益肾化瘀泄浊法调节慢性肾衰竭患者血清IL-13的临床研究

目的:评价益肾化瘀泄浊汤对慢性肾衰竭(CRF)的治疗作用并探讨其作用机制.方法:60例脾肾气虚,瘀浊阻滞型CRF患者随机分为益肾化瘀泄浊汤组(治疗组)30例,尿毒清颗粒剂组(对照组)30例.观察CRF患者血清白细胞介素13(IL-13)在治疗前后的水平变化,探讨IL-13在CRF病程中的作用、意义及与肾功能变化之间的相互关系.结果:CRF患者血清IL-13水平随着肾功能损害程度的加重而增高,且与内生肌酐清除率(Ccr)呈负相关;益肾化瘀泄浊汤组可明显改善CRF血清IL-13水平,其血清IL-13降低水平明显优于尿毒清颗粒剂组(P＜0.01).益肾化瘀泄浊汤可降低血肌酐、血尿素氮,提高Ccr水平,可明显改善肾功能(P＜0.01).结论:(1)CRF患者血清IL-13升高,可能是体内部分免疫活化的反映;(2)益肾化瘀泄浊汤具有疗效确切及副作用少等优势,并能降低CRF患者血清IL-13水平,可能是其获得疗效的机制之一.     

慢性肾衰竭患者甲状旁腺素变化的临床分析

目的：寻找降低CRF患血清TPH的有效途径，评价不同PTH水平患的营养状况，方法：应用放射免疫法测定CRF患HD，CAPD，肾移植皇血清TPH值，测定营养生化指以及用人体测量法来评价不同PTH水平患的营养状况。结果：肾移植后患较HD，CAPD患血清PTH值下降明显；务清PTH值处于65－200pg/ml的患营养指数高。结论：肾移植是清除PTH的有效治疗手段，患的血清PTH水平与营养指数密切相关。     

慢性肾衰竭患者血浆NT—proBNP水平的研究

目的探讨慢性肾衰竭患者血浆脑钠肽前体N末端片段（N—terminal-pro—brain natriuretic prptide，NT-proBNP）水平与慢性肾功能不全之间的关系。方法选择临床诊断慢性肾衰竭患者59例，根据肾小球滤过率将患者分为氮质血症期25例、肾衰竭期20例、尿毒症期14例，对照组20例。检测血浆NT—proBNP水平、测量超声心动图并收集患者临床资料。对比不同肾功能状态患者的血浆NT—proBNP水平差异及其与肾功能损害等临床指标及心脏结构功能改变之间的相关性。结果慢性肾衰竭各期患者血浆NT-proBNP水平明显升高，且与左心室后壁厚度、血磷水平正相关，与左室射血分数呈负相关。结论慢性肾衰竭患者血浆NT-proBNP水平升高，其浓度与患者心脏结构和功能的改变以及肾功能下降有关。血浆NT-proBNP水平可作为慢性肾衰竭患者心血管疾病的生化指标。     

肾衰合剂治疗慢性肾衰竭的临床研究

目的观察肾衰合剂对慢性肾衰竭(CRF)患者肾功能的保护作用。方法217例CRF患者给予肾衰合剂50ml口服，每日2次，连续1个月。观察CRF患者治疗前后肾功能、血内皮素、血液流变学及血色素的变化。结果肾衰合剂能显著降低CRF患者血肌酐(SCr)、血尿素氮(BUN)，并且可显著降低血内皮素，提高肌酐清除率(Ccr)，但对患者血液流变学没有显著影响。结论肾衰合剂可以降低CRF患者血内皮素，改善患者肾功能。     

内皮素受体拮抗剂阿魏酸钠对慢性肾衰竭患者肾功能和血浆内皮素及D-二聚体的影响

目的：研究内皮素受体桔杭剂阿魏酸钠对慢性肾衰竭患血浆内皮素(KT)、D—二聚体(DDi)及肾功能的影响。方法：应用常规治疗加注射用阿魏酸钠治疗慢性肾衰竭非透析患45例，观察治疗前后血浆KT—1、DDi及血肌酐(Scr)、尿素氮(BUN)改变，并与21例常规治疗组、35例健康对照组相比较。结果：常规治疗组与常规治疗加阿魏酸钠组治疗前血浆KT—1及血水平明显高于健康对照组(P＜o．01)，常规治疗组与常规治疗加阿魏酸钠组治疗前血浆KT—1及DDi无明显差异(P＞o．05)。常规治疗加阿魏酸钠组治疗后，其血浆KT—1、DDi及Scr、BUN均显下降，与治疗前相比较，差异显(P＜0．01)；常规治疗组治疗后，其血浆KT—1、DDi及Scr、BUN无显性差异(P＞0．05)。结论：阿魏酸钠能够降低慢性肾衰竭患KT及DDi水平，改善肾功能，延缓慢性肾衰竭进展。     

