目的 观察连续性血液透析滤过在治疗MODS患者的临床疗效。及其容量平衡的情况。方法 中南大学湘雅二医院20例MODS患者行床旁CBP治疗，采用Aquarius机器、AV600ｓ透析膜行床旁连续性静脉-静脉血液透析滤过（CVVHDF）治疗，置换液流量2～4L/h，透析液流量4～6L/h，治疗时间6～10h/天，观察治疗前、后患者血清尿素氮(BUN)、肌酐（SCr）、尿酸（UA）及血清电解质钾、钠、氯、钙、磷及二氧化碳结合力的变化，比较设定治疗剂量与实际治疗剂量，设定净超滤量与实际净超滤量的差值。结果 20例患者均很好地耐受治疗。治疗后BUN、SCr及Ua下降率分别为（42±13）%、（36±9）%及（52±11）%,血清钾、钠、氯、钙及二氧化碳水平无显著变化，血磷水平明显下降（P＜0.01）。设定治疗量为（47.2±8.1）L，而实际治疗量为（45.8±6.7）L，误差率为2.9%（中位数，95%范围0.3%～8.3%）。设定净超滤量为（3112±1002）ml，实际净超滤量为（2921±927）ml，误差率为6.8%（中位数，95%范围2.9%～9.9%）。总的容量误差率为0.51%（中位数，95%范围0.21%～0.96%）。结论 连续性血液透析滤过能有效用于MODS患者的救治，毒素清除能力强，能保持水、电解质及酸碱平衡，很好地保持容量平衡。

本研究通过观察同型半胱氨酸（HCY）对人外周血单个核细胞（PBMC）白细胞介素（IL）-6表达及过氧化物增生体激活型受体（PPAR）-γ激动剂对其的干预作用，为防治慢性血液透析患者动脉粥样硬化（MIA）综合征提供新的思路。

目的 了解多发性骨髓瘤（MM）肾损害患者临床特征及其发生的相关因素。方法 对经临床、病理明确诊断的MM肾损害患者的临床特征太实验室检查进行统计学分析。结果 MM肾损害的发生率为40.9%（18/44），临床症候群以肾功能不全）血肌酐>177µmol/L）最为常见（77.8%），其次为肾病综合征（16.7%）、无症状尿检异常（5.56%）。血清轻链阳性率为72.2（13/18），尿中轻链阳率为77.8%(14/18例)，均以λ链为主。骨髓浆细胞数最和尿本周蛋白（BP）与肾功能损害之间有显著相关关系（P<0.01；P<0.05），贫血及多发性骨损害与肾脏损害有相关关系（P<0.05）。结论 MM伴肾损害患者临床症候群以肾功能不全多见，血清与尿液中轻链以λ为主。骨髓将细胞增殖及尿轻链蛋白产生可能是多发性骨髓肾脏损害的主要原因。

Although some studies have suggested that troglitazone could retard the progression of glomerulosclerosis, its effects on renal tubulointerstitial fibrosis have not been completely larified. The aim of this study was to investigate the effects of troglitazone on the secretion of connective tissue growth factor (CTGF) and fibronectin (FN) in human renal proximal tubular pithelial (HK-2) cells induced by transforming growth factor-β1 (TGF-β1). The mRNA of CTGF and FN were measured by semi-quantitative RT-PCR. CTGF and FN protein were detected by Western blot and ELISA, respectively. Our results revealed that troglitazone could inhibit CTGF and FN expression in a dose-dependent manner in human renal proximal tubular epithelial cells induced by TGF-β1, which may be one of the mechanisms of troglitazone contributing to retard progression of renal ubulointerstitial fibrosis.

Aim: Peritoneal matrix accumulation is a characteristic of peritoneal fibrosis (PF). Continuous ambulatory peritoneal dialysis (CAPD) patients with up-regulation of transforming growth factor-β1 (TGF-β1) in their drained effluent show an increased risk of PF. Inhibition of TGF-β1 expression in human peritoneal mesothelial cells (HPMC) may provide a potential treatment for PF. Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists are increasingly used in patients with diabetes, but their effects on extracellular matrix (ECM) turnover are unknown. The aims of this study were to investigate the effects of the PPAR-γ agonist troglitazone on TGF-β1 expression and matrix production in HPMC. Methods: Human peritoneal mesothelial cells were cultured from human omentum by an enzyme digestion method, grown in a medium containing 30 mmol/L D-glucose. TGF-β1 expression and matrix production and turnover were measured in HPMC in the presence and absence of 15 μmol/L troglitazone. The mRNA expressions of TGF-β1, Collagen I (Col I) and fibronectin (FN) were determined by semiquantification reverse-transcriptive polymerase chain reaction (RT-PCR). The protein of TGF-β1 was determined by ELISA and proteins of Col I, FN were determined by western blot. Results: The mRNA expression and protein of TGF-β1, Col I, FN were significantly increased in HPMC stimulated with 30mmol/L D-glucose compared to the control group with F12 media (P<0.01), which was reversed in the presence of troglitazone (15μmol/L). Obvious decrease of TGF-β1 was found in troglitazone-treated groups as compared to groups stimulated with GS (P<0.05). Exposure of HPMC to troglitazone reduced collagen I secretion (P<0.05), and fibronectin secretion (P<0.05). Conclusion: Troglitazone reduce the expression of TGF-β1 in HPMC stimulated by 30 mmol/L D-glucose, and reduces ECM production. These studies suggest that the PPAR-γ agonists may have a specific role in ameliorating the course of progressive peritoneal fibrosis under long-term peritoneal dialysis states.