从热、虚、瘀辨证论治小儿过敏性紫癜

从热、虚、瘀三个方面论述了小儿过敏性紫癜的病因病机特点，抓住病因病机的核心，确定了热伤血络、阴虚火旺、气不摄血三个本证证型和风热、热毒、湿热、血瘀四个标证证型。采用本证和标证相结合的方法对小儿过敏性紫癜进行辨证论治，并从理论上探讨了该方法的科学性和实用性。     

免疫性血小板减少性紫癜辨证分型与血小板表面相关抗体及T淋巴细胞亚群的关系

为探讨免疫性血小板减少性紫癜（ITP）中医辨证分型与免疫机理的关系,将ITP患者中医辨证分型结合血小板相关抗体（PAIg）及T淋巴细胞亚群进行分析。发现作为本病主要抗体的PAIgG脾肾阴亏型明显高于脾虚失统型（P<0.01）;OKT₈⁺值亦显著高于脾虚失统型（P<0.05）,OKT₄⁺/OKT₈⁺比值则明显低于脾虚失统型（P<0.05）。提示脾肾阴亏型的免疫损伤程度较脾虚失统型严重。     

大鼠抗GBM肾炎模型的建立及不同病期的生化指标和肾组织病理学观察

目的：为研究人类新月体抗肾炎的发病机制，建立大鼠抗肾小球基底膜（BGM）肾炎的动物模型，方法：提取S－D大鼠GBM抗原，将此抗原免疫新西兰白兔获得抗血清，再将此抗血清从尾静脉一次性注射给S－D大鼠。实验分2组：肾炎模型组及正常对照组。定期于第4天、第14天第第21天检测大鼠24h尿蛋白，血肌酐及血尿素的含量和肾组织病理学改变。结果：大鼠肾炎模型组：大鼠注射抗血清后于第4天出现大量蛋白尿，第14天血肌酐，血尿素显著升高，并持续上升，肾组织病理表现为肾小球内细胞数明显增加，大量新月体形成及蛋白管型，GBM呈不规则增厚，足突融合，内皮细胞脱落，坏死，免疫荧光检查见IgG、鼠IgG沿GBM线形分布，大鼠正常对照组以上指标均无明显改变。结论：通过动态观察大鼠抗GBM肾炎的病变变化，证实该模型病变与人类新月体性肾炎的病变较为一致，该模型可用于探讨人类新月体体肾炎的实验研究。     

Fiberglass or silica exposure and increased nephritis or ESRD (end-stage renal disease)

The U.S. multiplant cohort mortality study of workers producing manufactured mineral fibers is finding increasing mortality from nephritis and/or nephrosis. We examine other data sets to see if similar effects can be identified. In a case-referent study among Michigan patients with end-stage renal disease (ESRD), men with exposures to silica have elevated odds ratio for ESRD. In a California occupational mortality study based on 1979–81 data, a number of the construction trades, farmers, and farm laborers show excess mortality for renal disease. The highest mortality ratio is found in the category including insulation workers. This ratio remains significantly elevated when adjusted for estimated exposures to smoking, alcohol, and for socio-economic status. California mortality data from 20 years earlier (1959–61) fail to show much excess renal disease in construction workers, but do for farmers. In Singapore, granite workers with a long-term exposure to silica have excess excretion of albumin and similar compounds compared to less exposed controls, leading to the presumption that silica exposure can lead to silica nephrotoxicity. Balkan nephropathy has been associated with consumption of well water high in silica. In the Negev of Israel, dust storms are a vehicle for increasing respiratory uptake of silica. The Beduin, thought to be a population with maximal exposures, have higher rates of ESRD than do Jews in the age groups over 60 years. Although high blood concentrations of silica are found in persons with renal failure, the close association with elevated creatinine has been interpreted as evidence that the buildup of silica is due to renal failure, rather than vice-versa. The evidence is consistent with, but not yet compelling, that exposure to silica, which can be readily absorbed (or dissolved) from the lung, may increase the long-term risk of renal disease including renal failure. © 1993 Wiley-Liss, Inc.     

Subacute (acute,persistent) thrombotic microangiopathy

Six patients with prolonged acute courses of thrombotic microangiopathy are reviewed. These patients had in common courses of acute disease requiring plasma support for more than 3 months, with subsequent complete remission. Plasma support requirements may be prodigious, and the acute course may require more than 100 plasma exchanges before a stable remission is achieved. These patients appear to represent a subset of thrombotic microangiopathy distinct from the more common acute T.T.P. course, which resolves in 3–6 weeks, and the chronic relapsing pattern, which may have a short or prolonged acute course. © 1992 Wiley-Liss, Inc.     