血清降钙素原水平鉴别血液透析炎症发热初探

目的探讨血清降钙素原（PCT）水平在尿毒症患者血液透析（HD）炎症性发热时的变化及临床意义。方法在106例有发热表现的尿毒症HD患者中，根据有关临床表现和实验室检查，分为细菌感染组和其它致热源感染组，分别检测血清PCT水平和C反应蛋白（CRP）水平，并与尿毒症HD稳定无发热组进行比较分析。结果慢性肾功能衰竭（CRF）患者血清PCT水平不受原发病，肾功能衰竭程度和HD治疗的影响。细菌感染组与其它致热源发热组相比，前者血清PCT水平升高显著，差异有显著性（P〈0．01），CRP在两组患者血清中都升高，无显著差异性（P〉0．05）。细菌感染组患者血清PCT水平检测的敏感性和特异性高于CRP的检测。结论血清PCT水平的检测为合并细菌感染的HD治疗的CRF患者提供了一个较好的敏感性和特异性早期诊断指标，其检测细菌感染的特异性和敏感性高于CRP。     

狼疮肾炎患者血清和尿白细胞介素-18水平检测及其临床意义

目的：检测狼疮肾炎(LN)患外周血清和尿液白细胞介素—18(IL—18)水平并探讨其临尿意义。方法：血清和尿液IL-18含量采用酶联免疫吸附方法(ELISA)。结果：LN组血清IL—18水平显高于正常对照组(P＜0、01)，活动期LN血清IL—18水平显高于缓解期患(P＜0．01)3LN组尿IL—18水平显高于正常对照组(P＜0．05)，活动期LN患尿IL—18水平显高于缓解期患(P＜0．05)。LN患血清IL—18水平与SLEDAI、抗dsDNA抗体成正相关关系，与补体C3呈负相关关系，而与血白蛋白、血肌酐无相关关系；活动期LN患尿IL—18水平与狼疮肾组织活动性指数(AI)、24h尿蛋白排泄量均呈正相关关系。结论：LN血清和尿IL—18水平显增高，IL—18可能在LN的病理生理过程中起重要作用。LN血清和尿IL—18水平均与狼疮病情活动密切相关，可作为判断狼疮疾病活动性的候选参考指标。     

联机血液透析滤过治疗尿毒症的临床应用研究

目的：探讨联机血液透析滤过（On-line hemodiafiltration,On-line HDF)对尿毒症患不同分子量物质的清除率、患耐受性及临床疗效。方法：回顾性分析18例伴有血透并发症及不适症状的尿毒症患行后稀释法On-line HDF 231例次，并与23例仍行常规血液透析（HD）治疗的患（887例次）进行比较，观察Kt/V，血清肌酐（Scr)、尿素氮（BUN）、血磷（SP）、β2－微球蛋白（β2－M）下降率及治疗中患血透常见并发症和不良反应发生率。结果：患对联机HDF治疗效果和耐受性显优于HD，透析并发症和不适症状发生率显低于HD（P＜0．01），联机HDF治疗后血清Scr、BUN、SP、β2－M水平显降低，KT／V明显增高。结论：后稀释法联机HDF能有效清除尿毒症患血中大、中、小分子物质，透析效果显提高，患对该法治疗的耐受性明显提高，适用于易出现血透并发症及不适症状的尿毒症患。     

氯沙坦对早期慢性肾衰竭患者蛋白尿和肾功能的影响

目的：观察氯沙坦对早期慢性肾衰竭(CRF)患血压、蛋白尿和肾功能的可能有利效应。方法：早期CRF病人(Scr135～442μtool／L或Ccr30～50ml／min)56例,其中慢性肾小球肾炎31例,2型糖尿病肾病15例,高血压肾小动脉硬化症10例。随机分为两组,氯沙坦组(N=30)给予氯沙坦50mg每日1次;对照组(N=26)给予洛汀新10mg每日1次,共4个月。观察血压、尿蛋白、BUN、Scr和Cer、等指标。结果：氯沙坦与洛汀新一样均能有效降低血压、减少尿蛋白、降低BUN和Scr、增加肾小球滤过率。其对轻中度慢性肾衰竭的患疗效较好,治疗期间未见严重毒副作用和过敏反应。结论：氯沙坦具有良好的降血压、减少蛋白尿作用,能延缓早期CRF患肾功能的进展,其副作用少,病人耐受性好。但有关氯沙坦对中重度高血压、大量蛋白尿及CRF晚期患的疗效尚需大样本的长期研究来证实。     

