慢性肾功能不全患者的脑干听觉诱发电位分析

本文对54例慢性肾功能不全(CRF)患者的脑干听觉诱发电位(BAEP)检查结果进行分析。全部患者均有不同程度的贫血,血红蛋白平均为53g/L,非蛋白氮平均为25.44mmol/L,肌酐平均为510μmol/L。患者组BAEP有不同程度异常,主要表现为Ⅰ～Ⅴ各波潜伏期和Ⅲ～Ⅴ、Ⅰ～Ⅴ波间期延长(P<0.05和<0.01),波幅降低,波形分化不清或消失。本病患者有神经系统损害,特别是脑干损害者尤为明显。应用BAEP对CRF患者并发尿毒症脑病的可进行早期诊断,脑干的电生理变化因体内毒性物质的有害影响而产生异常。     

80例慢性肾功能不全的疗效及护理

目的 探讨治疗慢性肾功能不全的临床护理效果.方法 对慢性肾功能不全患者80例分成两组,分别进行结肠透析治疗和传统灌肠治疗及系统化护理,观察疗效.结果 两组患者治疗后常见临床症状明显减轻或消失,治疗组明显优于对照组(P<0.05).结论 结肠途径治疗机治疗慢性肾功能不全,克服了传统灌肠方式只能达直肠段的缺点,能更充分彻底地清除体内的有毒物质,并促进肠黏膜吸收药物,达到治疗目的,其治疗效果优于传统的灌肠法;值得推广使用.     

不同程度慢性肾功能不全患者血清醛固酮水平变化

目的:探讨慢性肾功能不全患者肾功能不同程度减退时血清醛固酮(Ald)水平的变化趋势及两者的相关性。方法:各种病因导致的慢性肾功能不全而未开始替代治疗的患者共42例按Cockcroft-Gault计算的内生肌酐清除率(Ccr)的不同分成三组,第1组Ccr≥60ml(min·1.73m2),第2组20ml/(min·1.73m2)≤Ccr<60ml/(min·1.73m2),第3组Ccr<20ml/(min·1.73m2)但未开始透析,比较三组患者的血浆肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)和血清Ald浓度(SACs),并对Ccr和SACs两者行相关性分析;PRA、AngⅡ和SACs的检测用放射免疫分析。结果:第3组患者的SACs较第1、2组显著升高(P<0.01),第2组患者的SACs也较第1组患者显著升高(P<0.05)。Ccr与SACs呈高度负相关(r=-0.685,P<0.001)。结论:慢性肾功能不全的患者,随着Ccr下降,SACs有逐渐升高的趋势。     

慢性肾功能不全患者血清瘦素水平的分析

本文侧重探讨血清瘦素（leptin）水平在慢性肾功能不全患者中的意义，尽早发现营养不良，探讨营养不良的原因，对改善慢性。肾功能不全患者的预后有重要意义。     

多普勒超声对慢性肾功能不全患者心血管改变的诊断价值

目的:观察分析多普勒超声在慢性肾功能不全（CKD）患者心血管改变评估中的诊断价值。方法:按照美国肾脏病与透析病人生存质量指导指南（KDOQI）选取轻中度肾功能不全即CKD 2~3期患者共80例,选取患者住院治疗同时间段80名健康志愿者作为对照组,使用彩色多普勒超声诊断仪检测两组患者左心室结构及功能参数和颈动脉血管结构及弹性参数,对比分析两组患者各项参数变化。结果:CKD组患者动脉血压收缩压及舒张压均高于健康对照组,CKD组患者心率较快,差异有统计学意义（P<0.05）,CKD 2~3期患者左心室结构及功能参数与正常对照组比较,E/A值和Em值均明显降低,E/Em、EF、LVID、DTE、LAD、LVMI均明显升高,差异有统计学意义（P<0.05）,E、RWT变化不明显,差异无统计学意义（P>0.05）,CKD 2~3期患者颈动脉血管结构及弹性参数与正常对照组患者比较,PWVcf、PWVβ、Ep、IMT、D、β均明显升高,差异有统计学意义（P<0.05）。结论:多普勒超声技术可无创且准确地对CKD早期患者左室结构及功能、血管结构及弹性改变进行较为完整的评估,能为临床治疗提供准确有效的指导。     

慢性肾功能不全患者的瞬目反射

本文报道10例慢性肾功能不全患者的瞬目反射(BR)结果,并和正常对照组进行对照分析,以探讨慢性肾功能不全对BR的影响.     

