高糖透析液对大鼠腹膜结缔组织生长因子表达的作用

目的探讨腹膜透析液对大鼠腹膜结缔组织生长因子（CTGF）的表达及细胞外基质（ECM）合成的影响。方法将中南大学湘雅二医院动物实验中心提供的SD大鼠随机分为4组：正常对照组（Con）、生理盐水组（NS）、低糖透析液组（LG）、高糖透析液组（HG）。4周后,评价腹膜的功能。VG染色镜下测量腹膜胶原组织厚度。免疫组织化学方法检测CTGF、TGF-β1及纤连蛋白（FN）蛋白质的表达。采用RT-PCR检测大鼠腹膜组织中CTGF和TGF-β1mRNA的表达。结果LG、HG组与Con、NS组相比较,超滤量均显著下降（P〈0.05）;HG组与LG组比较,其超滤量明显减少（P〈0.05）。D/Pcr的比较：HG组比Con、NS组升高（P〈0.05）;D/DO的比较：HG组比Con、NS组明显下降（P〈0.05）,LG组比Con组低（P〈0.05）。HG组腹膜胶原厚度比与其余各组均增厚（P〈0.05）;LG组比Con组增厚（P〈0.05）;HG组CTGF、TGF-β1、FN蛋白表达水平显著高于其他各组（P〈0.05）;LG组显著高于Con、NS组（P〈0.05）。在Con及NS组中,TGF-β1、CTGFmRNA呈低水平表达,TGF-β1、CTGFmRNA在HG组中表达最高（P〈0.05）。结论腹膜透析液尤其是高糖腹膜透析液,能明显诱导大鼠腹膜CTGF的表达增强,并促使腹膜纤维化发生。     

血液透析患者出现热原反应原因调查

为探寻血液透析患者出现热原反应的原因,进行了微生物污染与消毒剂浓度调查。结果,消毒透析器所用过氧乙酸浓度低至０．０５％～０．１６％,贮罐中自来水、反渗水及透析器入口处透析液的细菌总数分别高达 １１ ２００ｃｆｕ／ｍｌ、 １５８０ｃｆｕ／ｍｌ与 １２５０ｃｆｕ／ｍｌ,透析液、反渗水细菌内毒素阳性率均为 １００％（ ２０／ ２０）。经确保过氧乙酸浓度≥０．３％,缩短消毒周期,改善液体过滤除菌设备,液体微生物检测均达标,未再出现热原反应。     

贝朗Dialog~＋血液透析机透析液回路结构与功能分析

论述了贝朗Dialog＋血液透析机透析液回路,包括透析液除气加热、透析液配比、超滤以及消毒等过程的构成与功能,分析了有关功能对透析患者的影响,以提高操作者或护士的工作效率,达到为患者实施安全高效血液透析的目的。     

低钙透析液在低甲状旁腺素伴高磷血症患者中的应用

目的观察低钙（1．25mmoL／L）透析液加大剂量碳酸钙口服对血液透析患者高磷血症、高钙血症及低甲状旁腺素（PTH）的作用。方法选择长期使用1．50mmol／L浓度钙透析液，同时伴血磷、血钙水平升高，血PTH水平降低的患者27例，观察其在改用1．25mmol／L浓度钙透析液后血钙、血磷、钙磷乘积及血PTH水平的变化。结果使用1．25mmol／L浓度钙透析液2周后血钙水平较使用前即有明显下降（P〈0．01），6周后（加用大剂量碳酸钙口服4周后），血钙水平有所回升（P〈0．05），血磷水平显著下降（P〈0．01），钙磷乘积下降（P〈0．05），血PTH水平显著升高（P〈0．01）。结论低钙透析液可显著降低血液透析患者血钙水平，升高PTH水平，同时口服大剂量碳酸钙可改善高磷血症，降低钙磷乘积，可能起到防止低转运骨病的作用。     

透析用水和透析液细菌污染原因分析及对策

目的:了解透析用水和透析液细菌污染的原因及对策.方法:按卫生部《医院感染管理规范》(2000版)的透析液菌落数标准检测细菌含量.结果:整改前与整改后的透析器入口处透析液、透析器出口处透析液、透析B液的菌落数差异有统计学意义(P＜0.05);整改前与整改后的反渗水、透析A液的菌落数差异无统计学意义(P＞0.05).结论:输送反渗水到透析机的管道和配制A液、B液的过程是造成透析液被污染的主要原因,应加强各容器和管道的消毒,并建议修改透析器入口处透析液的细菌学标准.     