HD组方对血透患者内皮素与降钙素基因相关肽影响的临床研究

目的：观察中药HD组方在血液透析中对血透患内皮素(ET)、降钙素基因相关肽(CGRP)的影响，探讨如何进一步提高尿毒症终末期维持性血透患的透析效率和生活质量。方法：选择终末期肾衰竭(ESRD)患66例，已作维持性血液透析(HD)治疗1年以上，随机分为常规治疗组32例，中药治疗组34例；另设正常对照组20例。常规治疗组：继续进行常规血液透析；中药治疗组：在常规治疗组透析的基础上，将常规透析液中加入中药HD组方。并定期观察各组患的收缩压(SBP)、舒张压(DBP)、内皮素(ET)、降钙素基因相关肽(CGRP)，疗程均为6个月。结果：治疗6个月后，中药治疗组与治疗前及常规治疗组相比SBP、DBP、ET水平显降低(P＜0．01)，而CGRP水分显增高(P＜0．05)。结论：HD组方的应用可通过改善血循环状态，调节患ET、CGRP代谢失衡状况，从而调节血管舒、缩功能，有利于降低血压。     

Hemodialysis with Regenerated Cellulosic Membranes Does Not Reduce Plasma Selenium Levels in Chronic Uremic Patients

Abstract: Selenium (Se) is considered an essential and very important trace element for humans. Se blood levels are frequently low in end-stage renal disease (ESRD) patients, but very little has been established concerning the mechanisms that could modify Se status in uremia, including a supposed dialysis-mediated Se depletion. In order to verify whether hemodialysis (HD) can induce a loss of Se, thereby leading or contributing to a low plasma Se concentration, we investigated the effect of HD procedure with the most commonly used regenerated cellulosic membrane (Cuprophan) on plasma Se levels in 20 uremic patients on HD for 62.5 ± 49.4 months. Plasma Se levels were also determined in 15 chronic renal failure (CRF) nondialyzed patients and in 28 age-matched healthy controls. Se concentration was determined by atomic absorption spectrophotometry. Plasma Se levels of both HD patients (61.3 ± 8.5 μ/L) and CRF nondialyzed patients (56.4 ± 10.1 μg/L) were significantly lower than in normal subjects (78.3 ± 9.7 μg/L, p < 0.001). In CRF nondia-lyzed patients, a significant (p < 0.05) negative correlation was found between the plasma Se concentration versus serum creatinine values. Within the HD group, plasma Se levels significantly increased after the HD procedure (72.8 ± 17.2 μg/L, p < 0.02) together with hemat-ocrit and total plasma protein values (p < 0.05 and p < 0.001, respectively). In the hollow fiber dialyzer during an HD session, the Se concentration increased but not significantly from the blood inflow site (64.6 ± 12.5 μg/L) to the outflow site (72.6 ± 17 μg/L) and decreased, again not significantly, from the dialysate entrance (5 ± 1.9 μg/L) to the outlet (4.8 ± 2.5 μ?.). In HD with low-flux regenerated cellulosic dialyzer, very likely due to the high molecular weight of Se-binding proteins, the replacement treatment did not induce a Se loss in chronic uremic patients with a low plasma Se concentration.     

Neuroendocrinology of chronic renal failure and renal transplantation.