SCL-90对慢性肾功能不全患者的测评分析

目的 了解慢性肾功能不全患者的心理健康状况。方法 对34例慢性肾功能不全患者，应用90项症状校核量表（SCL-90），根据各自的实际情况作出独立测试，测试结果由神经心理医生进行测评。分析、结果 慢性肾功能不全患者躯体化、强迫、人际关系、焦虑、抑郁、敌对，恐怖等因子分值显著高于国内常模。结论 慢性肾功能不全患者在躯体疾病的基础上，还存在着不同程度的社会心理问题。     

慢性肾功能不全32例临床特点

目的 探讨慢性肾功能不全的临床诊断治疗问题;方法积极治疗原发病,去除诱因及对症治疗,注意低磷、低脂、优质低蛋白饮食,必需氨基酸的补充,中医治疗以及适时开始透析治疗;结果存活24例;结论加强对慢性肾病的早期防治,实施慢性肾脏病一体化治疗以及在使用西医治疗的同时应用中医药辨证治疗.     

11例小儿慢性肾功能不全的病因及临床特点

目的了解小儿慢性肾功能不全的病因及临床特点。方法回顾了我院收治的11例慢性肾功能不全患儿,男7例,女4例,年龄最小4个月,最大14岁,平均5岁。大于5岁小儿5例,小于1岁小儿6例。结果6例小婴儿慢性肾功能不全中婴儿型多囊肾1例,双肾发育不全1例,先天性肾病综合征1例,双肾发育异常伴尿道瓣膜、室间隔缺损、胆总管囊肿各1例。多以肾外症状就诊如：生长发育迟缓、腹包块、抽风、贫血等。5例较大的小儿为膀胱输尿管尿液返流Ⅳ级伴返流型肾病1例,原发性肾病综合征伴肾衰2例,慢性间质性肾炎1例,肾固缩1例,肥胖相关性肾病1例。结论小婴儿慢性肾功能不全多由先天性肾发育畸形所致,且多以肾外症状为表现,应引起重视。较大的小儿慢性肾功能不全多由获得性肾脏疾患所致;这些患儿如若尿改变不明显,肾功能异常明显,排除肾前、肾后因素所致者,应做肾穿刺活检明确病因。     

彩色多普勒超声诊断子宫恶性滋养细胞肿瘤的探讨

目的 评价彩色多普勒血流显像(CDFI)及脉冲多普勒(PD)检测恶性滋养细胞肿瘤的早期诊断疗效观察及判断疾病转归的应用价值。方法 应用CDFI及PD检测恶性滋养细胞肿瘤患者32例,并以正常妊娠20例作对照。结果 CDFI恶性滋养叶肿瘤表现为丰富而敏感的彩色血流,PD为低速的动静脉血流。正常妊娠为不甚敏感的点状或多条状的不规则血流,PD为单相或双相的低速动脉血流。阻力指数(RI)显著性差异(P<0.01)。结论 CDFI和PD检测可做为一种新的方法,不仅可对滋养叶细胞肿瘤作出早期诊断,亦可用于观察化疗效果,判断疾病的转归。     