长期使用低钙透析液对血液透析患者钙磷代谢的影响

目的:研究应用钙离子1.25mmol/L透析液进行透析6个月对患者免疫反应性甲状旁腺素(iPTH)及钙磷水平的影响。方法:在规律性血透的患者中,选择透前或透后高钙血症的患者16例。入选前,所有患者均采用钙离子1.75mmol/L透析液,每周透析3次,每次4小时,均使用聚砜膜透析器,面积为1.3m2。使用钙离子1.25mmol/l(DCa1.25)透析液透析期间,患者饮食中钙磷的摄入量稳定,且根据需要伴高磷血症的患者同时口服碳酸钙(钙尔奇D),6个月。观察DCa1.25透析液单次治疗前、后至下一次透析前以及治疗1、2、3、6个月时患者透前血钙(校正的血清总钙)、血磷、iPTH水平(检测采用放免法)。结果:使用DCa1.25透析液单次透析4小时后血钙浓度下降,透后血iPTH(221.3±67)pg/ml较透前(163.7±78)pg/ml明显升高(P<0.05),至下次透析前血钙浓度及血iPTH(163.9±101.1)pg/ml基本恢复至上次透析前水平。使用低钙透析液透析1、2、3、6个月后,患者血钙水平呈下降趋势,在低钙透析2个月时,血钙水平显著低于治疗前水平(2.925±0.25)mmol/l,达(2.55±0.25)mmol/l,P<0.05,这种趋势持续至治疗6个月时,血钙水平(2.6±0.2)mmol/l,P<0.05。低钙透析对患者的iPTH水平有明显的影响,呈上升趋势,在低钙透析3个月时,差异有统计学意义,血iPTH上升至(294.4±134.1)pg/ml(P<0.05),低钙透析治疗6个月时,血iPTH达(295.5±192.3)pg/ml(P<0.05),所有患者均完成了6个月的临床观察,其中6名患者因治疗后的iPTH升高超过300pg/ml,而开始应用活性维生素D,有1例患者iPTH升高达821pg/ml,接受了活性维生素D的冲击治疗。血磷水平在进行低钙透析治疗后有所上升,但差异无统计学意义。结论:在维持性血液透析患者中,单次应用DCa1.25的透析液进行透析,透析后血iPTH升高,但至下一次透析前血iPTH基本恢复至上次透前水平。持续应用低钙透析6个月,钙负荷减轻,血iPTH升高。     

Comparison of dialysis adequacy at two dialysate potassium concentrations

SUMMARY: It has been suggested that haemodialysis adequacy is greater dialysing against a 3 mmol/L potassium dialysate concentration than against a 1 mmol/L potassium concentration. As most dialysis patients dialyse against 1 or 2 mmol/L potassium, the dialysis adequacy at these two potassium concentrations was compared. Ten stable haemodialysis patients were randomly assigned to dialyse against 1 mmol/L potassium dialysate (K1) followed by 2 mmol/L potassium dialysate (K2) or vice versa. All other dialysis parameters were held stable. The mean urea reduction ratio was 68.3 ± 6.2 using K1 and 69.5 ± 6.4 using K2 ( P < 0.05 using Wilcoxon for paired data). The Kt / V , however, did not differ (1.39 ± 0.23 for K1 and 1.41 ± 0.23 for K2). The urea rebound was also not different between K1 and K2, with a trend to higher rebound using K2. The percentage rebound in urea was 6.0 ± 2.5 for K1 and 7.1 ± 2.8% for K2. In this setting, K2 dialysate offered no advantage in terms of urea rebound or Kt/V. Based on previously published data, a dialysate potassium concentration of 3 mmol/L may be required to achieve significant benefit in terms of dialysis adequacy.     

Calcium free hemodialysis: Experience in the treatment of 33 patients with severe hypercalcemia

Objective To assess the efficacy, adverse effects and relevance of calcium-free hemodialysis (CFHD) in the treatment of major hypercalcemia.Design Retrospective chart review.Setting Medical ICU.Patients All patients admitted over a 9-year period for hypercalcemia requiring urgent treatment and who underwent hemodialysis.Interventions CFHD with an acetate dialysate.Main results Thirty-three patients with severe hypercalcemia from various etiologies received CFHD. Marked and rapid decrease of serum total calcium was obtained during all sessions (mean decrease: 1.71±0.54 mmol/l). Calcium rebound within 24 h after CFHD was observed in all evaluable cases (1±0.45 mmol/l; mean delay 13.7±5.8 h). Adverse cardiovascular effects occurred in 17 of 48 sessions (35%) and in 13 of 30 evaluable patients (43%).Conclusions Adverse effects are frequent during CFHD. After correction of hypovolemia, its use should be restricted to patients with severe clinical symptoms or advanced renal impairment.     

Albumin catabolism measurement by a double tracer technique in uraemic patients during a single dialytic treatment

Abstract. In order to explain the pathogenesis of protein depletion in chronic uraemia, 13 measurements of albumin catabolism were performed in uraemic patients undergoing haemo-or peritoneal dialysis treatment, during either the early phase or steady uraemic state. Catabolism was determined during a single haemo-or peritoneal dialysis by a double tracer technique (Human Serum Albumin and sodium iodide labelled with two different isotopes of iodine). The output from both albumin and iodine systems was measured in the dialysis solution flowing out from the peritoneum or artificial kidney. The radioactive iodide arising in dialysate from albumin breakdown was concentrated by the use of an anion exchange resin. Catabolic rate was three times the normal in 3 patients showing clinical features of hypercatabolism (true rapid loss of body weight) in the early phase of uraemia, or during relapse of it; albumin turnover rate returned to normal in 2 of these patients, when measured during clinical steady state conditions. This behaviour suggests highly increased catabolism, not counterbalanced by a correspondingly increased synthesis, as the cause of albumin depletion in chronic uraemia.