脂蛋白肾病1例报道及文献复习

近期重庆市中医院肾病科收治脂蛋白肾病(Lipoprotein glomerulopathy,LPG)1例。现回顾分析病例资料、中西医诊疗及随访情况,并进行文献复习、中医传统理论阐述及讨论。以提高临床对中医药诊治该病的认识。     

2-Dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione,isolated from the root of Averrhoa carambola L., protects against diabetic kidney disease by inhibiting TLR4/TGFβ signaling pathway

ObjectiveDiabetic kidney disease (DKD) is the leading cause of death and disability of diabetes mellitus. However, there is still a lack of specific drugs for the treatment of DKD. The chief aim of this research is to investigate the role and mechanism of 2-Dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione (DMDD) for DKD.MethodsWild type and TLR4 knockout mice were induced to diabetes. After 4-week treatment with DMDD, blood sugar, renal function, blood lipid and pathological changes were assessed. Real-time PCR, western blotting, and immunohistochemistry were employed to detect the expressions of TLR4, TGFβ1 and Smad2/3 in the renal tissue.ResultsDMDD improved the serum lipid and decreased fasting blood glucose levels in diabetic mice. CysC and urinary albumin levels increased markedly in the diabetic group, and they were obviously decreased after 4 weeks of DMDD treatment. Compared with the WT diabetic mice, the urinary albumin and CysC in the TLR4^-/- mice were expressed at lower levels. HE and Masson’s staining revealed that DMDD clearly ameliorated pathological changes and renal fibrosis. When TLR4 gene was knock out, the pathological was improved. Mechanistically, TLR4, TGF-β1 and Smad2/3 were obvious up-regulation in the renal tissues of diabetic mice. The expressions of these proteins were significantly down-regulated after DMDD treatment (p < 0.05). In the TLR4^-/- mice, mRNA and protein levels of TGF-β1 and Smad2/3 were obviously lower than those in the WT mice. In addition, IHC revealed that a strong in situ expressions of TLR4, TGF-β1 and Smad2/3 were seen in the kidney tissues of diabetic mice, which were distinctly weakened in the DMDD-treated mice. In the TLR4^-/- mice, however, expressions of TGF-β1 and Smad2/3 were not remarkable increase in the diabetic mice compared with normal mice.ConclusionsThese results strongly indicate that TLR4 is essential for DMDD protection against renal dysfunction in diabetic mice. Its hypoglycemic and anti-fibrosis effects were likely mediated by the TLR4/TGFβ signaling pathway.     

谭新华从肝肾论治男科疾病临证经验

谭新华教授采用温肾补肝、益肾疏肝、填精消癥、养肾柔肝、补肾泻肝之法治疗男性不育症、勃起功能障碍、前列腺增生症、精索静脉曲张、慢性前列腺炎等男科疾病临床疗效显著。本文结合典型案例对谭教授从肝肾论治男科疾病经验进行总结。     

“三焦针法”改善慢性肾脏病患者失眠症的临床观察

[目的]通过"三焦针法"对慢性肾脏病合并不寐患者辨证施治,探讨"三焦针法"治疗慢性肾脏病患者失眠症的临床疗效。[方法]对天津市第一中心医院慢性肾脏病管理中心长期随访的89例慢性肾脏病3、4期未透析患者以匹兹堡睡眠质量指数量表(PSQI)评价睡眠质量。筛选出失眠症患者为研究对象,并随机选取30例患者实施"三焦针法"针灸治疗,其余患者作为对照组给予综合治疗。针灸治疗总疗程为3个月,继续随访至6个月。全部患者治疗前、3个月疗程结束、6个月随访结束后记录患者一般情况、实验室指标、PSQI评分、中医症状评分、SF-36生活质量评分以及评估的肾小球滤过率(eGFR),评价干预前后上述各项指标的变化。[结果]全部患者中男性占60.7%,平均年龄52.5岁,平均eGFR 48.9 mL/(min·1.73 m~2)。至6个月随访结束,针灸治疗组PSQI评分与基线评分比较下降值明显高于对照组。针灸治疗组各项中医症状评分改善情况优于对照组,失眠缓解率明显高于对照组。两组之间eGFR及SF-36评分变化无明显差异。[结论]"三焦针法"可以显著改善CKD3、4期未透析患者的失眠症,各项中医症状也得到相应改善。     

