糖尿病肾病患者血清肝细胞生长因子水平变化分析

目的 探讨肝细胞生长因子(HGF)在糖尿病肾病发生发展中的作用.方法 测定正常人、糖尿病组(单纯糖尿病组、微量白蛋白尿组、蛋白尿肾功能正常组、终末期肾功能衰竭组)共150例研究对象的血清HGF水平,并分析其与尿微量白蛋白等指标的关系.结果 糖尿病组血清HGF水平明显比正常对照组高(P＜0.05).糖尿病组中,微量白蛋白尿组和蛋白尿肾功能正常组两个亚组血清HGF水平明显比单纯糖尿病组高(P＜0.05),终末期肾功能衰竭组血清HGF水平明显比单纯糖尿病组高(P＜0.05),但低于微量白蛋白尿和蛋白尿肾功能正常组(P＜0.05).在出现终末期肾功能衰竭前HGF与尿微量白蛋白正相关(F=6.29、P＜0.05).结论 糖尿病患者随着肾损害的出现其HGF水平亦逐渐增高,但进入终末期肾功能衰竭后HGF水平明显降低.HGF与糖尿病肾病发生发展有关.     

血清胱抑素C测定对早期糖尿病肾病的诊断价值

目的观察血清胱抑素C测定对早期糖尿病肾病的诊断价值。方法对2015年1月—2016年6月该院189例糖尿病患者血清胱抑素C及尿微量蛋白进行检测,尿微量白蛋白0~30 mg/L为正常,Cys-C 0.55~1.05 mg/L为正常范围。超过此正常范围即为异常。结果 189例患者尿微量白蛋白值为(32.5±5.8)mg/L,阳性检出率为24.3%(46/189),血清胱抑素C测定值为(1.35±0.65)mg/L,阳性检出率为41.2%(78/189),血清胱抑素C测定阳性检出率高于尿微量白蛋白测定阳性检出率,P0.05。结论血清胱抑素C测定是诊断糖尿病肾病的灵敏指标,可以及早监测糖尿病肾病,尽早干预,改善预后。     

高铁蛋白血症与糖尿病肾病的关系

对６２例糖尿病患者和２０例正常对照者检测血尿铁蛋白，血清β２微球蛋白（β２－ＭＧ）及尿Ｔａｍｍ－Ｈｏｒｓｆａｌｌ糖蛋白（ＴＨＰ），白蛋白，发现糖尿病高铁蛋白血症患者的β２－ＭＧ较血清铁蛋白正常者明显升高，而尿ＴＨＰ排泄明显减少，其肾病的发生率增高，此提示高铁蛋白血症与糖尿病肾病有关。     

血清CRP与2型糖尿病肾病的关系

根据尿白蛋白排泄率(UAER)将糖尿病患者分为正常蛋白尿组、微量白蛋白尿组和临床蛋白尿组，并设立对照组。采用免疫透射比浊法测定血清CRP浓度。结果：血清CRP浓度在糖尿病各组均较对照组明显升高，并且随着UAER的增加而增高。结论：血清CRP与2型糖尿病及糖尿病。肾病的程度有一定的相关性。     

血清CRP与2型糖尿病肾病的关系

根据尿白蛋白排泄率(UAER)将糖尿病患者分为正常蛋白尿组、微量白蛋白尿组和临床蛋白尿组,并设立对照组.采用免疫透射比浊法测定血清CRP浓度.结果血清CRP浓度在糖尿病各组均较对照组明显升高,并且随着UAER的增加而增高.结论血清CRP与2型糖尿病及糖尿病肾病的程度有一定的相关性.     

2型糖尿病患者急性时相蛋白与糖尿病肾病的关系

目的 探讨糖尿病肾病不同时期血清急性时相蛋白浓度的变化及其意义。方法 正常对照组30例和2型糖尿病组100例进入本研究，根据尿白蛋白排泄率(UAER)将糖尿病患者分为正常蛋白尿组(39例)、微量白蛋白尿组(30例)和临床蛋白尿组(31例)。采用数率散射比浊法测定血清C反应蛋白、α1-酸性糖蛋白(α1-AAG)、铜蓝蛋白(cER)浓度，用快速比色法测定唾液酸(SA)。结果 (1)2型糖尿病患者血清急性时相蛋白浓度较对照组明显升高。(2)急性时相蛋白浓度随UAER的增加而增加。(3)多元逐步回归分析表明部分急性时相蛋白(α1-AAG，CER，SA)与甘油三酯及胆固醇相关。结论 2型糖尿病患者中存在急性时相反应，而且急性时相反应的强度与糖尿病肾病的程序存存一致性。     

