75例糖尿病合并蛋白尿患者的病因分析

分析糖尿病患者合并蛋白尿的原因，发生率及其与病程的关系。给临床提供有效的防治措施。方法对７５例糖尿病合并蛋白尿患者的清晨第１次中段尿测定尿蛋白的含量。并统计各种病因对蛋白尿发生的影响。结果７５例糖尿病患者合并蛋白尿的病因中以合并泌尿系感染者占首位，依次为糖尿病肾病，高血压，心功能不全，酮症，高渗昏迷和休克。     

2型糖尿病周围神经传导速度与病程及尿清蛋白的关系：附66例报告

目的：了解２例糖尿病病程及尿清蛋白（白蛋白）排泄率对周围神经传导速度的影响。方法：测定６６例２型糖尿病患者的周围神经传导速度,并就其与病程及尿蛋白排泄的关系进行分析。结果：在病程不到５年、５￣１０年和超过１０年的患者的右尺神经感觉电生理异常的发生率分别为７５％、８６％和９２％;右腓肠神经感觉电生理异常分别为７３％、７１％和９２％。而运动神经病变早期多不明显,仅在病程超过１０年的患者中,其神经传导速     

检测两种尿微量蛋白评估糖尿病早期肾损害

目的：通过尿液白蛋白（Ａｌｂ）和α１－微球蛋白（α１－ＭＧ）含量测定,以早期诊断糖尿病肾损害,方法：采用免疫速率散射比浊法,对３９例健康者,７３例糖尿病（ＤＭ）患者Ａｌｂ,α１－ＭＧ联合检测。结果：尿Ａｌｂ和α１－ＭＧ排泄水平均有明显增加（Ｐ〈０．０１）,尿α１－ＭＧ升高者占７５．３％,Ａｌｂ升高者占４５．２％,结论：尿α１－ＭＧ测定在早期发现糖尿病有更大的敏感性。     

糖尿病肾病的早期诊断与糖尿病病程及糖化血红蛋白、血糖的关系探讨

目的：探讨糖尿病肾病与糖尿病病程、糖化血红蛋白及血糖的关系。方法：测定246例常规尿蛋白阴性糖尿病患者的晨尿微量白蛋白／尿肌酐，以大于2．5mg/mmol，为诊断糖尿病肾病标准，并比较不同病程、糖化血红蛋白、血糖的糖尿病肾病检查结果。结果：共检出糖尿病肾病59例，病程＞15年者与病程＜5年者比较，糖尿病肾病检出率有显著性差异（P＜0．01）；糖化血红蛋白＞11％者与糖化血红蛋白＜6．5％者比较，糖尿病肾病的检出率有高度显著性差异（P＜0．01）；空腹血糖＞11．1mmol/L者与＜7．8mmol/L者比较，糖尿病肾病的检出率有显著性差异（P＜0．05）。结论：测定晨尿微量白蛋白／尿肌酐来诊断糖尿病肾病方法简单可靠。糖尿病病程长及血糖、糖化血红蛋白控制越差者，其糖尿病肾病发生率越高。     

Ⅱ型糖尿病微白蛋白尿与缺血性心脏病的临床研究

目的 对Ⅱ型糖尿病患者微白蛋白尿与缺血性心脏病的关系进行研究。方法 根据有无尿微白蛋白，将81例Ⅱ型糖尿病患者分为以下两组：①微白蛋白尿组；②无微白蛋白尿组。详细记录患者的临床资料及生化检验结果。结果 Ⅱ型糖尿病微白蛋白尿组的病程显著长于无微白蛋白尿组；空腹血糖、餐后2h血糖及合并IHD的发病率显著高于无微白蛋白尿组（P均＜0．05）。ECG活动平板运动负荷试验，Ⅱ型糖尿病微白蛋白尿组的运动时间、运动试验阳性显著低于无微白蛋白尿组；运动试验阳性率显著高于无微白蛋白尿组（P均＜0．05）。结论 Ⅱ型糖尿病患者出现微白蛋白尿者，其缺血性心脏病的发病率更高。     