一个成人多囊肾疾病家系研究分析

目的通过一个家系分析,探讨常染色体显性遗传性多囊肾疾病的病因学、病理学、遗传学因素。方法通过对一个多囊肾家系三代20例家庭成员进行调查,并对六例患者进行B超、肝肾功能检查。结果患者主要表现为双侧肾脏多发性囊肿,部分患者合并肝脏多发性囊肿,多于35岁以后起病,伴有腹胀,高血压,血尿等症状,部分患者行囊肿去顶开窗手术,有一例患者合并多囊脾。家系遗传分析表明该疾病属于常染色体显性遗传性多囊肾疾病,其中多囊肝为肾外表现。结论本病发病机制与基因缺陷相关,尤其是PKD1、多囊蛋白-1、PKD2、多囊蛋白-2、PKD3等,家系中如果亲代发病,子代中亦会有发病,年龄在35岁以后为多。     

Quality of life in patients with chronic kidney disease

AIM:

To compare the dimensions of quality of life in the stages of chronic kidney disease and the influence of sociodemographic, clinical and laboratory data.

INTRODUCTION:

The information available on the quality of life of patients on conservative treatment and the relationship between the quality of life and glomerular filtration rate is limited.

METHODS:

155 patients in stages 1–5 of chronic kidney disease and 36 in hemodialysis were studied. Quality of life was rated by the Medical Outcomes Study Short Form 36-Item (SF-36) and functional status by the Karnofsky Performance Scale. Clinical, laboratory and sociodemographic variables were investigated.

RESULTS:

Quality of life decreased in all stages of kidney disease. A reduction in physical functioning, physical role functioning and in the physical component summary was observed progressively in the different stages of kidney disease. Individuals with higher educational level who were professionally active displayed higher physical component summary values, whereas men and those with a higher income presented better mental component summary values. Older patients performed worse on the physical component summary and better on the mental component summary. Hemoglobin levels correlated with higher physical component summary values and the Karnofsky scale. Three or more comorbidities had an impact on the physical dimension.

CONCLUSION:

Quality of life is decreased in renal patients in the early stages of disease. No association was detected between the stages of the disease and the quality of life. It was possible to establish sociodemographic, clinical and laboratory risk factors for a worse quality of life in this population.     

Polycystin-1 expression in fetal, adult and autosomal dominant polycystic kidney

The mutation of the PKD1 gene causes autosomal dominant polycystic kidney disease (ADPKD), and the PKD1 gene encodes polycystin-1 (PC-1). PC-1 is thought to be a cell-cell/matrix adhesion receptor molecule at the cell surface that is widely expressed in the kidney. However, there are controversies about the role of PC-1 protein and its expression when using different antibodies to detect it. We used two PC-1 antibodies; C-20 (Santa Cruz, sc-10372) as the C-terminal antibody, and P-15 (Santa Cruz, sc-10307) as the N-terminal antibody. We evaluated the PC-1 expression by performing immunoblotting on the human embryonic kidney (HEK) 293 cells and the renal proximal tubular epithelial cell (RPTEC) lysates. We characterized the expression of PC-1 in the fetal, adult and polycystic kidneys tissues by performing immunohistochemistry. We confirmed the PC-1 expression in the HEK 293 cells and the RPTEC lysates, but the expression was very low. The PC-1 proteins were diffusely expressed in the tubular epithelial cells cytoplasm in the fetal and adult kidneys, and the PC-1 expression was more prominent in the proximal tubules of the fetal kidney. In the ADPKD kidney, the PC-1 proteins were heterogenously and weakly expressed in the tubular or cyst lining epithelial cells. Our data suggests that the development of the kidney may regulate the expression of PC-1, and an altered PC-1 expression may contribute to cyst formation in ADPKD.     