非布司他治疗慢性肾脏病伴高尿酸血症的临床效果分析

目的对非布司他治疗慢性肾脏病伴高尿酸血症的临床效果进行研究.方法46例慢性肾脏病伴高尿酸血症患者,随机分为常规组与科研组,各23例.常规组采用别嘌醇片治疗,科研组采用非布司他治疗.比较两组治疗前后尿酸、血尿素氮、血肌酐水平及药物不良反应发生情况.结果治疗后,科研组血尿酸、血尿素氮及血肌酐水平分别为(290.92±59.12)μmmol/L、(13.06±5.23)mmol/L、(269.12±52.42)μmmol/L,低于常规组的(520.81±60.14)μmmol/L、(15.81±5.73)mmol/L、(293.34±56.18)μmmol/L,差异有统计学意义(P<0.05).科研组药物不良反应发生率4.35%低于常规组的43.48%,差异有统计学意义(P<0.05).结论慢性肾脏病伴高尿酸血症采用非布司他进行治疗,能够明显降低患者的尿酸、血尿素氮、血肌酐水平,不良反应少,安全性高,疗效确切.     

“两阶段三部曲”在结直肠癌辅助化疗期的应用＊

辅助化疗有助于改善高危II/III期结直肠癌患者的生存。然而，辅助化疗的不良反应影响患者的生活质量，严重的不良反应甚至可能导致化疗的延期或终止，使得患者不能从辅助化疗中获益。中国中医科学院西苑医院杨宇飞教授根据多年临床经验，创新性提出辅助化疗期的“两阶段三部曲”，即补肾健脾序贯疗法，第1阶段应用自拟六君安胃方健脾和胃，针对化疗导致的胃肠道反应；第2阶段运用芪菟二至方健脾益肾，针对化疗导致的骨髓抑制；以及辛凉解表感冒方，针对化疗期间的外感。临床应用取得了显著的疗效。文章详细阐述“两阶段三部曲”提出的背景及其主要内容。     

CDC42 promotes vascular calcification in chronic kidney disease

Vascular calcification is prevalent in patients with chronic kidney disease (CKD) and a major risk factor of cardiovascular disease. Vascular calcification is now recognised as a biological process similar to bone formation involving osteogenic differentiation of vascular smooth muscle cells (VSMCs). Cell division cycle 42 (CDC42), a Rac1 family member GTPase, is essential for cartilage development during endochondral bone formation. However, whether CDC42 affects osteogenic differentiation of VSMCs and vascular calcification remains unknown. In the present study, we observed a significant increase in the expression of CDC42 both in rat VSMCs and in calcified arteries during vascular calcification. Alizarin red staining and calcium content assay revealed that adenovirus-mediated CDC42 overexpression led to an apparent VSMC calcification in the presence of calcifying medium, accompanied with up-regulation of bone-related molecules including RUNX2 and BMP2. By contrast, inhibition of CDC42 by ML141 significantly blocked calcification of VSMCs in vitro and aortic rings ex vivo. Moreover, ML141 markedly attenuated vascular calcification in rats with CKD. Furthermore, pharmacological inhibition of AKT signal was shown to block CDC42-induced VSMC calcification. These findings demonstrate for the first time that CDC42 contributes to vascular calcification through a mechanism involving AKT signalling; this uncovered a new function of CDC42 in regulating vascular calcification. This may provide a potential therapeutic target for the treatment of vascular calcification in the context of CKD. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Hepcidin – Potential biomarker of contrast-induced acute kidney injury in patients undergoing percutaneous coronary interventions

PurposeContrast-induced acute kidney injury (CI-AKI) is a common and potentially serious complication of percutaneous coronary interventions (PCI). In this study, we tested the hypothesis whether serum and urinary hepcidin could represent early biomarkers of CI-AKI in patients with normal serum creatinine undergoing PCI. In addition, we assessed serum and urinary neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, eGFR and serum creatinine in these patients.MethodsSerum and urinary hepcidin and NGAL, serum cystatin C, were evaluated before, and after 2, 4, 8, 24 and 48 h after PCI using commercially available kits. Serum creatinine was assessed before, 24 and 48 h after PCI.ResultsWe found a significant rise in serum hepcidin as early as after 4 and 8 h when compared to the baseline values. Serum NGAL increased after 2, 4 and 8 h, and in urinary NGAL after 4, 8 and 24 h after PCI. We found a significant fall in urinary hepcidin after 8 and 24 h after PCI. Serum cystatin C increased significantly 8 h after PCI, reaching peak 24 h after PCI and then decreased after 48 h. The prevalence of CI-AKI was 8%. Urine hepcidin was significantly lower 8 and 24 h after PCI in patients with CI-AKI, while serum and urine NGAL were significantly higher in patients with CI-AKI.ConclusionsOur findings suggest that serum hepcidin might be an early predictive biomarker of ruling out CI-AKI after PCI, thereby contributing to early patient risk stratification. However, our data needs to be validated in large cohorts with various stages of CKD.