal after interaction with its natural ligand FasL. In contrast to the extensive tissue distribution of Fas, constitutive expression of FasL is relatively limited. We examined Fas and FasL expression by neutrophils in healthy subjects, patients with CRF, and patients on hemodialysis (HD) and peritoneal dialysis (PD). Fas expression was significantly higher among patients with CRF compared with control subjects, HD patients, and PD patients. FasL expression was significantly higher among patients with CRF compared with control subjects. At 24 h, neutrophil apoptosis was higher among patients with CRF compared with control subjects. Furthermore, high-neutrophil Fas expression was paralleled by a higher sensitivity to Fas-mediated apoptosis. There was a strong correlation between Fas-stimulated apoptosis and creatinine clearance as well as Fas expression. Finally, we found that uremic serum increased the expression of neutrophil-associated Fas and FasL proteins, when compared with normal serum. Further studies are under way to examine the regulation of this pathway in the uremic environment.     

Assessment of erythropoietin levels and some iron indices in chronic renal failure and liver cirrhosis patients

This study was constructed to investigate the relationship between renal anaemia and erythropoietin (EPO) concentrations in chronic renal failure (CRF) patients and to evaluate the possible role of the liver. Serum EPO levels were measured in blood samples from 20 CRF patients on hemodialysis (HD), 20 liver cirrhosis (LC) patients, 20 patients having both CRF and LC and undergoing HD, and 20 normal control subjects. Blood cell counts, iron indices (iron, total iron-binding capacity (TIBC) and ferritin), renal function (blood urea nitrogen (BUN) and creatinine), hepatic function (ALT, AST, ALP and bilirubin) investigations were carried out for all the subjects enrolled in this study. CRF patients without LC had serum EPO concentration of 6.21 +/- 0.53 mU/ml (mean +/- SE), which was significantly higher than that in patients having both CRF and LC (4.32 +/- 0.52) (p < 0.01). Both groups showed significantly lower values than the controls (12.75 +/- 0.70) (p < 0.001). LC patients with intact kidneys had significantly higher EPO level (22.70 +/- 1.70) (p < 0.001). No correlation was found between EPO level and any of the hematologic or iron indices.     

慢性肾功能衰竭患者血液透析和肾移植前后凝血-血栓形成指标的变化

目的:观察慢性肾功能衰竭(CRF)患者血液透析(血透)和肾移植前后凝血-体外血栓形成指标的变化。方法:CRF病人53例,46例采用血透治疗,7例采用同种异体肾移植。分别于治疗前、血液透析10次后、肾移植18个月后检查血浆内皮素-1(ET-1)、抗凝血酶-Ⅲ(AT-Ⅲ)水平以及体外血栓形成的长度和重量。结果:CRF患者ET-1增加,AT-Ⅲ降低,体外血栓较长、较重,与健康对照组比较P均<0.01;血透治疗后ET-1有所降低,AT-Ⅲ有所增加,但体外血栓长度和重量无显著变化(P>0.05);肾移植治疗后血浆ET-1、AT-Ⅲ以及血栓长度和重量均较治疗前有非常显著性统计学差异,P均<0.01,接近健康对照组水平。结论:ET-1和AT-Ⅲ异常变化可促进CRF患者凝血功能增强和血栓形成,肾移植能改善凝血功能,防治血栓形成。