Neuroendocrine activity in normal subjects was compared to patients with chronic renal failure on maintenance hemodialysis (CRF-HD) and to cyclosporine-treated renal transplantation (RT) recipients in an effort to further define the mechanisms underlying their associated fluid, electrolyte, and hemodynamic abnormalities. To evaluate neuroendocrine function in CRF and RT patients, plasma levels of angiotensin II (A-II), vasopressin (AVP), atrial natriuretic peptide (ANP), neuropeptide Y, neuropeptide Y (NPY), epinephrine (E), and norepinephrine (NE) were measured before and after HD and RT. Plasma concentrations of A-II, AVP, ANP, and NPY were significantly elevated in patients with CRF. HD did not produce a significant change in plasma concentrations of AVP, ANP, NPY, E, or NE. NE plasma levels, but not E levels, increased pre- and post-HD. A-II plasma levels were elevated basally in CRF patients and significantly increased following HD. Following RT, plasma levels of A-II, AVP, NPY, and creatinine decreased significantly over the first week, but AVP and NPY did not normalize. Plasma levels of ANP were elevated during the first month, then decreased to normal levels in RT patients. NE levels, but not E levels, were elevated both pre- and post-RT. Despite antihypertensive treatment, the group mean arterial pressure increased post-RT from 100 +/- 4.4 to 116 +/- 3.7 mmHg by POD 6.     

Lipid and apolipoprotein profiles of uremic dyslipoproteinemia--relation to renal function and dialysis

To study the effect of renal function on the development of lipid and apolipoprotein abnormalities in human renal disease, we have investigated 75 patients at different stages of renal insufficiency. The patient population consisted of 19 patients with less advanced renal failure (CRF:1) characterized by a mean glomerular filtration rate (GFR) of 37.4 +/- 14 ml/min, 31 patients with advanced renal failure (CRF:2) having a mean GFR value of 7.9 +/- 7.3 ml/min and 25 patients on maintenance hemodialysis (CRF:HD). Patients in the CRF:1 group had normal plasma triglyceride (TG) and total cholesterol (TC) levels. In the CRF:2 and CRF:HD group, TG levels were increased two- to threefold, together with a moderate elevation of TC levels. All patient groups had elevated levels of VLDL cholesterol and slightly decreased levels of HDL cholesterol. The apolipoprotein profile of all patient groups was characterized by significantly reduced levels of apolipoprotein (Apo)A-I and ApoA-II and significantly increased levels of ApoC-III. CRF:2 and CRF:HD patients had also moderately elevated levels of ApoB, ApoC-I and ApoC-II. Levels of ApoE were only elevated in CRF:HD patients. All patients, regardless of TG levels, had significantly lower ApoA-I/ApoC-III ratios than controls. GFR was positively correlated with ApoA-I and inversely correlated with TC, TG and ApoC-III. CRF:HD patients had slightly higher ApoA-I and ApoA-II and lower ApoB levels compared to CRF:2 patients. Patients with vascular disease had higher TC, TG, ApoB, ApoC-II and ApoE than patients without vascular disease. These results demonstrate that the dyslipoproteinemia with CRF is already manifested at the early stages of disease through its abnormal apolipoprotein rather than lipid profile.     

Polymorphonuclear leukocyte rigidity is defective in patients with chronic renal failure.

BACKGROUND: The purpose of the study was to investigate the rigidity of polymorphonuclear leukocytes (PMNs) in non-dialysed chronic renal failure (CRF) and haemodialysis (HD) patients. METHODS: PMN rigidity as well as tumour necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) plasma levels were assessed in 10 early-stage CRF, 10 late-stage non-HD, and 10 HD patients, before and during dialysis. In HD patients both cellulose acetate and polysulphone membranes were used. Ten healthy subjects served as controls. Rigidity was tested by counting the deformability in morphologically passive PMNs by the micropipette method. Cytokine levels were measured by enzyme-linked immunosorbent assay. RESULTS: PMN rigidity was significantly increased in end-stage CRF patients regardless of HD but not in early-stage CRF. In HD patients PMN rigidity increased significantly 60 min after initiation of HD. There was an increase of TNF-alpha and IL-1beta levels in end-stage non-HD and HD patients and a further increase at 60 min after initiation of HD. The percentage of morphologically activated PMNs was increased only during dialysis. The nature of the HD membrane had no influence on rigidity, PMN activation, or cytokine production. CONCLUSIONS: The results indicate that PMN rigidity is defective in end-stage chronic CRF patients and is further increased 60 min after initiation of HD, regardless of the nature of the HD membrane used. PMN activation, increased TNF-alpha and IL-1beta levels, or a direct PMN impairment may cause the observed cell rigidity.     

