黄葵胶囊联合替米沙坦治疗早中期糖尿病肾病临床研究

目的：观察黄葵胶囊联合替米沙坦治疗早中期糖尿病肾病的疗效。方法：采用黄葵胶囊联合替米沙坦治疗本病,并设对照组观察24 h尿蛋白定量、血尿素氮、血肌酐、血尿酸、三酰甘油、总胆固醇等变化,并进行组间比较。结果：治疗后,24 h尿蛋白定量两组均有显著下降（P〈0.05）,以治疗组下降更为显著,与对照组比较有显著性差异（P〈0.05）。治疗组40例,其中显效16例,有效18例,无效6例,有效率80.5%,治疗后尿蛋白定量、血尿酸、血尿素氮、血肌酐、三酰甘油、总胆固醇均有明显下降（P〈0.05）,且与对照组比较各指标下降显著（P〈0.05）。结论：黄葵胶囊联合替米沙坦治疗早中期糖尿病肾病有较好协同作用,且能有效减轻蛋白尿,从而保护肾脏,且无明显不良反应。     

Recombinant human hepatocyte growth factor (HGF), but not rat HGF,elicits glomerular injury and albuminuria in normal rats via an immune complex‐dependent mechanism

1. Hepatocyte growth factor (HGF) has the therapeutic potential to improve renal fibrosis and proteinuria in rodents with chronic kidney disease. In contrast, long‐term administration of human HGF to normal rats reportedly elicits proteinuria. Thus, the role of HGF during proteinuria remains contentious. The aim of the present study was to demonstrate that human HGF is antigenic to rodents and that immune complex formation causes proteinuria. 2. We administered either human or rat HGF to normal rats for 28 days. Albuminuria was evaluated by sodium dodecyl sulphate–polyacrylamide gel electrophoresis. The renal phenotypes of the two HGF treatments were examined using histological techniques. 3. Administration of human HGF (1 mg/kg per day, i.v.) to rats led to severe albuminuria and glomerular hypertrophy in association with increased blood levels of anti‐human HGF IgG and IgG deposition in mesangial areas. Furthermore, an immune complex between human HGF and anti‐human HGF IgG stimulated the production of proteinuric cytokines (including transforming growth factor‐β) in rat cultured mesangial cells. In contrast, treatment of healthy rats with rat HGF for 4 weeks caused neither mesangial IgG deposition nor elevated anti‐HGF IgG in the blood. Overall, rat HGF did not provoke albuminuria. 4. We conclude that human HGF produces pseudotoxic effects in normal rat kidneys via an immune complex‐mediated pathway, whereas syngenic HGF is safe due to less deposition of glomerular IgG. Our results affirm the safety of the repeated use of syngenic HGF for the treatment of chronic organ diseases, such as renal fibrosis and liver cirrhosis.     

氯沙坦钾联合金水宝胶囊治疗2型糖尿病肾病的疗效观察

目的:观察氯沙坦钾联合金水宝胶囊对2型糖尿病肾病患者的治疗作用。方法:2型糖尿病肾病40例,随机分成两组(每组20例),治疗组以氯沙坦钾联合金水宝胶囊治疗,对照组以氯沙坦钾治疗,疗程为2个月。比较各组治疗前后尿微量蛋白排泄率(UAER)、24 h尿蛋白(UTP/24 h)、血肌酐(Scr)、尿素氮(BUN)的变化。结果:两组患者治疗后,UAER、UTP/24 h均有所下降(P<0.05),治疗组下降尤为明显,与对照组比较差异显著(P<0.05),Scr、BUN无明显改变(P>0.05)。结论:氯沙坦钾联合金水宝胶囊治疗2型糖尿病肾病,能明显降低患者蛋白尿,显著改善肾功能。     

氟伐他汀与缬沙坦对糖尿病肾病患者CTGF表达的影响

目的：探讨糖尿病肾病（Diabetic Nephropathy,DN）发病过程中结缔组织生长因子（Connective tissuegrowth factor,CTGF）的作用及氟伐他汀对CTGF表达的影响。方法：38名糖尿病肾病患者（24h尿白蛋白定量为150~500mg）,随机分成缬沙坦治疗组、氟伐他汀治疗组、氟伐他汀＋缬沙坦治疗组,观察3个月,用ELISA方法计算24h尿白蛋白定量（UAER）及血CTGF浓度,进行治疗组间及治疗前后比较。结果：氟伐他汀降低血CTGF浓度及减轻24h尿白蛋白增长趋势,氟伐他汀联合缬沙坦效果更明显。结论：氟伐他汀具有肾脏保护作用,延缓糖尿病肾病病情进展。     

糖尿病患者血清肝细胞生长因子水平及临床意义

目的 探讨血清肝细胞生长因子（HGF）在2型DM不同肾损害期中的变化、临床意义及糖尿病肾病发生发展中的作用。方法将2型DM患者92例分为不同的组别,其中尿白蛋白正常组30例,尿白蛋白微量组32例,尿白蛋白明显增高组30例;糖耐量异常患者33例,采用ELISA法检测血清HGF水平,同时用化学发光法检测尿微量白蛋白。结果糖耐量异常组和尿白蛋白正常组HGF浓度明显高于对照组（P〈0．05）;尿白蛋白微量组及尿白蛋白明显增高组HGF浓度明显低于对照组（P〈0．05）;且尿白蛋白明显增高组又显著低于尿白蛋白微量组（P〈0.05）。结论2型DM患者不同肾损害期HGF浓度差别有统计学意义,检测血HGF水平可为糖尿病肾病的诊断和治疗监测提供可靠依据。     

Abnormal plasma noradrenaline response and exercise induced albuminuria in type 1 (insulin-dependent) diabetes mellitus

Submaximal exercise provokes an abnormal elevation in albuminuria in type 1 (insulin-dependent) diabetes mellitus. Plasma catecholamines might be involved in this phenomenon by a renal vasoconstrictive effect. Twelve healthy subjects (Controls: albuminuria < 10 μg min^-1), 13 normoalbuminuric type 1 diabetic patients (DNormo: albuminuria < 10μg min^-1) and 13 microalbuminuric type 1 diabetic patients (DMicro: albuminuria 10–200 μg min^-1) performed a fixed bicycle workload (600 kpm for 20 min + urine collection 40 min post exercise). None of the patients suffered from autonomic neuropathy or hypertension. Fractional albumin clearance (FalbCl) rose in DNormo (p=0.02) and DMicro (p=0.01) but not in the Controls (p=0.40). Basal plasma adrenaline and noradrenaline were not different in the three groups. The increments in noradrenaline were more pronounced in DNormo and DMicro than in Control (Controls < DNormo, p < 0.05; Controls < DMicro, p < 0.01). The changes in FalbCl were significantly correlated with the changes in noradrenaline (all subjects r=0.65, p < 0.001). The increments in adrenaline were not different in the diabetic groups compared to the controls, and were not related to the changes in FalbCl. Multiple regression analysis showed that changes in plasma noradrenaline (p < 0.002) and in mean arterial pressure (p < 0.005) independently contributed to the changes in FalbCl (multiple r=0.73).

It is concluded that the exercise-induced plasma noradrenaline response is increased in normo-and microalbuminuric type-1 diabetic patients. Noradrenaline appears to contribute in the exercise-induced changes in renal protein handling, possibly by its effect on renal haemodynamics.