围绝经期妇女血清瘦素水平的测定及其意义

本文采用放射免疫测定法 (RIA)检测了 138例围绝经期妇女 (其中月经紊乱期 81例 ,绝经期 5 7例 )血清FSH、LH、E2 、瘦素水平 ,并与 4名育龄妇女各项指标对照比较。在此基础上探讨它们在围绝经期妇女正常生理过程中的相互关系。结果表明 :瘦素在月经紊乱期妇女 (P <0 .0 5 )和绝经期妇女 (P <0 .0 1)中都有较明显变化 ;FSH、LH、E2 亦有显著变化 (P <0 .0 1) ,提示瘦素参与了围绝经期妇女的正常生理变化 ,并通过一些途径参与了激素的调节     

2型糖尿病患者血清瘦素水平及临床意义

目的：观察2型糖尿病（DM2）患者血清瘦素（leptin）水平及其与肥胖、血糖、血脂的关系。方法：采用放射免疫分析（RIA）测定42例DM2患者和38例正常对照组的血清leptin水平。结果：DM2组血清leptin水平明显高于对照组（P〈0．01）;血清leptin与体重指数（BMI）、血清胰岛素（INS）、总胆固醇（TC）、甘油三酯（TG）、脂蛋白LDL-C呈正相关。结论：DM2患者的高leptin血症与肥胖、血脂异常及胰岛素抵抗（IR）密切相关。     

肾病患者血清HA水平及临床意义

为探讨血清HA在肾病中的诊断意义。我们采用放射免疫分析 (RIA)测定 4 0例肾病患者血清HA水平。1　对象和方法1 1　对象　肾病组 4 0例 (男 2 2 ,女 18) ,均为我院住院病人 ,年龄 (4～ 78)岁 ,平均 4 0 8岁。其中尿毒症 12例 (男 5 ,女 7) ,年龄 (38～ 78)岁 ,平均 5 1 7岁 ;肾小球肾炎 15例 (男11,女 4 ) ,年龄 (4～ 6 7)岁 ,平均 4 2 3岁 ;肾病综合征 13例(男 6 ,女 7) ,年龄 (7～ 4 5 )岁 ,平均 38 5岁。正常对照组 30例 (男 17,女 13) ,年龄 (18～ 5 0 )岁 ,平均 39 7岁。均为健康体检者。1 2　方法　尿毒症患者均于血透前抽取静脉…     

慢性肾衰竭血透患者血清瘦素水平及其意义

为探讨慢性肾衰竭（CRF）血透患者的血清瘦素水平及其与残余肾功能、人体构成和营养状况的关系，分别采用放射免疫分析技术、生物电阻 抗技术和常规生化方法测定31例终末期CRF血透患者的血清瘦素水平、人体构成和营养相关指标。结果显示，CRF患者血清瘦素水平显著高于对照组（P＜0．001）；瘦素水平与体重指数和脂肪百分比呈正相关，与去脂体重呈负相关（P均＜0．001），与肌酐清除率、血肌酐、尿素氮以及血白蛋白、胆固醇、血红蛋白无相关性（P均大于0．05）。结论：终末期CRF患者存在高瘦素血症，其瘦素水平与残余肾功能无关，但可能导致去脂体重丢失。瘦素可以作为评价机体脂肪含量的营养指标，但没有在终末期CRF患者蛋白质营养不良中发挥显著作用。     

IgA肾病患者纤溶酶原激活物的变化及临床意义

目的：探讨IgA肾病患者纤溶酶原激活物（PA）的变化及临床意义。方法：以纤维蛋白平板法检测108例IgA肾病及34例健康自愿者尿PA活性，同时以免疫组化方法观察了27例IgA肾病及6例正常人肾组织t-PA、u-PA抗原表达，分析其与临床病理资料的关系。结果：正常人肾组织t-PA偶见少量表达于肾小球毛细血管袢，u-PA则表达于所有节段的肾小管上皮细胞。IgA肾病肾组织t-PA阳性率及单个肾小球t-PA平均积分明显高于正常人。轻度增生的肾小球其t-PA阳性率明显增高，中度增生的肾小球t-PA阳性率明显高于轻度增生者，硬化的肾小球不表达t-PA。u-PA表达明显下调，尿PA活性下降。伴血肌酐升高、肾小管间质病变严重、肾小动脉病变较重或大量蛋白管型形成的患者尿PA活性下降更为明显。结论：IgA肾病早期肾组织t-PA表达增加，晚期下降。肾组织u-PA表达减少。蛋白管型的形成可能与尿PA活性下调有关。尿PA活性的检测有助于判断IgA肾病的病情。     

血清瘦素水平与2型糖尿病肾病的关系探讨

本文对64例2型糖尿病患者血清瘦素水平进行放射免疫分析(RIA),以探讨其与糖尿病肾病(DN)的关系,现将结果报告如下.     