发色三肽底物测定血浆蛋白C活性及临床应用

建立了血浆蛋白Ｃ活性水平测定的发色三肽底物法，并对临床５６例病例进行了检测。以正常人血浆蛋白Ｃ活性平均值为１００％作对照，３０例肝硬化病人血浆蛋白Ｃ活性平均为（６１．４±２７．３）％；７例慢性肾功能不全病人血浆蛋白Ｃ活性平均为（５１．２±２５．７）％，１８例正常晚期妊娠妇女血浆蛋白Ｃ活性平均为（１３８．０±２３．５）％。与正常对照组比较，结果差异均有显著性。在的１例血栓性血小板减少性紫癜（ＴＴＰ）     

Inhibition of Complement Regulation Is Key to the Pathogenesis of Active Heymann Nephritis

Crry (complement receptor 1–related protein/gene y) is a key cellular complement regulator in rodents. It is also present in Fx1A, the renal tubular preparation used to immunize rats to induce active Heymann nephritis (HN), a model of membranous nephropathy. We hypothesized that rats immunized with anti-Fx1A develop autoantibodies (auto-Abs) to Crry as well as to the megalin-containing HN antigenic complex, and that anti-Crry Abs promote the development of injury in HN by neutralizing the complement regulatory activity of Crry. Rats immunized with Fx1A lacking Crry remained free of proteinuria and glomerular deposits of C3 during a 10-wk follow-up despite typical granular immunoglobulin (Ig)G deposits in glomeruli. Anti-Fx1A auto-Abs were present in their sera at levels that were not different from sera pooled from proteinuric rats with HN induced with nephritogenic Fx1A. Passive administration of sheep anti-Crry Abs to rats immunized with Crry-deficient Fx1A led to proteinuria and glomerular C3 deposition, which were not seen in such rats injected with preimmune IgG, nor in rats with collagen-induced arthritis injected with anti-Crry IgG. To directly examine the role of Crry in HN, rats were immunized with Crry-deficient Fx1A reconstituted with rCrry. This led to typical HN, with 8 out of 15 rats developing proteinuria within 14 wk. Moreover, the extent of glomerular C3 deposition correlated with proteinuria, and anti-Crry Abs were present in glomerular eluates. Thus, Crry is a key nephritogenic immunogen in Fx1A. Formation of neutralizing auto-Abs to Crry impairs its function, leading to unrestricted complement activation by Abs reactive with the HN antigenic complex on the epithelial cell surface.     

高脂饲料加重大鼠阿霉素肾病的实验病理学研究

探讨高脂饲料加剧阿霉素肾病大鼠高脂血症及肾组织形态学改变的作用。用ＡＤＲ静脉注射建立大鼠肾病模型，饲喂含１．５％胆固醇、５％猪油的高脂饲料，观察大鼠尿蛋白排泄量，测定血肖中脂质有关指标以及检查肾组织形态学改变。饲喂高脂饲料的ＡＤＲ肾病大鼠，血清脂质水平在整个试验过程中均明显高于饲喂基础饲料的ＡＤＲ肾病大鼠，肾小球病变也显著加重，饲喂高脂饲料所致高脂血症是导致大鼠ＡＤＲ肾病进行性进展的重要因素之一。     

Role of β2 integrins in glomerular leucocytes in Henoch-Schoenlein purpura nephritis: an age-matched comparative study with immunoglobulin A nephropathy

SUMMARY: A comparative immunohistological study was performed for the glomerular deposition of complements (C1q and C3c), fibrin/fibrinogen‐related antigen (FRA), the expression of intercellular adhesion molecule‐1 (ICAM‐1), and the infiltration of leucocytes bearing β₂ integrins (leucocyte function associated antigen‐1 (LFA‐1), complement receptor 3 (CR3) and complement receptor 4 (CR4)) on renal biopsy specimens from 49 cases with Henoch‐Schoenlein purpura nephritis (HSPN), and 49 age‐matched cases with immunoglobulin A nephropathy (IgAN). the glomerular expression of ICAM‐1 was signifcantly correlated with the glomerular infiltration of leucocyte function associated antigen (LFA)‐1⁺ leucocytes in both diseases, and with that of CR3⁺ leucocytes in HSPN. the expression of ICAM‐1 was closely localized with the infiltration of LFA‐1⁺ leucocytes in the study with double immunostaining. the incidence and intensity of glomerular deposition of FRA were significantly higher in HSPN than in IgAN (P< 0.001), and those of C3c were significantly lower in HSPN than in IgAN (P< 0.001). the glomerular deposition of FRA was significantly correlated with the glomerular infiltration of CR4⁺ leucocytes in HSPN (P<0.05) but not in IgAN. In contrast, the glomerular deposition of C3c was significantly correlated with the glomerular infiltration of CR4⁺ leucocytes in IgAN (P<0.05), but not in HSPN. Studies with double immunostaining revealed a close association of CR4⁺ leucocytes with FRA deposition in HSPN and with C3c deposition in IgAN, respectively. the number of glomerular leucocytes bearing β₂ integrins was significantly correlated with urinary protein at the time of renal biopsy in both diseases. These results suggested the differential roles of β₂ integrins in the induction of glomerular injury in HSPN and IgAN. the ICAM‐1/LFA‐1 interaction may commonly be involved in the glomerular infiltration of leucocytes in both diseases. the ICAM‐1/CR3 interaction may be involved only in HSPN. Complement receptor 4 may function as a fibrin/fibrinogen receptor in HSPN, while CR4 may function as a complement receptor in IgAN.