缺血修饰性白蛋白指数与2型糖尿病合并早期肾病的关系

目的探讨血清缺血修饰性白蛋白(IMA)水平与2型糖尿病(T2DM)合并早期肾病(EDN)的关系。方法测定94例T2DM患者和32例健康者的空腹血糖(FPG)、糖化血红蛋白(HbA1c)、血清白蛋白及尿微量白蛋白,应用白蛋白-钴结合(ACB)法测定受试者的血清缺血修饰白蛋白(IMA)水平,计算IMA指数、尿微量白蛋白排泄率(UMAER)及体重指数(BMI),并依据UMAER将T2DM患者分为单纯糖尿病组(SDM组)及合并早期肾病组(EDN组)。结果 T2DM患者BMI、血清IMA、IMA指数均明显高于对照组,而EDN组患者的BMI、IMA、IMA指数均高于SDM组患者;单因素简单相关显示,IMA与BMI、UMAER呈显著正相关(r=0.256、0.408,均P<0.01),而IMA指数仅与UMAER呈显著正相关(r=0.463,P<0.01)。结论 IMA增高,尤其是IMA指数增高与T2DM早期肾病的发病有关,其机制可能是通过肾小管内皮损伤所致的氧化应激所致。     

2型糖尿病患者血清护骨素水平与糖尿病肾病的关系

目的 2型糖尿病(T2DM)患者血清护骨素水平与糖尿病肾病(DN)的关系.方法 110例T2DM患者根据尿白蛋白排泄率(UAER)分为正常白蛋白尿组 38例、微量白蛋白尿组 36例及大量白蛋白尿组 36例,同时选择年龄、性别相匹配的40例健康者为对照组.血清护骨素采用ELISA法测定.结果 在T2DM各组中,大量白蛋白尿组患者的血清护骨素水平[(4.45±0.76)ng/L]显著高于微量白蛋白尿组[(3.62±0.70)ng/L]、正常白蛋白尿组[(2.77±0.78)mg/L]和对照组[(2.29±0.37)ng/L](均P＜0.01);微量白蛋白尿组患者的血清护骨素水平高于正常白蛋白尿组.血清护骨素水平与空腹血糖(FPG)、糖化血红蛋白(HbA1c)、超敏C反应蛋白(hs-CRP)及UAER呈明显正相关.血清护骨素水平是DN的重要影响因素.结论 DN患者血清护骨素水平明显升高,护骨素可能在DN的发生中起一定作用.     

不同尿白蛋白水平的糖尿病患者单核细胞趋化蛋白-1和尿N-乙酰β-D-氨基葡萄糖苷酶的含量变化及其临床意义

目的观察不同尿白蛋白水平的糖尿病患者单核细胞趋化蛋白1(MCP1)和尿N乙酰βD氨基葡萄糖苷酶(NAG)的含量变化及其临床意义。方法将60例糖尿病患者按尿白蛋白排泄率(UAER)的不同分为正常白蛋白尿组、微量白蛋白尿组和大量白蛋白尿组3组。分别测定血清和尿MCP1的含量、尿NAG含量以及血肌酐(Scr)、糖化血红蛋白(GHbAlc),进行组间比较,并与对照组比较,同时做尿MCP1与GHbAlc、UAER、NAG的相关分析。结果尿MCP1含量及NAG含量在所有患者中均升高,明显高于对照组,且大量白蛋白尿组升高最明显,其升高程度与尿白蛋白排泄率增高程度一致,即随糖尿病肾病加重而逐渐升高。而血清MCP1水平较低,与对照组比较无显著性差异;尿MCP1与GHbAlc、UAER、NAG呈正相关关系。结论尿中MCP1升高与糖尿病肾病的发生发展有密切关系,尤其与肾小管间质损伤有更密切的关系。     