粘附分子选择素在IgA肾病中变化的临床意义

目的：为探讨ＩｇＡ肾病患者血和肾组织中Ｐ选择素必变与疾病的关系。方法：采用酶联免疫吸附法、免疫组化及原位杂交技术检测了４５例ＩｇＡ肾病患者血浆和肾组织中Ｐ选择素含量及表达水平。结果：ＩｇＡ肾病患者血浆Ｐ选择素含量明显高于正常人,其中肾病综合征组和肾功能减退组含量又较肉眼血尿组、尿检异常组和肾炎综合征组显著增高造反素在患者肾组织中广泛表达,其中在Ⅳ级和Ⅴ级ＩｇＡ肾病肾小球中表达水平明显高于Ⅱ级和Ⅲ级     

IgA肾病患者肾间质肥大细胞浸润的临床意义

目的 研究肥大细胞（MC）在IgA肾病患者肾间质中的分布及间质纤维化的关系。方法 采用甲苯蓝特殊染色法及MC特异酶（即类酶蛋白酶,tryptase）免疫组化染色法,对12例IgA肾病患者肾活检标本中的MC进行了观察。结果 （1）肾脏皮、髓质均可见到MC,多见于纤维化区域、血管周围、萎缩或扩张小管周围及肾小球周围。（2）系膜细胞的增殖程度与MC数无关,而随着IgA肾病患者MC的数增加,间质纤维化加重,差异显著（P＜0．05）。结论 IgA肾病患者的肾间质中存在MC,并与肾间质的纤维化有关。     

高血压病患者血清瘦素水平的变化

瘦素 (Ｌｅｐｔｉｎ ,Ｌｐ)为肥胖基因的产物 ,是由脂肪细胞合成分泌的一种蛋白激素 ,分子量为 1 60 0 0 ,由 1 67个氨基酸组成。瘦素作为一种重要的机体能量平衡的调节因子 ,参与机体能量的摄取、储存和释放 ,与机体的肥胖、糖代谢异常、胰岛素抵抗、脂代谢异常等密切相关[1 ] 。为了解高血压病患者的血清瘦素水平 ,我们测定了 35例高血压病患者的血清瘦素含量。探讨瘦素与高血压的发病关系。材料和方法一、对象 :(一 )高血压病组 :35例 (男 2 1 ,女 1 4 ) ,年龄 40～ 81岁 (平均 60 2 6± 1 2 90岁 )。均系我院住院病人。本组病人均符合…     

人类白细胞抗原与IgA肾病关联及其临床意义

７５例经肾穿刺证实ＩｇＡ肾病患者来自上海驻族患者检测了ＨＬＡ－Ａ、Ｂ、ＤＲ抗原和５９例ＨＬＡ－ＤＱ抗原，发现ＨＬＡ－ＤＲ４抗原频率明显增高，ＨＬＡ－ＤＲ５一型频率降低；ＨＬＡ－ＤＲ４抗原阳性者在大量蛋白尿组和肉眼血尿组均增高。     

炎症介质在IgA肾病中的临床应用价值探讨

目的探讨hs-CRP、IL-6、IL-18、TNF-α和TGF-β1在Ig A肾病中的临床应用价值。方法选取2010年6月至2013年11月肾穿刺活检确诊的Ig A肾病患者71例,根据病理Lee氏分级的结果将Ig A肾病组分为3个亚组,轻度组(Ⅰ级+Ⅱ级)32例,中度组(Ⅲ级)17例,重度组(Ⅳ级+Ⅴ级)22例;同时选取35例健康对照。检测各组血清Scr、Urea、CysC和尿UTP水平及血清炎症因子hs-CRP、IL-6、IL-18、TNF-α和TGF-β1水平,并比较各炎症因子与Scr、Urea、CysC和尿UTP的相关性。结果 Ig A肾病患者各组血清hs-CRP、IL-6、IL-18、TNF-α和TGF-β1水平逐渐增高,与健康对照组有显著性差异(P<0.05);随着疾病进展,重度组各炎症因子水平与轻度组和中度组比较有显著性差异(P<0.05);各炎症因子与Scr、Urea、CysC和尿UTP呈正相关(P<0.05)。结论炎症介质可以监测肾损伤程度,炎症损伤与Ig A肾病进展有密切关系。     

