308例IgA肾病中医证候分布多中心前瞻性研究

目的用临床流行病学的研究方法,对IgA肾病的中医证候分布进行新的探索.方法病例问卷采用横断面调查,共收集合格病例308份,用因子分析的统计方法进行分析.结果共得出6个共因子,即6个类证候,它们是类气阴两虚证、类肾阳虚、类风热袭肺证、类舌脉证、类大肠湿热证,其中类气阴两虚证所占比例最大.结论用临床流行病学的方法对中医证候的探索性研究具有一定意义.     

商陆粗提物对阿霉素肾病大鼠治疗作用的实验研究

目的：观察商陆粗提物对大鼠阿霉素肾病模型的影响及作用。方法：经大鼠尾静脉分次注射阿霉素合计7．5mg／kg制备肾病模型，分别灌以商陆粗提物4g／kg.d^-1和1g／kg.d^-1以及强的松16mg／kg．d^-1，均连续2周，观察用药组间动物血清白蛋白、尿蛋白及血脂的改变。结果：商陆粗提物对阿霉素肾病模型大鼠具有减少尿蛋白、提高血清白蛋白的作用（与模型组比较，P〈0．05），且与激素比较无统计学差异（P〉0．05）。结论：商陆对阿霉素肾病具有治疗作用，为开发中药商陆提供了实验依据。     

维生素B6对大鼠早期糖尿病肾病的防治作用

目的:探讨维生素B6对糖尿病肾病(DN)大鼠肾功能的保护作用及可能的机制.方法:利用链脲菌素(STZ)腹腔注射法诱导建立DN大鼠模型,将其随机分为模型组(D组)、维生素B6治疗组(B组)、氨基胍治疗组(A组),并与正常对照组(C组)比较,每组10只大鼠;A、B组每天分别用氨基胍、维生素B61g溶于1L蒸馏水中,C、D组仅给予1L蒸馏水,24 h后自由饮用.观察治疗期间大鼠的一般状况、空腹血糖(FBG)、糖化血红蛋白(HbA1c)、血三酰甘油(TG)、血总胆固醇(TC)、血肌酐(SCr)、肾小球滤过率(GFR)、24 h尿白蛋白排泄率(UAER)、肾小球提取物糖基化终末产物(GTE-AGEs)、肾组织病理等改变.结果:(1)造模组大鼠均出现肾脏功能损害.(2)维生素B6对FBG及HbA1c无影响,但能降低DN大鼠的TG、TC、SCr、24h-UAER,增加GFR.(3)维生素B6能降低DN大鼠肾小球AGEs,其作用效果与氨基胍相当.结论:(1)维生素B6无降糖作用,但对肾脏功能有一定的保护作用;(2)维生素B6能降低糖尿病大鼠的高脂血症;(3)维生素B6具有与氨基胍相似的抑制肾脏AGEs在糖尿病大鼠肾脏蓄积的作用,发挥其对糖尿病肾病的防治作用.     

厄贝沙坦与开博通治疗糖尿病肾病的临床观察

目的探讨厄贝沙坦开博通治疗糖尿病肾病的疗效。方法选择60例2型糖尿病并发肾脏病变患者,随机分为厄贝沙坦治疗组(30例),与开搏通对照组(30例)。两组患者治疗前后监测血压、24h尿蛋白定量、血肌酐、尿素氮、血钾、血糖、血β2-MG、尿β2-MG等,疗程16周。结果两组病人治疗前后血压、24h尿蛋白定量、血β2-MG、尿β2-MG、血肌酐均有明显下降(P<0·05)。结论厄贝沙坦和开博通均有降压及肾脏保护作用,厄贝沙坦的肾脏保护作用优于开博通,而厄贝沙坦同时具有改善胰岛β细胞功能的作用。且厄贝沙坦副作用较小。     

商陆粗提物对阿霉素肾病大鼠治疗作用的实验研究

目的:观察商陆粗提物对大鼠阿霉素肾病模型的影响及作用。方法:经大鼠尾静脉分次注射阿霉素合计7.5mg/kg制备肾病模型,分别灌以商陆粗提物4g/kg.d-1和1g/kg.d-1以及强的松16mg/kg.d-1,均连续2周,观察用药组间动物血清白蛋白、尿蛋白及血脂的改变。结果:商陆粗提物对阿霉素肾病模型大鼠具有减少尿蛋白、提高血清白蛋白的作用(与模型组比较,P<0.05),且与激素比较无统计学差异(P>0.05)。结论:商陆对阿霉素肾病具有治疗作用,为开发中药商陆提供了实验依据。     

葛根素注射液与维生素C联用治疗2型糖尿病肾病52例临床研究

目的：观察葛根素注射液联用维生素C对2型糖尿病肾病的治疗作用及机制。方法：将确诊为2型糖尿病肾病的145例患者随机分为3组。治疗组52例，在常规治疗基础上给予葛根素注射液静脉滴注，并口服维生素C；对照A组48例，在常规治疗基础上加用葛根素静脉滴注；对照B组45例，在常规治疗基础上加服维生索C，3组均以2周为1个疗程。观察3组治疗前后尿紊氮、血肌酐、血脂、糖化血红蛋白、丙二醛、超氧化物歧化酶、24小时尿白蛋白排泄率等指标的变化。结果：治疗组治疗后除尿素氮、血肌酐、糖化血红蛋白外其他各项指标与治疗前相比均有显著改善（P〈0．01）。结论：葛根素注射液、维生素C均有较好的改善肾功能及降低尿蛋白排泄率的作用。二者合用有协同作用，治疗2型糖尿病肾病的疗效比单用葛根素或维生素C好。     