手牵法治疗颈椎病220例

１对象与方法１．１对象２２０例均为中医骨伤科门诊及住院患者，男１３３例，女８７例，年龄２８～６５岁，平均４６．５岁，病程短者３d，长者８年。根据颈椎病分型主要分为神经根型８３例、椎动脉型７７例、落枕型（颈型）６０例。病因与职业：病因分慢性劳损８９例（占４０．５％），外感风寒湿邪６４例（占２９．１％），急性损伤３６例（占１６．４％），原因不明３１例（１４％），职业：工人４６例占（２０．９％），教师２３例（占１０．５％），机关文员８８例（占４０％），商人４４例（占２０％），其他１９例（占８．６％）。…     

20例非胰岛素依赖型糖尿病并高血压的动态血压分析

观察非胰岛素依赖型糖尿病并高血压患者动态血压的特点，方法：分析２０例ＮＩＤＤＭ伴高血压患者的动态血压。结果：７５％的患者２４小时收缩压及舒张压均〉１７．３／１０．６ｋＰａ（１３０／８０ｍｍＨｇ），８５％患者夜间平均血压下降率〈１０％，且夜间平均血压下降与糖尿病病程呈相关。     

2型糖尿病患者视网膜病变分期与肾脏损害的研究

目的：探讨2型糖尿病患者视网膜病变分期与糖尿病肾脏损害程度的关系。方法：对101例不同时期的2型糖尿病视网膜病变（DR）患者进行研究,按DR分期分为5组,对各组患者的糖尿病病程、24h尿蛋白定量、血清肌酐、肾小球滤过率（GFR）等资料进行分析。结果：各组间糖尿病病程、血清肌酐水平比较差异无统计学意义,24h尿蛋白定量随DR分期的严重而依次升高,组间比较差异有统计学意义（P〈0．05）,DRⅢ期患者GFR低于0期患者,Ⅳ期患者GFR明显低于Ⅰ、Ⅱ期患者,GHbA1c水平Ⅱ、Ⅳ期相对较高。随着DR分期的增加,GHbA1c有所升高,反映肾损害的指标如24h蛋白尿定量呈现增高趋势、肾小球滤过率呈现下降趋势。结论：随着DR的进展,肾损害程度加重。临床上应该积极地对合并DR的2型糖尿病患者进行蛋白尿的筛查;同样,对进入临床蛋白尿期的2型糖尿病患者也需常规行眼底检查以尽早发现病变尽早治疗,提高生存质量。     

尿微量蛋白检查对糖尿病早期肾损伤的诊断价值

目的：观察糖尿病患者尿液检查对糖尿病早期肾损伤的诊断价值及其监控作用。方法：用速率散射比浊法检测分析102例不同病程糖尿病患者及50名健康对照者尿蛋白定性及尿徽量蛋白[微量白蛋白(MA)、α1-微球蛋白(α1-M)、β2-微球蛋白(β2-M)、转铁蛋白(TRF)和免疫球蛋白(IgG)]，对检测结果进行统计、分析。结果：糖尿病组尿蛋白定性及尿微量蛋白测定结果均明显高于健康对照组，其差异有统计学意义；糖尿病组中，尿蛋白定性阳性率只有22．5％，尿MA、α1-M、β2-M、TRF和IgG阳性率分别为54．9％、63．7％、27．3％、59．1％和22．7％；尿MA和尿α1-M联合检测总阳性率为75．5％；尿蛋白定性和尿MA、尿α1-M联合检测时，102例糖尿病者尿蛋白定性阴性者中有51％MA或尿α1-M阳性；糖尿病者随病程增加尿蛋白定性、尿MA和尿α1-M阳性检出率不断增高，尿MA和尿α1-M水平不断升高。结论：尿蛋白定性阴性不能除外糖尿病早期肾损伤；尿微量蛋白联合检测对早期发现糖尿病肾损伤有重要意义。     

肾移植术后蛋白尿病因及转归的临床研究

目的:研究肾移植术后蛋白尿形成的主要原因及转归.方法:对105例肾移植术后蛋白尿患者进行回顾分析,研究其形成病因及其与转归的关系.结果:在105例肾移植尿蛋白患者中,由于排斥反应引起的占55.2％,由新发或复发性肾病引起的占34.3％,其余高血压、CNI肾毒性等原因的占10.5％.术后排斥反应和新发或复发性肾病导致肾移植术后蛋白尿总治愈率分别为93.10％和91.67％,两组比较差异无统计学意义(P＞0.05).与由高血压等其他原因所致蛋白尿患者比较,差异均有统计学意义(P＜0.05).结论:导致肾移植术后蛋白尿的主要原因是排斥反应和新发或复发性肾病,应根据移植肾穿刺后病理学诊断,及早进行相应临床治疗,以免造成不可逆性移植肾损伤.     