Aberrant sialylation of serum IgA1 was associated with prognosis of patients with IgA nephropathy

Aberrant glycosylation of serum IgA1 was considered as an initial event and involvement in the pathogenesis of IgAN. We previously demonstrated that aberrant glycosylation of serum IgA1 was associated with pathologic phenotype of IgAN. The present study is to investigate if abnormal sialylation of IgA1 affects renal survival of IgAN. 127 patients with biopsy-proven IgAN were enrolled and followed up to 8 years. Seventy-nine healthy and 75 patients with non-IgAN renal diseases were selected as controls. Alpha 2, 6 sialic acid (SA) of serum IgA1 was measured by sandwich-ELISA. Renal survival rate was estimated by Kaplan-Meier method. Alpha 2, 6 SA level in patients with IgAN was lower than that in healthy controls (0.92+/-0.14 vs. 0.98+/-0.12, P=0.001) and non-IgAN glomerulonephritis (0.92+/-0.14 vs. 1.00+/-0.18, n=53, P=0.001). Patients with IgAN in Low SA Group were no significant differences compared with patients in Normal SA Group in age, gender, hypertension, serum creatinine, and excretion of proteinuria. Renal cumulative survival rate was 53.3% in patients in Low SA Group and 83.5% in Normal SA Group (P=0.0008). The lower the alpha 2, 6 SA level of serum IgA1 in patients with IgAN was, the worse their renal survival rate was. Although patients in Low SA Group had worse renal function evaluated by eGFR, there was no significant difference in various CKD stages in non-IgAN renal function controls (n=42, P=0.352). Alpha 2, 6 SA level of serum IgA1 was associated with the prognosis of patients with IgAN and could serve as a predictor of poor prognosis in IgAN.     

Urinary IgA in IgA nephropathy and Henoch-Schoenlein purpura

To determine the concentrations and molecular forms of urinary IgA in IgA nephropathy and Henoch-Schoenlein purpura, we studied 29 patients with these IgA-associated renal diseases (IgAN). Control groups comprised 10 patients with other diverse renal diseases and 11 healthy volunteers. Urinary IgA and IgG concentrations were higher in IgAN than in either control group and correlated positively with the serum creatinine concentration as well as the urinary protein excretion (P<0.01). However, IgA/IgG ratios did not differ among the three groups. Polymeric IgA (p-IgA) in the urine predominated only in normals; in IgAN and patients with other renal diseases, monomeric IgA (m-IgA) occurred almost exclusively. Serum IgA concentrations were generally normal in IgAN; four patients had concentrations greater than 500 mg/dl. Although the fraction of p-IgA in serum (median, 18%) was increased above normal (5–10%) in 13 of 16 (81%) subjects, neither the concentration of IgA or IgG nor the amount of p-IgA correlated with the serum creatinine concentration. These data suggest that the molecular form and concentration of urinary IgA are not discriminating for IgAN and are independent of these characteristics of serum IgA.     

The level of urinary secretory immunoglobulin A (sIgA) of patients with IgA nephropathy is elevated and associated with pathological phenotypes

Recent studies have demonstrated deposition of secretory immunoglobulin A (sIgA) in glomeruli of some patients with IgA nephropathy (IgAN). The aim of this study is to investigate the levels of urinary sIgA in IgAN patients with different pathological phenotypes and whether it could be used as a non‐invasive biomarker for assessment of kidney injury in IgAN. Urine samples from 202 patients with IgAN were collected on the day of renal biopsy. Forty‐eight fulfilled the histopathological criteria of Haas‐I or II (group 1), 60 fulfilled Haas‐III (group 2) and 94 patients fulfilled Haas‐IV or V (group 3). Urine samples from 60 healthy sex‐ and age‐matched volunteers with negative urinalysis were collected as normal controls. Urinary sIgA was detected by sandwich enzyme‐linked immunosorbent assay and was corrected by urinary creatinine. In comparison with normal controls, the levels of urinary sIgA were significantly higher in IgAN [2·22 (0–43·82) μg/mg Cr versus 1·08 (0–16·49) μg/mg Cr, P < 0·001]. The levels of urinary sIgA were significantly higher in group 3 than that in group 2 and group 1 [3·54 (0–43·82) μg/mg Cr versus 1·63 (0–15·88) μg/mg Cr versus 0·91 (0–11·79), P < 0·001], and group 2 than group 1 (P = 0·014). The levels of urinary sIgA were associated positively with proteinuria (r = 0·443, P < 0·001), serum creatinine (r = 0·376, P < 0·001) and histopathological parameters, such as ratio of global sclerosis (r = 0·356, P < 0·001), ratio of total crescents (r = 0·339, P < 0·001) and ratios of cellular crescents (r = 0·231, P < 0·001). The levels of urinary sIgA were associated closely with histopathological phenotypes of IgAN and might be used as a non‐invasive biomarker to evaluate kidney injury in IgAN.     

