Más difícil todavía: tratar una glomerulonefritis rápidamente progresiva grave en el seno de una neumonía por COVID-19

We present the case of a male patient with severe SARS-CoV-2 pneumonia, with simultaneous onset of p-ANCA positive rapidly progressive glomerulonephritis. We discuss the different therapeutic possibilities, emphasising the appropriateness of their administration according to the time in the course of the infection.     

Retinal disease in the C3 glomerulopathies and the risk of impaired vision

Background: Dense deposit disease and atypical hemolytic uremic syndrome are often caused by Complement Factor H (CFH) mutations. This study describes the retinal abnormalities in dense deposit disease and, for the first time, atypical haemolytic uremic syndrome. It also reviews our understanding of drusen pathogenesis and their relevance for glomerular disease. Methods: Six individuals with dense deposit disease and one with atypical haemolytic uremic syndrome were studied from 2 to 40 years after presentation. Five had renal transplants. All four who had genetic testing had CFH mutations. Individuals underwent ophthalmological review and retinal photography, and in some cases, optical coherence tomography, and further tests of retinal function. Results: All subjects with dense deposit disease had impaired night vision and retinal drusen or whitish-yellow deposits. Retinal atrophy, pigmentation, and hemorrhage were common. In late disease, peripheral vision was restricted, central vision was distorted, and there were scotoma from sub-retinal choroidal neovascular membranes and atypical serous retinopathy. Drusen were present but less prominent in the young person with atypical uremic syndrome due to a heterozygous CFH mutation. Conclusions: Drusen are common in forms of C3 glomerulopathy caused by compound heterozygous or heterozygous CFH mutations. They are useful diagnostically but also impair vision. Drusen have an identical composition to glomerular deposits. They are also identical to the drusen of age-related macular degeneration, and may respond to the same treatments. Individuals with a C3 glomerulopathy should be assessed ophthalmologically at diagnosis, and monitored regularly for vision-threatening complications.     

胰腺导管癌中血管生成、细胞增殖指数、DNA倍性检测的临床意义

目的:探讨血管生成、细胞增殖指数、DNA倍性在胰腺导管癌发生、发展中的作用及临床意义。方法:对29例胰腺导管癌和7例慢性胰腺炎患者的石蜡包埋标本作苏木精鄄伊红(HE)染色,CD34、Ki67免疫组织化学染色,镜下计算微血管密度(MVD)及Ki67阳性细胞比例,同时用流式细胞仪(FCM)检测细胞核DNA倍性,计算异倍体出现率及S期比例,并结合临床病理资料对各项指标作相关分析。结果:胰腺导管癌和慢性胰腺炎都有较多的新生血管。MVD值在胰腺导管癌高、中、低分化3组之间差异无显著性。按肿瘤直径分为≤1.5cm、1.6～2.9cm、≥3cm3组,此3组间MVD值、Ki67阳性细胞百分率、DNA异倍体出现率及肿瘤周围有无浸润的差异都非常显著(P<0.01)。肿瘤越大,MVD值、Ki67阳性细胞百分率及DNA异倍体出现率越高。结论:胰腺导管癌的发生、发展伴血管生成和DNA合成增加,联合测定MVD、Ki67阳性细胞百分率、DNA倍型可能为胰腺导管癌临床预后预测提供辅助参考指标。     

胃癌和胃癌前病变Cx43、PCNA的表达及意义

目的　通过观察间隙连接蛋白 Cx4 3和增殖细胞核抗原 (PCNA )在正常胃粘膜、胃癌前病变和胃癌中的表达和分布情况 ,探讨 Cx基因表达与胃癌发生的关系。　方法　运用 SP免疫组织化学方法检测 Cx4 3、PCNA在 70例原发性胃癌 ,6 2例中、重度不典型增生和 16例正常胃粘膜中表达规律。　结果　 Cx4 3在正常胃粘膜 ,中、重度不典型增生和胃癌中表达的阳性率分别为 10 0 % ,83.9%和 17.1% ,三者比较差异有显著性 (P<0 .0 5 )。 Cx4 3表达与胃癌的分化程度相关 (P<0 .0 1)。胃癌前病变、胃癌组中的 PCNA较正常胃粘膜组增高 (P<0 .0 1)。 Cx4 3表达与 PCNA呈负相关 (P<0 .0 1)。　结论　 Cx4 3表达降低在胃癌发生发展中起重要作用 ,Cx4 3可做为胃癌早期诊断的指标     

系膜细胞α-平滑肌肌动蛋白表达与细胞表型的关系

目的：探讨增殖性肾小球肾炎大鼠动物模型中系膜细胞α－平滑肌肌动蛋白（α－SMA）表达与细胞表型的关系。方法：应用单克隆抗体1－22－3（MoAb1-22-3)及Habu蛇毒素分别诱导大鼠增殖性肾小球肾炎动物模型。用免疫组化技术并结合计算机图像分析，检测两个不同诱因引起模型的各个阶段的系膜细胞内α－平滑肌肌动蛋白，SMeb的表达程度，系膜细胞增殖和细胞外基质（ECM）分泌的情况。结果：在MoAb1-22-3模型，随着系膜细胞增殖程度的加理，ECM积聚增多，α－SMA的表达程度也增加，三者平行变化并具有高度相关性，而Habu模型则系膜细胞增殖和ECM增加的同时α－SMA，SMemb表达不增加。结论：α－SMA不是系膜细胞被激活并处于增殖／分泌表型唯一标志。     

李松林副主任医师治疗肾小球肾炎的经验

李松林副主任医师将肾小球肾炎的病机概括为湿、热、毒、瘀、虚等方面，在中医辨证的基础上，结合现代医学对其病因和发病机理的认识及中草药药理作用，针对不同的病理机制和临床表现，提出清热解毒法，活血化瘀法，调补脾肾法，扶正固本法，并视症有机结合，恰当治疗，疗效显著。     

p53,p16,PCNA蛋白在食管癌中的表达及其临床意义

目的探讨p53,p16,PCNA蛋白在食管癌中的表达及临床意义。方法用免疫组织化学染色SP法对62例食管癌标本进行p53,p16,PCNA蛋白测定。结果62例食管癌中,p53,PCNA蛋白阳性表达均为71.0%(44/62),p16缺失率48.4%(30/62)。p16缺失与肿瘤浸润深度、淋巴结转移密切相关(P<0.05、P<0.01)。而p53,PCNA蛋白同时表达56.5%(35/62),亦与肿瘤浸润深度、淋巴结转移密切相关(P<0.05、P<0.01)。结论食管癌p53,PCNA蛋白同时表达及p16缺失可视为危险预后因素。     

柴苓小方对大鼠肾小球系膜细胞异常增殖的影响

目的：探讨柴苓小方对大鼠肾小球系膜细胞（GMCs）异常增殖的影响及相关机制。方法：采用脂多糖刺激系膜细胞异常增殖。MTT法检测柴苓小方对㈣异常增殖的影响；免疫细胞化学方法检测药物作用后增殖细胞核抗原（PCNA）的表达；乳酸脱氢酶释放实验检测柴苓小方的细胞毒作用。采用RT—PCR检测药物作用不同时间点细胞周期蛋白依赖性激酶抑制剂p21的表达。结果：柴苓小方可以剂量依赖性的抑制系膜细胞异常增殖并显著减少PCNA阳性细胞数而没有明显的细胞毒作用。并且柴苓小方可以显著地上调p21基因的表达（P〈0．05）。结论：柴苓小方可剂量依赖性的抑制GMC8异常增殖．其机制可能与上调p21mRNA表达有关。