血清尿酸与2型糖尿病及糖尿病肾病关系研究

目的探讨血清尿酸与2型糖尿病及血清尿酸与糖尿病肾病的关系。方法选择该院收治的56例2型糖尿病患者作为研究对象,将其作为病例组,选择同期在该院进行体检的100名健康志愿者,将其作为对照组。测定两组血清尿酸及其他代谢指标,比较其差别分析血清尿酸水平与2型糖尿病关系;同时将病例组根据24 h尿微量白蛋白排泄率分为3组:正常尿蛋白组,微量白蛋白组及临床白蛋白组,以正常尿蛋白组作为对照组,分别测定各组的血清尿酸水平及其他代谢指标,分析在糖尿病肾病发展中不同阶段的变化水平。结果病例组血清尿酸水平较健康对照组高,但差异无统计学意义(P0.05),高尿酸血症发生率糖尿病组明显高于对照组(P0.01),代谢综合征发生率糖尿病组也明显高于对照组(P0.001);临床白蛋白组的血尿酸平均水平明显高于正常尿蛋白组(P0.05),微量白蛋白组的血尿酸平均水平明显高于正常尿蛋白组(P0.001);在临床蛋白尿组与微量白蛋白组中,血清尿酸水平差异无统计学意义(P0.05)。结论血尿酸升高在2型糖尿病及慢性糖尿病肾脏病发生和发展中可能起到一定作用,为以后进一步的研究提供依据。     

糖尿病肾病重度浮肿患者短时低效每日透析的疗效分析

目的:研究短时低效每日血液透析(STSLEDD)在糖尿病肾病(DN)重度浮肿患者的临床应用情况,为改善糖尿病患者的临床症状提供一个新方法。方法:选择DN伴重度浮肿患者31例,随即分为两组(A、B)。A组采用STSLEDD加DN常规药物治疗;B组单纯DN常规药物治疗。A组每日行血液透析9h,连续3~5d,同时观察两组患者尿蛋白、血浆蛋白、肾功能、浮肿等变化情况。结果:A、B两组治疗后尿蛋白减少、血浆蛋白上升、肾功能均得到不同程度的改善。A组所有患者浮肿均完全消退。A组较B组临床症状改善更明显(P<0.05)。结论:STSLEDD对DN合并重度浮肿患者有明显疗效。     

IgA肾病血尿误诊为尿路感染血尿三例分析

目的 探讨IgA肾病的病理特点,提高诊断合格率.方法 回顾性分析3例有血尿症状的IgA肾病患者被误诊为尿路感染血尿的经过和原因.结果 3例患者均为系膜增生性IgA肾病患者,HaasⅠ级2例、HaasⅡ级1例,均于发病前出现过尿路感染,确诊后均已治愈.结论 IgA肾病的复杂性和隐匿性使其易被误诊,临床诊断要全面掌握IgA肾病的临床与病理特点,不能局限于表面症状的诊断.     

端粒缺陷相关蛋白在IgA肾病中的表达研究

目的 观察IgA肾病患者血液、尿液中4种端粒缺陷相关蛋白CRAMP、stathmin、EF-1α和chitinase表达变化,评估其对IgA肾病肾损伤程度的预测价值。方法 以浙江省人民医院肾内科收治的177例IgA肾病患者为研究对象,同时选取83名健康对照者作为对照,其中IgA肾病患者根据肾穿刺活检病理分期分为IgANⅠ~Ⅱ组和IgAN Ⅲ~Ⅴ组。收集纳入者血浆及尿液标本,采用酶联免疫吸附法(ELISA)及Chitinase分析试剂盒检测CRAMP,EF-1α和stathmin浓度及chitinase酶活性。结果 (1)IgAN组血浆中CRAMP浓度及chitinase酶活性较对照组增高,且IgAN Ⅲ~Ⅴ组升高更为明显。联合CRAMP及chitinase对于区分IgA肾病和健康对照具有较高的灵敏度(88.2%)及特异度(92.5%)。(2)IgAN组尿液中CRAMP浓度及chitinase酶活性较对照组增高,IgAN Ⅲ+组chitinase酶活性升高更为明显。联合CRAMP及chitinase对于区分IgA肾病和健康对照具有较高的灵敏度(74.3%)及特异度(84.2%)。结论 端粒缺陷相关蛋白CRAMP及chitinase在IgA肾病表达增加,且二者对IgA肾病肾损伤程度具有较高的预测价值。     

IgA Nephropathy with Minimal Change Disease

Background and objectives

Patients with IgA nephropathy typically present with hematuria and subnephrotic proteinuria. Nephrotic syndrome is uncommon in IgA nephropathy, and when present, it is usually associated with severe histologic features, such as endocapillary proliferation, segmental sclerosis, and crescent formation. Rarely, patients with IgA nephropathy present with nephrotic syndrome and only mild mesangial disease. This study sought to better characterize these patients.