IgA polyspecific autoantibodies in IgA nephropathy.

The specificity of circulating and kidney-bound IgA during IgA nephropathy is still a matter of discussion. In the present study, high levels of IgA antibodies directed against a panel of self and non-self antigens were found in the serum from patients with IgA nephropathy and were eluted from four out of the seven kidney biopsies studied. After immunoadsorption of pooled selected serum samples on TNP and actin-coated columns, polyspecific IgA antibodies were eluted. This supports the hypothesis that IgA-bearing B cells clones most probably producing polyspecific antibodies are a major feature of human IgA nephropathy. These findings also suggest that it may be hazardous to draw conclusions from the finding of apparently monospecific IgA antibodies in this condition.     

Lower serum bilirubin is associated with poor renal outcome in IgA nephropathy patients

Aims: IgA nephropathy (IgAN) is the most prevalent primary glomerulonephritis worldwide. We conducted this study to explore the relationship between serum bilirubin and renal outcome of patients with IgAN.Methods: A total of 1492 biopsy proven IgAN patients were recruited and divided into two groups according to their median serum bilirubin concentration: the low bilirubin group (serum bilirubin≤9.7umol/L, n=753) and high bilirubin group (serum bilirubin>9.7umol/L, n=739). Basic clinical characteristics were assessed at the time of renal biopsy and the relationships between serum bilirubin and the combined endpoints were analyzed. The combined endpoints were defined as a 50% decline in estimate glomerular filtration rate (e-GFR), end-stage kidney disease (ESKD), renal transplantation and/or death. In addition, propensity score matching (PSM) was then performed to improve balance and simulate randomization between patients in different groups. Kaplan-Meier survival analysis was applied to explore the role of serum bilirubin in the progression of IgAN. Three clinicopathological models of multivariate Cox regression analysis were established to evaluate the association of serum bilirubin and renal prognosis of IgAN.Results: During median 5-year follow-up period, significant differences were shown in Kaplan-Meier analysis. In the unmatched group, 189 (12.7%) patients progressed to the renal combined endpoints.Among this, 122 in 753 patients (16.2%) were in low bilirubin group and 67 in 739 patients (9.1%) were in high bilirubin group (p<0.001). After PSM, there were 134 (11.8%) patients reached the combined endpoints, which included 77 in 566 patients (14.6%) in low bilirubin group and 57 in 566 patients (10.1%) in high bilirubin group (p=0.039). The results of three models (including demographics, pathological, clinical indicators and serum bilirubin) demonstrated that a lower basic serum bilirubin level was significantly associated with a higher risk of reaching combined endpoints in IgAN patients both in unmatched and matched cohort.Conclusion: Serum bilirubin level may be negatively associated with the progression of IgAN.     

Abnormalities of the IgA immune system in members of unrelated pedigrees from patients with IgA nephropathy.

In the last few years many investigators have reported the recurrence of primary IgA nephropathy (IgAN) or the presence of persistent microhaematuria and/or proteinuria in family members of patients with IgAN. Our study was undertaken to investigate the relevance of abnormalities in the regulation of the IgA and IgM immune system in microhaematuric and asymptomatic family members of IgAN patients. Fifty-four out of 120 members of nine unrelated pedigrees were examined by urinalysis; polymeric IgA (pIgA), IgA rheumatoid factor (IgARF), IgA1-IgG immune complexes (IgA 1-IgG IC) and IgA 1-IgM IC, and other immunoglobulins were measured in serum samples. Moreover, we studied the production of immunoglobulins, pIgA and IgARF by peripheral blood mononuclear cells (PBMC) in basal conditions and after pokeweed mitogen (PWM) stimulation. Our data demonstrate that persistent microhaematuria was present in 24% of relatives. High serum levels of IgA, mainly pIgA and IgARF, IgA 1-IgG IC and IgA 1-IgM IC occurred in 66% of relatives. Abnormal spontaneous production of IgA by PBMC and after PWM stimulation was present in 64% of family members. Interestingly, high serum levels of IgM and abnormal production of this immunoglobulin by PBMC were observed in relatives. However, the immunological abnormalities did not correlate in any way with the presence of urinary abnormalities such as microhaematuria, which was most likely determined by an underlying glomerular alteration.     