弹性酶与脂必妥对糖尿病高脂血症及微量蛋白尿的疗效观察

目的：探讨弹性酶与脂必妥对糖尿病高脂血症及对早期糖尿病肾病的疗效。方法：８４例非胰岛素依赖型糖尿病患者随机分为弹性酶组和脂必妥组,比较２种药物对糖尿病高脂血症及微量蛋白尿的治疗效果。结果：总胆固醇（ＴＣ）、甘油三酯（ＴＧ）、高密度脂蛋白胆固醇（ＨＤＬＣ）在弹性酶组治疗６周末分别下降了１０％、１９％和上升了８％（Ｐ均＜０．０１）;脂必妥组６周末分别下降了１１％、１６％和上升了７％（Ｐ均＜０．０１）。尿蛋白排泄率在脂必妥组平均上升了２．４％（Ｐ＞０．０５）,弹性酶组平均下降了２５．７％（Ｐ＜０．０１）。结论：弹性酶与脂必妥对糖尿病高脂血症均有非常显著的疗效,而对尿蛋白排泄率（ＵＡＥＲ）的影响弹性酶优于脂必妥。     

膀胱残余尿量水平监测及2型糖尿病患者排尿习惯的临床分析

目的探讨2型糖尿病患者临床排尿习惯的改变及超声表现。方法观察154名糖尿病患者排尿次数（次／d）、排尿时间（s）、每次尿量（ml）B超残余尿量（ml）及膀胱壁厚度（mm）。并观察随膀胱残余尿量的改变尿培养阳性率和肾功能异常发生率的改变。结果随着糖尿病病程的延长患者排尿习惯出现改变，膀胱残余尿量及膀胱壁厚度增加。同时膀胱残余尿量增加的患者更易合并尿路感染，肾功能异常发生率更高。结论神经原性膀胱诊断应结合临床。超声检查能清晰显示膀胱壁厚度、测量膀胱内残余尿量，有明确的临床诊断价值。     

The light diffusion technique for estimation of the size of urine particles in patients with type 2 diabetes mellitus in the Tamm-Horsfall protein precipitation

Tamm-Horsfall uroprotein accounts for more than 50% of the urinary proteins in healthy individuals. In abnormalities, it creates a favorable background for detecting smaller-sized uroproteins and for diagnosing pathological processes from the results of native urine tests. In this connection, there is a need for precipitating Tamm-Horsfall glycoprotein while applying laser correlation spectroscopy to analyze the size of urine particles in patients with type 2 diabetes mellitus. Eighty patients with this condition concurrent with different stages of diabetic nephropathy and 23 apparently healthy individuals were examined. The findings suggest that the subfraction urine composition before and after Tamm-Horsfall protein precipitation is different in apparently healthy individuals and patients with type 2 diabetes mellitus concurrent with diabetic nephropathy. This is most likely to be due to the change in the qualitative composition of protein as renal lesion progresses, to the specific features of protein excretion at different stages of a pathological process, and to different concentrations of other low and high molecular-weight proteins.     

Etiology and prognostic significance of albuminuria in diabetes

Persistent clinical proteinuria (i.e., urinary protein excretion greater than 0.5 g/24 h) is an ominous development in a person with diabetes. It eventually leads to a decline in the glomerular filtration rate and ultimately to end-stage renal failure or premature cardiovascular mortality. Progression of renal disease appears to be related to arterial blood pressure and protein intake and is primarily independent of the metabolic state. More sensitive immunoassays for detecting low concentrations of albumin in urine have led to recognition of subclinical increases in albumin excretion rates in nonclinically proteinuric diabetic patients, a phenomenon named microalbuminuria. Studies have shown that patients with microalbuminuria have a significantly increased risk for clinical proteinuria and cardiovascular mortality. Microalbuminuria is rarely found during the first 5 yr of a patient's diabetes, suggesting that it is a sign of early glomerular damage rather than a marker for susceptibility to it. In patients with non-insulin-dependent diabetes mellitus (NIDDM), an association has been found between microalbuminuria and coronary heart disease, but this relationship needs further investigation. In patients with insulin-dependent diabetes mellitus (IDDM), this subclinical form of proteinuria is associated with poor metabolic control and, more important, with marginal elevation of blood pressure. Correction of hyperglycemia by intensified insulin treatment might arrest progression to persistent clinical proteinuria; moreover, restricted protein intake and lowering of blood pressure have been shown to reduce the albumin excretion rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Characterization of diabetic nephropathy by urinary proteomic analysis: identification of a processed ubiquitin form as a differentially excreted protein in diabetic nephropathy patients