The alteration of QT dispersion in hemodialysis subjects

OBJECTIVE: We attempted to observe the alterations in QTd and QTcd in chronic renal failure (CRF) patients before and after hemodialysis (HD) to determine the relevant determinants of QTc duration in HD. METHODS: The HD was carried out 2 or 3 times/week in a standard setting for 4-4.5 h. No drug therapy was applied during HD, except for isotonic NaCl infusions and sodium heparin. Maintenance drug therapy, including digitalis, antihypertensive, anti-anginal, and beta-blocking agents, was not changed. In the study, we investigated the alterations in QTd and QTcd in 68 CRF patients before and after HD with 12-lead ECG. Plasma Na(+), K(+), ionized Ca, creatinine, urea nitrogen, and hemoglobin were also controlled before and after HD. RESULTS: In our study QTd and QTcd significantly increased at the end of HD (p < 0.01). Plasma Na(+) and K(+) decreased, and ionized Ca increased after HD (p < 0.05, 0.01). Plasma Na(+), K(+), ionized Ca levels, ultrafiltration volume and myocardial ischemia appear to be the main determinants of QTc duration in HD, not hypertension, gender, patient age, or duration of chronic HD. CONCLUSION: Changes in plasma Na(+), K(+) and ionized Ca, the ultrafiltration volume and presence of ischemic heart disease in HD have significant effects on QTcd. ECG data demonstrate that the risk of arrhythmia could be higher with decreased plasma Na(+) and K(+), increased ionized Ca, the presence of ischemic heart disease and an increased ultrafiltration rate during HD. These results might provide some valuable references for proper HD programs.     

Alteration in plasma antioxidant capacity in various degrees of chronic renal failure

AIM, PATIENTS AND METHODS: To obtain a more comprehensive profile of extracellular antioxidant capacity in chronic renal failure (CRF), markers of oxidative stress (malondialdehyde, MDA and hydrogen peroxide), protein SH groups (as an important chain-breaking antioxidant) and activity of antioxidant enzymes (glutathione peroxidase, [GPX], catalase and superoxide dismutase, [SOD]) were studied in plasma of 36 non-dialyzed patients with various degrees of CRF and 10 hemodialyzed (HD) patients. RESULTS: The results show that plasma MDA concentrations significantly increase with the severity of kidney dysfunction (r = -0.543, p < 0.01). A marked and profound fall in plasma thiol group levels was observed in all groups tested, independent of the degree of renal failure (r = 0.082, p > 0.05). Plasma SOD activity increased in CRF patients with the progression of renal insufficiency (r = -0.370, p < 0.05). On the other hand, plasma GPX activity decreased progressively in strong correlation with endogenous CCr (r = 0.712, p < 0.001). However, despite this imbalance between extracellular SOD and GPX activities, plasma concentration of hydrogen peroxide remained unchanged in non-dialyzed CRF patients. Catalase activity in non-dialyzed CRF patients was increased, suggesting the significant involvement of catalase in the regulation of plasma hydrogen peroxide level. CONCLUSION: In hemodialyzed patients significantly lower plasma catalase activity, associated with higher hydrogen peroxide levels, was found. It seems reasonable to assume that the imbalance in the activity of extracellular antioxidant enzymes in chronic renal failure may result in accumulation of free radical species, and in unscheduled oxidation of susceptible molecules.     

Pentraxin 3 is elevated in haemodialysis patients and is associated with cardiovascular disease.

BACKGROUND: Pentraxins are mediators of inflammation as well as markers of the acute-phase reaction. While elevation of C-reactive protein (CRP) in patients with renal failure and its association with cardiovascular disease is well described, there are no data on pentraxin 3 (PTX3) in this population. METHODS: Plasma was obtained from 44 chronic haemodialysis (HD) patients, 35 peritoneal dialysis (PD) patients, 39 patients with chronic renal failure (CRF) not on dialysis therapy and 14 age-matched normal subjects. PTX3 production in whole blood was also investigated in samples taken before and during HD. RESULTS: PTX3 plasma levels were significantly higher in HD patients (5.8 +/- 0.6 ng/ml) compared with the other three groups. There were no significant differences between PD patients (1.5 +/- 0.4 ng/ml), CRF patients (1.5 +/- 0.4 ng/ml) and normal subjects (0.76 +/- 0.2 ng/ml). In dialysis patients, PTX3 levels correlated significantly with time on renal replacement therapy (RRT) and with weekly erythropoietin dose. PTX3 levels were significantly higher in patients with coronary artery disease and peripheral artery disease compared with those without. During a single HD session, PTX3 production was higher in whole blood samples taken after 3 h HD compared with samples taken before HD. CONCLUSIONS: PTX3 levels are markedly elevated in HD patients. The increase in PTX3 production in whole blood after HD indicates that the HD procedure itself contributes to elevated PTX3 levels in HD patients. The association between PTX3 and cardiovascular morbidity suggests a possible connection of PTX3 with atherosclerosis and cardiovascular disease in HD patients.     