Binding capacity and pathophysiological effects of IgA1 from patients with IgA nephropathy on human glomerular mesangial cells

IgA deposition in glomerular mesangium and the interaction with mesangial cells may well be the final common pathway to IgA nephropathy (IgAN). Altered hinge-region O-glycosylation of IgA1 from patients with IgAN may predispose to mesangial deposition and activation of the mesangial cell (MC) by IgA1, via a novel IgA1 receptor, and may be a key event in the pathogensis of IgAN. The aim of this study was to investigate the binding capacity and biological effects of IgA1, from both patients with IgAN and healthy controls, on human mesangial cells (HMC). Serum IgA1 was isolated with jacalin affinity chromatography, heated to aggregated form (aIgA1) and labelled with (125)I. Binding capacity of aIgA1 in vitro to cultured primary HMC was evaluated by a radioligand binding assay and the specificity of binding was determined by a competitive inhibition assay. Intracellular calcium release was studied by confocal analysis and phosphorylation of extracellular signal-regulated kinase (ERK) was determined by Western blot analysis. Change of cell cycles was demonstrated by flow cytometry and HMC proliferation was evaluated by direct cell count. Expression of TGF-beta mRNA and production of supernatant fibronectin were tested by RT-PCR and indirect competitive ELISA, respectively. aIgA1 from both the patients with IgAN and normal controls bound to HMC in a dose-dependent, saturable manner, and was saturated at approximately 500 pmoles per 0.5 ml of aIgA1. aIgA1 from patients with IgAN, however, bound to HMC at a higher speed and Scatchard analysis revealed a Kd of (8.89 +/- 2.1) x 10(-8)m versus (4.3 +/- 1.2) x 10(-7)m for aIgA1 from healthy controls (P = 0.026).The binding was specific because it was only inhibited by unlabelled Mono-IgA1 (mIgA1) and not by serum albumin or IgG. aIgA1 from patients with IgAN could induce release of intracellular calcium, phosphorylation of ERK, DNA synthesis, proliferation of HMC, expression of TGF-betamRNA and secretion of fibronectin in HMC in a similar time-dependent manner as aIgA1 from healthy controls, but the effects were much stronger and the durations were much longer (P < 0.05, respectively). We conclude that aIgA1 from patients with IgAN has a higher binding capacity to HMC and stronger biological effects than aIgA1 from healthy controls. This suggests that direct interaction between IgA1 and HMC and subsequential pathophysiological responses may play an important role in the pathogenesis for IgAN.     

Expression profile of Fc receptor-like molecules in patients with IgA nephropathy

BackgroundFc receptor-like (FCRL) molecules were considered to play a role in the pathogenesis of certain autoimmune diseases. Nonetheless, the clinical significance of FCRLs in IgA nephropathy (IgAN) remains unclear.ObjectiveThis study is aimed at investigating the expression levels of FCRLs molecules in IgAN patients and determining its relevance to disease activity.MethodsThe mRNA expression levels of FCRLs were determined in peripheral blood mononuclear cells (PBMCs) of 42 IgAN patients and 48 healthy controls by quantitative real-time PCR (qRT-PCR). FCRLs proteins expression in B cells of 25 IgAN patients, 14 patients with non-IgAN glomerulonephritis, and 29 healthy controls were detected by Flow cytometry. The Spearman correlation test was used to assess the correlation of FCRLs expression with clinical parameters of IgAN patients.ResultsOur results indicated significant down-regulation of FCRL2 and FCRL3 mRNA levels in IgAN patients compared to healthy subjects. Surface protein expression of FCRLs molecules confirmed the qRT-PCR results. But FCRL2 and FCRL3 protein levels did not correlate with clinicopathologic phenotypes of IgAN patients. However, we found a significant positively correlation of FCRL2 and FCRL3 mRNA expression with the core 1 β1,3-galactosyltransferase (C1GALT1) and its molecular chaperone (Cosmc) mRNA levels in IgAN patients.ConclusionsFCRL2 and FCRL3 expression levels in IgAN patients are significantly decreased and correlated with CIGALT1 and Cosmc mRNA expression.