Design, setting, participants, & measurements

A retrospective review of cases of IgA nephropathy diagnosed from 2004 to 2011 identified patients with nephrotic range proteinuria and histologically mild IgA nephropathy. Specifically, using the Oxford Classification of IgA Nephropathy, we identified cases that lacked endocapillary proliferation or segmental sclerosis.

Results

The cohort consisted of 17 patients, including 10 men and 15 adults. The median serum creatinine was 0.9 mg/dl (range=0.7–3.1), median 24-hour urine protein was 8.0 g/d (3.0–18.0 g), and 14 patients were fully nephrotic, whereas the remaining 3 patients fulfilled two of three criteria for nephrotic syndrome. Biopsies revealed IgA-dominant or codominant deposits accompanied by mesangial proliferation in 14 patients (82.4%). Electron microscopy showed mesangial deposits and extensive foot process effacement (median=90%). Initial treatment consisted of corticosteroids, although many patients required additional agents to maintain remission status. Over a median follow-up of 20 months (2.2–82 months), 14 patients experienced a complete response, and 3 patients showed a partial response, with a median response time of 2 months (0.5–27 months). At least one relapse of nephrotic syndrome occurred in nine patients (53%). All patients exhibited stable or improved renal function over the follow-up period.

Conclusions

The findings in this cohort and previous studies suggest that rare cases of mild IgA nephropathy with nephrotic range proteinuria exhibit a clinical presentation, biopsy findings, treatment response, and outcome more typical of IgA nephropathy with superimposed minimal change disease. This study favors the view that such cases represent a dual glomerulopathy.     

Effects of Eicosapentaenoic Acid Supplementation on Immunoglobulin A Nephropathy

Eicosapentaenoic acid (EPA), which is purified from fish oil, attenuates inflammatory responses by decreasing eicosanoid and cytokine production. EPA reportedly improves renal survival in patients with immunoglobulin (Ig)A nephropathy; however, this is unconfirmed. We studied the effects of EPA on IgA nephropathy patients. Eighteen biopsy-confirmed IgA nephropathy patients (aged 31 ± 3 years) were enrolled. The prognoses based on glomerular findings were good (N = 5), relatively poor (N = 12), and poor (N = 1). EPA was administered at 1.8 g/day for 12 months. Five biopsy-confirmed IgA nephropathy patients were enrolled as control subjects. Administration of other drugs used to treat IgA nephropathy was not changed. The estimated creatinine clearance (eCCr), serum creatinine (Cr) concentration, urinary protein creatinine ratio (U/P), and other clinical parameters were checked. In the EPA group, the Cr went from 0.8 ± 0.2 mg/dL to 0.7 ± 0.2 mg/dL after 12 months of EPA treatment, and the U/P went from 550 ± 580 mg/g Cr to 330 ± 920 mg/g Cr. The values did not differ significantly; however, Cr and U/P tended to improve, with no adverse effects from the EPA. The eCCr improved significantly (99 ± 7–110 ± 8 mL/min, P = 0.001) in the EPA group, but not in the control group (126 ± 12–120 ± 13, P > 0.05). The effect of EPA in patients with IgA nephropathy is not pronounced, but these results suggest that EPA is a safe and worthwhile supplement to the drugs used to treat this disease.     

肾上腺髓质素与糖尿病肾病肾小管间质病变的关系研究

目的研究肾上腺髓质素(ADM)水平的变化对糖尿病肾病(DN)肾小管间质病变的关系。方法将42例糖尿病患者分为单纯糖尿病组(A组)、早期糖尿病肾病(DN)组(B组)、临床期DN组(C组),另选11例健康志愿者为D组。检测其ADM、内皮素-1(ET-1)水平,分析其与肾小管间质损伤标志物尿α1-MG、β1-MG水平的相关性。结果 4组研究对象血浆ADM及ET-1水平比较,差异均有统计学意义(P<0.05);血浆ADM与肾小管间质损伤标志物血、尿α1-MG,尿β1-MG水平呈正相关(均P<0.05)。结论 DN早期的肾脏血流动力学紊乱,ADM在肾小管间质病变的发展中可能起着重要的作用。     