Levels of serum ascorbate and its metabolites in hemodialysis patients

The status of ascorbic acid (AA) in dialysis patients is the subject of debate. Some reports have found AA to be deficient in dialysis patients, while others have found that AA is not deficient. In an attempt to confirm AA serum concentrations in dialysis patients, we analyzed the concentrations of AA as well as its metabolites using the specific determination of AA with chemical derivatization and the HPLC method. We studied 131 patients under maintenance hemodialysis therapy (HD), 23 patients with chronic renal failure (CRF) and 48 healthy controls (C). Serum concentrations of AA and the AA metabolites dehydroascorbic acid (DHA) and 2, 3-diketogulonate (DKG) were measured by HPLC. Nine HD patients were taking AA supplements. Seventy-six (62.3%) of the 122 HD patients not taking AA supplements exhibited deficient levels of AA (< 20 microM), while 13 (56.5%) of the 23 CRF patients and 9 (18.8%) of the 48 C showed deficient levels of AA. Analysis of AA metabolites in the normal-range AA (20-80 microM) group revealed that the DHA/AA ratio in HD patients was significantly higher than in C (3.3 +/- 2.6% and 1.2 +/- 2.2%, respectively). The DKG/AA ratio in HD patients was higher than in CRF patients (3.6 +/- 5.2% vs. 0.9 +/- 1.9%), whereas DKG was not detected in C. When compared to serum levels before the start of dialysis, serum AA, DHA and DKG concentrations at the end of the dialysis session decreased by an average of 74.2, 84.0 and 78.8% respectively. In HD patients, serum levels of thiobarbituric reactive substances (TBARS) were significantly lower in the higher AA (> 80 microM) group than in the deficient and normal-range AA groups. In 12 AA-deficient patients, after 1 month of taking AA supplements (200 mg/day), serum AA levels rose to 79.9 microM, while serum TBARS level declined when compared with levels before supplementation. In conclusion, the frequency of AA deficiency in dialysis patients is extremely high. AA deficiency in HD patients may result in high TBARS levels, which reflect increased oxidative stress. Adequate AA supplementation should therefore be considered in such patients.     

Plasma protein thiol oxidation and carbonyl formation in chronic renal failure

BACKGROUND: Myeloperoxidase-catalyzed oxidative pathways have recently been identified as an important cause of oxidant stress in uremia and hemodialysis (HD), and can lead to plasma protein oxidation. We have examined patterns of plasma protein oxidation in vitro in response to hydrogen peroxide (H2O2) and hypochlorous acid (HOCl). We measured thiol oxidation, amine oxidation, and carbonyl concentrations in patients on chronic maintenance HD compared with patients with chronic renal failure (CRF) and normal volunteers. We have also examined the effect of the dialysis procedure on plasma protein oxidation using biocompatible and bioincompatible membranes. METHODS: Plasma proteins were assayed for the level of free thiol groups using spectrophotometry, protein-associated carbonyl groups by enzyme-linked immunosorbent assay, and oxidation of free amine groups using a fluorescent spectrophotometer. RESULTS: In vitro experiments demonstrate HOCl oxidation of thiol groups and increased carbonyl formation. In vivo, there are significant differences in plasma-free thiol groups between normal volunteers (279 +/- 12 micromol/L), CRF patients (202 +/- 20 micromol/L, P = 0.005) and HD patients (178 +/- 18 micromol/L, P = 0.0001). There are also significant differences in plasma protein carbonyl groups between normal volunteers (0.76 +/- 0.51 micromol/L), CRF patients (13.73 +/- 4.45 micromol/L, P = 0.015), and HD patients (16.95 +/- 2.62 micromol/L, P = 0.0001). There are no significant differences in amine group oxidation. HD with both biocompatible and bioincompatible membranes restored plasma protein thiol groups to normal levels, while minimally affecting plasma protein carbonyl expression. CONCLUSIONS: First, both CRF and HD patients have increased plasma protein oxidation manifested by oxidation of thiol groups and formation of carbonyl groups. Second, HD with biocompatible and bioincompatible membranes restored plasma protein thiol groups to normal levels. Third, these experiments suggest that there is a dialyzable low molecular weight toxin found in uremia that is responsible for plasma protein oxidation.