2型糖尿病患者糖尿病性肾病不同阶段血脂谱的差异

目的:比较2型糖尿病患者糖尿病肾病不同阶段的血脂谱。方法:收集我院2型糖尿病患者144例,根据尿蛋白定量、尿微量白蛋白定量分成三组:无肾病组22例,早期肾病组78例,临床期肾病组44例。所有患者测定血甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A(apoA)、载脂蛋白B(apoB)、脂蛋白a。比较三组间血脂差异。结果:HDL-C水平在无肾病组、早期肾病组、临床期肾病组依次递减(1.363±0.535,1.161±0.327,1.060±0.281),三组间两两比较,差异均有显著性。TG水平依次递增(1.359±0.485,1.581±0.827,1.963±1.626),其中临床期肾病组较早期肾病组及无肾病组增高差异有显著性,早期肾病组与无肾病组间差异无显著性。脂蛋白a水平呈递增趋势(9.252±2.920,11.368±5.954,12.333±6.354),但组间差异无显著性。3组间TC、LDL-C、apoA、apoB无差异。结论:2型糖尿病患者脂代谢紊乱与糖尿病肾病的发生有一定相关性。     

The stressed neonatal kidney: from pathophysiology to clinical management of neonatal vasomotor nephropathy

The healthy term, and particularly the premature infant, is born with a very low glomerular filtration rate (GFR), controlled by a delicate balance of intrarenal vasoconstrictor and vasodilator forces. Vasoactive disturbances can easily further reduce the already low GFR. The newborn infant is thus prone to develop vasomotor nephropathy (VMNP) or acute renal failure (ARF). The main causes for ARF at this young age are prerenal mechanisms, and include hypotension, hypovolemia, hypoxemia perinatal asphyxia, and neonatal septicemia. Other causes include the administration of angiotensin converting enzyme inhibitors, indomethacin and tolazoline. The most-important factors governing the ultimate renal prognosis are the severity of the underlying disorder, the rapidity of an accurate diagnosis, prompt treatment, and avoidance of severe iatrogenic complications. The immediate treatment is of particular importance in VMNP, i.e., prerenal ischemic ARF, and consists of correcting abnormalities in fluid homeostasis and reduction of the complications of the acute azotemic state (uremia, hyperkalemia, acidosis, and hypertension). In severe and prolonged (established) ARF, temporary dialysis therapy may be indicated. Prerenal ARF with oliguria or anuria warrants immediate volume resuscitation. Special attention should be given to infants with congestive heart failure (CHF). The sick neonate with persistent oliguria and CHF should be treated with intravenous dopamine. Furosemide (FM) is the second line of therapy for babies with indomethacin-induced ARF. In most other conditions, the therapeutic effect of FM is limited to a transient increase in urine flow, without improving basic renal function. The special conditions of the maturing kidney have to be appreciated in order to protect babies from undue renal injury. With the increasing knowledge of the mechanisms governing the development of ARF, progress has been made in the development of new treatment modalities. For example theophylline, calcium antagonists, ATP-MgCl₂, thyroxine, and a variety of cytokines may in the near future be used to prevent or ameliorate VMNP and/or recently established ARF. With a combination of time-honored and new therapeutic strategies, there may well be a brighter future for neonates with vasomotor, prerenal, ischemic ARF. Received: 10 February 1999 / Revised: 16 June 1999 / Accepted: 22 June 1999     

Sporadic case of X-chromosomal Alport syndrome in a consanguineous family

Alport syndrome (AS) is a genetic disorder of basement membranes caused by mutations in type IV collagen genes that is characterized by chronic hematuria and progressive nephropathy leading to renal failure. The main extrarenal features include sensorineural hearing loss and ocular lesions. The mode of inheritance is X-linked dominant in about 80%–85% of the affected families, whereas autosomal transmission is rarely encountered. We report a male patient originating from a healthy consanguineous Lebanese family who presented with an unusual association of obstructive uropathy and AS. Hematuria and proteinuria were initially attributed to a suspected poststreptococcal glomerulonephritis (GN) and high-grade subpelvic ureteral stenosis. Persistence of symptoms after medical treatment of poststreptococcal GN and surgical correction of obstructive uropathy finally led to renal biopsy. The observed ultrastructural changes of the glomerular basement membrane were typical for AS.Molecular genetic studies revealed a previously undescribed de novo mutation in the COL4A5 gene, excluding maternal heterozygotic carrier status. This case report emphasizes the importance of hereditary nephritis in the differential diagnosis of chronic hematuria, and demonstrates the value of molecular studies for genetic counselling in AS. Received: 9 October 1998 / Revised: 15 February 1999 / Accepted: 24 August 1999     

野黄芩甙元对糖尿病大鼠肾脏保护作用的研究

目的:探讨野黄芩甙元(EB)对糖尿病大鼠肾脏病变的保护作用及作用机制。方法:观察 EB 对糖尿病大鼠肾病理、肌酐清除率(Ccr)、尿白蛋白排泄率(UAlb)的影响,以及对肾组织局部血管紧张素Ⅱ(AngⅡ)、转化生长因子β_1(TGF-β_1)含量的影响。结果:EB 可降低糖尿病大鼠 CCr、UAlb 及系膜基质含量,降低肾内局部 AngⅡ、TGF-β_1的水平。结论:EB 可能通过降低肾组织局部 AngⅡ及 TGF-β_1的含量起到对糖尿病肾病的保护作用。