BACKGROUND: Identification of markers for prediction of the clinical course of diabetic nephropathy remains a major challenge in disease management. We established a proteomics approach for identification of diabetic nephropathy-related biomarkers in urine. METHODS: We used SELDI-TOF mass spectrometry and SAX2 protein arrays to compare protein profiles from urine of 4 defined patient groups. Samples from patients with type 2 diabetes (DM; n = 45) without nephropathy and without microalbuminuria (DM-WNP), patients with DM with macro- or microalbuminuria (DM-NP; n = 38), patients with proteinuria due to nondiabetic renal disease (n = 34), and healthy controls (n = 45) were analyzed. Anionic exchange, reversed-phase fractionation, gel electrophoresis, and mass spectrometry were used to isolate and identify proteins with high discriminatory power. RESULTS: A protein with m/z 6188 (P <0.0000004) was strongly released in the urine of healthy controls, patients with proteinuria due to nondiabetic disease, and DM-WNP in contrast to DM-NP patients. An m/z 14 766 protein (P <0.00008) was selectively excreted in the urine of DM-NP patients, whereas the protein with m/z 11 774 (P <0.000004) was significantly excreted by patients with proteinuria and DM-NP. The m/z 11 774 and m/z 14 766 mass peaks were identified as beta(2)-microglobulin and UbA52, a ubiquitin ribosomal fusion protein, respectively. The protein with m/z 6188 was identified as a processed form of ubiquitin. CONCLUSION: The release of high amounts of UbA52 in urine of DM-NP patients could serve as a diagnostic marker, whereas the lack of the short form of ubiquitin raises interesting questions about the pathophysiology.     

Determination of urinary lysozyme for potential detection of tubular dysfunction in diabetic nephropathy

Seeking to study whether measurement of lysozyme (EC 3.2.1.17) in urine by a reliable radioimmunoassay can provide a suitable index of renal tubular function and how lysozymuria develops in temporal relation to proteinuria in diabetic nephropathy, we have compared the urinary excretion of lysozyme and beta 2-microglobulin with the 15-min excretion rate of phenolsulfonphthalein in 39 patients with Type 2 (non-insulin-dependent) diabetes and investigated the temporal relation between the onset of lysozymuria and proteinuria in 15 patients with Type 1 (insulin-dependent) diabetes. The concentrations of lysozyme and beta 2-microglobulin in urine increased in proportion to the decrease in the rate of excretion of phenolsulfonphthalein in these patients. The coefficient of correlation between lysozyme concentration and the 15-min excretion rate of phenolsulfonphthalein (r = -0.70) was higher than that between beta 2-microglobulin concentration and the 15-min excretion rate of phenolsulfonphthalein (r = -0.46). Abnormally high lysozymuria, suggesting the existence of tubular dysfunction, was demonstrated in six of the patients with Type 1 diabetes who showed no proteinuria or only a slight increase in urinary protein excretion. Lysozymuria may thus be added to a list of the indicators for diabetic nephropathy.     

Clinical features and health-care costs of diabetic nephropathy

The nephropathy complicating insulin-dependent diabetes mellitus (IDDM) has been well studied, but that complicating non-insulin-dependent diabetes mellitus (NIDDM) is less well defined. In patients with IDDM, the glomerular filtration rate is often increased early in the course of the disease, approaches normal with insulin therapy, but tends to remain slightly elevated throughout the ensuing 10-15 yr of insulin dependency. After the onset of overt azotemia, end-stage renal disease (ESRD) develops in approximately 5 yrs. Proteinuria may be intermittently positive in the earliest stages of diabetes, evolving into intermittent and then persistent microalbuminuria, which in turn blossoms into macroalbuminuria. Because 40-50% of IDDM patients develop proteinuria and two-thirds of this subpopulation develop ESRD, some 20-30% of any given cohort of IDDM patients eventually need dialysis or transplantation. Evidence indicates that diabetic nephropathy is associated with a greater incidence of eye, nerve, heart, and peripheral vascular disease. Nondiabetic renal disease complicating IDDM and NIDDM is associated with a lesser frequency and severity of these extrarenal manifestations. The prevalence of retinopathy increases with advancing nephropathy. Roughly two-thirds of the deaths from IDDM are related to renal failure, and most of the remainder are caused by associated cardiovascular disease. Transplantation from living relatives carries the best prognosis for survival, and little difference is seen between hemodialysis, peritoneal dialysis, and cadaver transplantation. The health-care costs of treating diabetic nephropathy are also reviewed.     