常染色体显性遗传多囊肾病发病相关信号转导通路的研究进展

<正>常染色体显性多囊肾病(autosomal dominantpolycystic kidney disease,ADPKD)是遗传性多囊肾疾病中最常见的一种,也是最常见的遗传性肾脏病,发病率约为1/1000-1/500。ADPKD的病程长、发展缓慢,一般在40岁以前常无症状,因此又称为成     

DNA flow cytometric analysis in renal neoplasms associated with acquired renal cystic disease

In order to better understand the potential malignancy of renal neoplasms arising in patients with acquired renal cystic disease and to try and establish differences from other renal tumours we analysed DNA ploidy as well as the level of S-phase fraction in 11 neoplasms associated with acquired cystic disease by means of flow cytometry. The results were correlated with known prognostic factors such as nuclear grade, size and stage, as well as the clinical behaviour of the tumours. We found a close relationship between DNA aneuploidy and high S-phase fraction and a poor clinical outcome. We also found some differences in the DNA ploidy profile of these tumours when compared with those reported in other renal neoplasms.     

Probing renal blood volume with magnetic resonance imaging

Damage to the kidney substantially reduces life expectancy. Renal tissue hypoperfusion and hypoxia are key elements in the pathophysiology of acute kidney injury and its progression to chronic kidney disease. In vivo assessment of renal haemodynamics and tissue oxygenation remains a challenge. Blood oxygenation level–dependent (BOLD) magnetic resonance imaging (MRI) is sensitive to changes in the effective transversal relaxation time (T₂*) in vivo, and is non‐invasive and indicative of renal tissue oxygenation. However, the renal T₂* to tissue pO₂ relationship is not governed exclusively by renal blood oxygenation, but is affected by physiological confounders with alterations in renal blood volume fraction (BVf) being of particular relevance. To decipher this interference probing renal BVf is essential for the pursuit of renal MR oximetry. Superparamagnetic iron oxide nanoparticle (USPIO) preparations can be used as MRI visible blood pool markers for detailing alterations in BVf. This review promotes the opportunities of MRI‐based assessment of renal BVf. Following an outline on the specifics of renal oxygenation and perfusion, changes in renal BVf upon interventions and their potential impact on renal T₂* are discussed. We also describe the basic principles of renal BVf assessment using ferumoxytol‐enhanced MRI in the equilibrium concentration regimen. We demonstrate that ferumoxytol does not alter control of renal haemodynamics and oxygenation. Preclinical applications of ferumoxytol enhanced renal MRI as well as considerations for its clinical implementation for examining renal BVf changes are provided alongside practical considerations. Finally, we explore the future directions of MRI‐based assessment of renal BVf.     

An autopsy case of chronic progressive external ophthalmoplegia with renal insufficiency

An autopsy of a 44-year-old Japanese woman with mitochondrial cytopathy confirmed the presence of chronic progressive external ophthalmoplegia (CPEO). Immunohistochemistry using antimitochondrial antibody was performed to observe the ultrastructure of the skeletal muscle and renal tissues. The patient was born of consanguineous parents, developed normally, and was of average intelligence. At 22 years of age, the patient noticed hearing loss, and subsequently, over time, developed a progressive generalized muscle weakness, which included limitation of eye movement and ptosis. At age 41, a muscle biopsy was performed using the modified Gomori trichrome method and demonstrated the presence of ragged red fibers. After the evaluation of her results in conjunction with her clinical course, she was diagnosed with CPEO. Renal insufficiency was discovered at age 30, and the patient died at the age of 44 of respiratory failure caused by respiratory muscle weakness and pneumonia. The autopsy revealed fiber size variation within the skeletal muscle, and an antimitochondrial antibody analysis demonstrated the accumulation of mitochondria between the bundles of myofibrils, as well as in subsarcolemmal locations. Ultrastructurally, abnormal mitochondria with disoriented cristae and paracrystalline inclusions were seen. Although no remarkable histological changes were noted in the kidneys, tubular epithelial cells exhibited accumulated abnormal mitochondria, similar to those seen in the skeletal muscle. Because mitochondrial diseases can affect other energy-dependent organs in addition to the skeletal muscle, immunohistochemical examina-tions employing an antimitochondrial antibody are useful for obtaining further ultrastructural observations that can assist in making a distinct diagnosis of this systemic disorder.