低蛋白饮食对环孢素A肾病大鼠肾间质纤维化的作用

Objective To investigate whether low-protein diet has protective effect on the progression of renal interstitial fibrosis in rats with cyclosporine A (CsA)-induced nephropathy. Methods Eighteen male Sprague-Dawley rats were randomly divided into three groups (6 rats in each group). The rats in control group (C group) received common diet; in model group (M group) low-salt diet; in intervention group (Ⅰ group) low-salt and low-protein diet. After diet adaptation period of one week, the rats in C group received subcutaneous injection of olive oil 1 mg/kg daily for 5 weeks, while M group and Ⅰ group subcutaneous injection of CsA (diluted into 25 g/L with olive oil) 1 ml/kg for 5 weeks. All the rats were sacrificed at the end of the 5th week. The food-intake and body weight were measured daily. The creatinine clearance (Ccr) was examined before rats were sacrificed. The semi-quantitative pathological analysis on kidney sections was performed. The mRNA and protein expression of transforming growth factor-β1 (TGF-βI) and type Ⅰ collagen (Col Ⅰ) in kidney tissue was determined with real time PCR and immunohistochemical staining, respectively. Results The food-intake and body weight of rats in M and I groups were significantly lower than those in C group (P<0.05). Compared with C group, the Ccr levels in M and Ⅰ groups were significantly reduced [(0.65±0.15) ml/min, (0.40+0.13) ml/min vs (1.55±0.29) ml/min, P<0.05], the relative fibrosis areas of kidney interstitium in M and I groups were significantly increased (3.60%±0.46%, 3.26%±0.75% vs 0.44%±0.24%, P<0.05), the mRNA and protein expression of TGF-β1 in M and I group was significantly up-regulated (by 2.6 and 3.1 times in mRNA and by 1.5 and 1.6 times in protein, respectively, P<0.05), and the mRNA and protein expression of Col Ⅰ in M and I groups was also significantly up-regulated (by 3.0 and 3.5 times in mRNA and by 2.3 and 2.1 times in protein, respectively, P<0.05). There were no significant differences between M and I groups in every parameters above-mentioned except the rat body weight and Ccr. Both the body weight and Ccr in Ⅰ group were significantly lower than those in M group (P<0.05). Compared with C group, the urine osmotic pressure in M group and in I group were deceased (for M group, P>0.05; for I group, P<0.05). Compared with C group, the serum cholesterol levels in M and I groups were significantly increased (P<0.05), and the serum phosphorus level in I group was significantly decreased (P<0.05). The levels of serum albumin and serum calcium of all three groups had no statistical differences (P>0.05). Conclusion Low-protein diet has no renoprutective effects on the rat model of cyclosporin A nephropathy, on the contrary, may induce body weight loss.     

慢性肾脏病与肾素-血管紧张素-醛固酮系统及高血压

慢性肾脏病(CKD)患者高血压发生率很高,尤其在出现慢性肾衰竭时.成人高血压患者中,CKD的患病率居第二位(仅次于原发性高血压,约占全部高血压的5%～10%);而在儿科高血压患者中,其患病率居首位(约占全部高血压的2/3).CKD患者的高血压危害极大,它不但诱发严重心脑血管并发症(约1/2终末肾脏病患者死于此并发症),而且能加速肾损害进展,促进慢性肾衰竭发生[1].     

无症状尿异常 肾小球性血尿和非肾小球性血尿鉴别诊断

尿沉渣显微镜检查高倍视野下红细胞数超过3个、或12小时尿Addis计数红细胞多于50方则称为血尿。轻者为镜下血尿,重者呈肉眼血尿(尿中含血量超过1ml/L即呈肉眼血尿)。血尿既可由原、继发肾小球疾病引起(肾小球性血尿),又可能由泌尿道疾病引起(非肾小球性血尿)。长期以来,临床医师一直在寻求一种简单易行的鉴别上述两种血尿的方法,以减少病人盲目检查的痛苦。近10余年来,毕竟已取得了很大进展,现作一简介。     

肺出血—肾炎综合征的诊断和治疗

Ernest Goodpasture 于1919年报告了首例患者在流感后咯血、贫血、死亡,尸解证实肺泡出血、坏死及肾炎.此后65年中又有500余例类似病例报道.1958年 Stanton 及 Tange 首先建议将其命名为 Goodpasture 综合征.文献中它还被称为肺出血—肾炎综合征及出血性肺—肾综合征等.1967年 Lerner 等证实在肺出血合并肾炎病例中相当一部份是由抗肾小球基膜(GBM)抗体致病,此后多数作者都主张将 Goodpasture 综合征的命名严格限制在这部份病例中.因此,本文所指肺出血—肾炎综合征应必备下列三个条件:(1)肺出血;(2)肾小球肾炎;(3)抗 GBM 抗体形成.病理改变一、肾脏病变:光镜下典型表现为新月体性肾炎.该新月体性肾炎之特点为不伴肾小球毛细血管     

肾脏病科临床实验诊断新知

70年代后期起,我国肾病学界已陆续开展许多新的临床诊断实验,应用至今已有一定经验,现试对其作一简要概括及评价。尿细胞学检查1.尿红细胞形态学检查:新鲜尿沉渣相差显微镜检查红细胞形态,在鉴别肾小球与非肾小球源血尿上意义极大,准确性高达95%以上,现已被普遍接受     

系统性疾病继发肾损害 狼疮性肾炎

系统性红斑狼疮（SLE）为自身免疫性疾病,常多器官系统侵犯,肾脏受累率尤高。本文仅就SLE及狼疮性肾炎（LN）的诊治予以讨论。 SLE的诊断 1988年全国风湿病学学术会议建议国内采用美国风湿病学会1982年标准（Arthritis Rh-eum 1982;25:1271）或上海标准（中华内科杂志1987;26:533）对SLE进行诊断,其中包括不少免疫学化验,如抗核抗体、抗双链DNA抗体、狼疮细胞、抗Sm抗体、血清补体C_3及皮肤狼疮带试验等。因此,要提高SLE诊断率必须开展上述化验。     

肾抗原在肾脏病中的致病作用

随着肾脏病学及免疫学的进展,对肾抗原通过自体免疫在肾脏病中的致病作用已渐获认识,现将有关问题做一综述。肾小球基膜抗原在原发性肾小球肾炎中的致病作用多种外因可作用于肾小球基膜(GBM),使其抗原结构改变,或得以暴露释放,如此便可引起机体对自体GBM的免疫反应,这些外因包括:某些具有交叉免疫反应的外源性抗原(如链球菌胞膜)或内源性抗原(如肾小管基膜及肺泡基底膜)的作用,免疫复合物的沉和,以及其它理化因素的损伤(如肾外伤)等。所引起的自体免疫能从体液免疫或