多项尿蛋白检测对早期糖尿病肾病诊断价值的研究

目的探讨糖尿病患者尿清蛋白（Alb）、β2微球蛋白（β2-m）、Tamm-Horsfall蛋白（T-H蛋白）、α1微球蛋白（α1-m）及视黄醇结合蛋白（RBP）的变化对早期糖尿病肾病的诊断价值。方法对103例糖尿病患者和40例健康人的尿标本采用放射免疫法检测Alb、β2-m、T-H蛋白和α1-m的水平，使用酶联免疫吸附试验检测RBP的含量。结果糖尿病患者尿Alb、β2-m、α1-m及RBP显著高于健康人（P〈0．01），而T-H蛋白则明显低于健康人（P〈0．05），尿RBP水平与尿Alb含量呈显著正相关（r=＋0．47，P〈0．05）。随着肾脏病变的进展而引起各项尿蛋白指标的异常改变更趋于显著。结论检测糖尿病患者尿Alb、β2-m、T-H蛋白、α1-m及RBP有助于早期诊断肾脏病变的部位及病变程度。     

Heterogeneity of causes of proteinuria in patients with non-insulin dependent diabetes mellitus

AIM: To make a retrospective clinicomorphological (autopsy) study of proteinuria causes. MATERIAL AND METHODS: The records have been analysed for 231 patients with non-insulin-dependent diabetes mellitus (NIDDM) over 60 years of age who died in a general hospital between 1990 and 1999. The choice of patients with diabetic nephropathy (DN) for a further morphological investigation was based on the presence of proteinuria (> 0.5 g/day), normal renal function. 72 patients met the above criteria. Of them 26 were women. RESULTS: Proteinuria occurred more frequently in men (63.4%). A morphological examination of the kidneys revealed diabetic glomerulosclerosis (diffuse and focal) in 48(67%) patients. In 24(33%) patients proteinuria resulted from non-diabetic affection of the kidneys: amyloidosis, atherosclerotic and/or hypertensive nephroangiosclerosis, membraneous and myelomic nephropathy, mesangioproliferative glomerulonephritis. Glomerular changes were not registered in 4 patients. 35(72%) DN patients had diabetic retinopathy which was not found in patients with non-diabetic renal affection. CONCLUSION: Diabetic retinopathy in patients with NIDDM and proteinuria allows to conclude that the latter is consequent to DN. The absence of diabetic retinopathy in such patients promotes a search for other causes of proteinuria.     

Stress tolerance test and SDS-PAGE for the analysis of urinary proteins in children and youths.

Excretion of urinary proteins (UP) is an important marker for the evaluation of patients with progressive renal disease. In order to analyze quantitative and qualitative variability of UP in relation to physical activity, we used standardized stress tolerance test and SDS-PAGE. Five urine samples were obtained from each patient at rest, during ordinary daily activity and after physical stress. Determination of total proteins was performed using Meulman's classic method with sulfosalicylic acid. UP were separated by ultrathin horizontal gradient SDS-PAGE according to G?rg. There were 142 patients; 40 with poststreptococcal glomerulonephritis (PSGN), 11 with diabetes mellitus, 16 with chronic pyelonephritis and 75 who attended for investigation of asymptomatic proteinuria. Functional proteinuria was established in 42 subjects, who displayed maximal UP excretion during stress and the presence of apolipoprotein AI on SDS-PAGE. Children with PSGN showed no significant increase of UP during stress. Some children with diabetes mellitus (27%) and chronic pyelonephritis (47%) displayed microproteinuria or overt proteinuria after stress. Quantitative and qualitative changes in total UP excretion can be detected by stress tolerance test and SDS-PAGE. It remains to be seen whether stress tolerance test can identify children and youths who are at higher risk for disease progression.