血清IgA—纤维连接蛋白聚合物在IgA肾病诊断中的意义

为探讨血清ＩｇＡ－纤维连接蛋白（ＦＮ）聚合物在ＩｇＡ肾病中的辅助诊断价值，对９１例ＩｇＡ肾病、１４例过敏性紫癜性肾炎、１１７例非ＩｇＡ肾脏病、２４例非肾脏病及２３４例健康人采用ＥＬＩＳＡ方法检测了血清中ＩｇＡ－ＦＮ聚合物水平。结果显示，ＩｇＡ肾病血清该聚合物水平及阳性率（６１．５％）显著高于狼疮性肾炎（３０．８％）、其他非ＩｇＡ肾脏病（８．８％）、非肾脏病（０．０％）及健康人群（５．１％）（Ｐ＜０．０５），但与过敏性紫癜性肾炎组（４２．９％）差异无显著性（Ｐ＞０．０５）。提示该聚合物对ＩｇＡ肾病具有一定的辅助诊断价值。但因在过敏性紫癜性肾炎及狼疮性肾炎时也有较高的阳性率，应注意鉴别。     

Time Dependency of IgA Nephropathy Induction in Alcohol Ingestion

We investigated the influence of the alcohol ingestion period on the incidence of IgA nephropathy in an animal model. A group of 41 rats received a continuous infusion of liquid diet and alcohol: "alcoholics." A further group of 41 control rats received an isocaloric diet in which the alcohol was replaced by glucose. IgA nephropathy was diagnosed by the presence of intense IgA deposition in the mesangium. At 6 weeks, 60% of the alcoholic rats had IgA nephropathy. The incidence increased until 100% of the alcoholic rats presented the renal disease at 16 weeks. IgA nephropathy was not found in any of the control animals. We conclude that, in this animal model, the incidence of IgA nephropathy is dependent on the time frame of the alcohol ingestion.     

Mechanisms of the impaired diuretic and natriuretic responses to a sustained and moderate saline infusion in rats with experimental cirrhosis

Kidney function and tubular handling of water and sodium by superficial nephrons, packed cell volume, total plasma proteins and albumin distribution space were studied in control and cirrhotic rats before and after a moderate and sustained saline infusion (3% body weight per 30 min + reposition of urinary losses). Tubular fluid samples were obtained from late proximal, early distal and late distal convolutions of superficial nephrons using micropuncture. Protein distribution was assessed by intravenous injection of 0.5 muCi of (125I)-albumin. In basal conditions, both groups of rats showed similar glomerular filtration rate and renal plasma flow, but cirrhotic animals had lower sodium excretion (fractional excretion of sodium = 0.04 +/- 0.01% vs. 0.22 +/- 0.02%, p less than 0.05) and urinary volume (4.31 +/- 0.41 vs. 7.57 +/- 0.53 microliter per min; p less than 0.05). After saline infusion, total plasma proteins decreased more in cirrhotic than in control rats (-18.5 +/- 2.7 vs. -12.9 +/- 2.2%, p less than 0.05). The opposite was observed for albumin distribution space (34.5 +/- 6.1 vs. 22.1 +/- 3.5%, p less than 0.05). Fractional sodium excretion increased to 2.98 +/- 0.15% in control rats but only to 0.61 +/- 0.080% in cirrhotic rats. The ratio single nephron glomerular filtration rate/glomerular filtration rate increased from 19.6 +/- 0.7 to 21.2 +/- 1.0 (X10(-6), p less than 0.005) in control animals but did not change in cirrhotic rats. These animals were unable to decrease adequately fractional fluid reabsorption in the proximal tubule and the loop of Henle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased expression of proliferating cell nuclear antigen mRNA in peripheral blood mononuclear cells from patients with IgA nephropathy.

Proliferating cell nuclear antigen (PCNA)/cyclin is an intranuclear polypeptide antigen whose appearance correlates with the proliferative state of cells. The authors investigated the expression of PCNA from peripheral blood mononuclear cells (PBMC) in 23 patients with IgA nephropathy and 10 healthy age-matched controls, using ribonucleic acid hybridization techniques. The majority of patients with IgA nephropathy (22 of 23 patients) showed elevated PCNA expression in PBMC, while no PCNA expression was detected in PBMC of normal controls. A positive correlation was noted between PCNA expression of PBMC and glomerular injuries and PCNA expression and urinary protein excretion. Sixty-three percent of patients with grade III and IV histological findings showed strong PCNA (more than ) expression in their PBMC. The urinary protein excretion in patients who showed more than ( ) PCNA expression was more than 2.5 g/d, while that in patients with less than (+) PCNA expression was less than 1.0 g/day. These findings indicate that abnormally regulated PCNA expression in PBMC may play an important role in the progression of IgA nephropathy, and that PCNA expression in PBMC may be a useful indicator of disease activity.