Mesangial autoantigens in IgA nephropathy: matrix synthesis and localization

Primary IgA nephropathy, a chronic nephritis with variable prognosis, is characterized by mesangial immunoglobulin A, frequently with codeposition of other immunoglobulin isotypes and complement components accompanying matrix expansion typically preceding glomerular scarring. Glomerular immunoglobulin G, when present, is localized to the mesangial periphery found variably in repeat biopsies. IgG anti-mesangial cell autoantibodies (IgG-MESCA) in sera of patients with IgA nephropathy, specific by F(ab')(2) binding to 48- and 55-kD autoantigen(s) could account for these deposits, but their in vivo localization, and the functional role in promoting scarring is unknown. A specific monoclonal antibody raised previously to these human mesangial cell autoantigen fractions, in this study localized to similar glomerular sites, reinforcing the view that immunoglobulin G deposition in vivo is a result of antibody-autoantigen binding. The propensity for immunoglobulin G more than other isotypes to enhance inflammation prompted study of its functional role in vitro. Using cultured human mesangial cells in a complement-free tritiated glycosaminoglycan synthesis single outcome assay, purified IgG fractions from patient sera increased matrix production in a dose-dependent manner compared with controls. At a constant total IgG concentration, matrix synthesis was proportional to the titre of IgG-MESCA. Autoreactive IgG stimulated matrix synthesis when compared with controls or IgA fractions. These findings are consistent with IgG-MESCA autoantibodies enhancing mesangial matrix synthesis in vitro, which suggests that in IgA nephropathy, similar prosclerotic autoimmune mechanisms might operate. Recombinant TGFbeta(1) also induced matrix synthesis, raising the possibility that both autoimmune mechanisms and those TGFbeta(1)-dependent are functional or inter-related. The pathogenesis of glomerular scarring and loss in IgA nephropathy may include, in part, these mechanisms.     

Mesangial proliferative glomerulonephritis

IgA nephropathy is by far the most popular mesangial proliferative glomerulonephritis which can induce nephrotic syndrome. The etiology and pathogenesis of IgA nephropathy are still elusive, however. The enigma is that the IgA molecules deposited in glomeruli are mainly IgA1 subclass produced in central lymphoid organs and not the IgA2 subclass produced in peripheral mucous membrane, contrary to the notion that mucosal defense mechanism may be exacerbated in patients with IgA nephropathy. Recent investigations have elucidated that clearance of IgA might be deteriorated in these patients due to the abnormalities in the O-glycosylation of the hinge region of IgA molecules. The etiopathogenesis of IgA nephropathy elucidated in recent years is discussed.     

The clinico-pathologic features of hepatitis B virus-associated glomerulonephritis

The frequency of hepatitis B surface antigen (HBsAg) was studied in the sera of 311 patients with various forms of primary glomerulonephritis and 43 patients with lupus nephritis. HBs antigenaemia was detected in 69 of the 311 patients (22 per cent) with primary glomerulonephritis and this prevalence of HBsAg carrier was significantly higher than that in the general population (p less than 0.001). These patients had no clinical or biochemical findings to suggest acute or chronic liver disease. A higher HBs antigenaemia carrier rate was not observed in patients with lupus nephritis. Three glomerulopathological entities, membranous nephropathy, IgA nephropathy, and mesangial proliferative glomerulonephritis, were found to be associated with a higher prevalence of HBs antigenaemia compared with the general population (p less than 0.001). Glomerular deposits of HBsAg and/or hepatitis core antigen (HBcAg) were detected in 41, 61, and 60 per cent of renal biopsy specimens from patients with membranous nephropathy, IgA nephropathy, and mesangial proliferative glomerulonephritis associated with persistent HBs antigenaemia respectively. During the mean study period of 40 months (range 12-180), 14 per cent of these patients with hepatitis-associated glomerulonephritis developed progressive renal failure, although none required maintenance dialysis. Our study suggests that hepatitis B virus antigenaemia may play a significant role in the development of specific forms of glomerulonephritis and that these hepatitis B virus-associated glomerulonephritides can run an indolent but relentless progressive clinical course.     

IgA nephropathy in a patient with dominant dystrophic epidermolysis bullosa

Dystrophic epidermolysis bullosa (DEB) is a rare and severe hereditary dermatosis. On the other hand, IgA nephropathy is the most common form of glomerulonephritis in childhood and adults, and clinically characterized by microhematuria and proteinuria and histologically by deposition of immunoglobulin A in mesangial lesions. Several renal complications of recessive DEB including IgA nephropathy and amyloidosis have been reported. However, there have been no reports on dominant DEB associated with IgA nephropathy. We report here for the first time a 17-year-old girl with dominant DEB associated with IgA nephropathy. The patient has suffered from episodes of urinary, upper airway, and skin infections. At 17 years of age, proteinuria and hematuria were detected, with a high value of serum IgA. Renal biopsy was performed, and immunofluorescence microscopic examination revealed segmental deposits of IgA in mesangial lesions, with many glomeruli exhibiting diffuse segmental mesangial-proliferative glomerulonephritis. We diagnosed dominant DEB associated with IgA nephropathy on the basis of proteinuria, hematuria, and deposits of IgA in mesangial lesions on immunofluorescence microscopic examination, and diffuse segmental mesangial-proliferative glomerulonephritis. These findings suggest that repeated skin infections might have contributed to the pathogenesis of IgA nephropathy in this patient.     

Oxidative metabolism of polymorphonuclear leukocytes (PMN) in patients with IgA nephropathy

The production of hydrogen peroxide (H₂O₂) by neutrophilic polymorphonuclear leukocytes (PMN) after stimulation and the infiltration of PMN in glomeruli were determined in 20 patients with primary IgA nephropathy. The H₂O₂ production of PMN after the stimulation was measured with a spectrophotometer using horseradish peroxidase as substrate. The results were as follows: (1) when PMN were pretreated with cytochalasine B, H₂O₂ production after stimulation with heataggregated IgG (IgG) or serum-treated zymosan (STZ) was significantly higher in patients with IgA nephropathy than in controls, and (2) there was an increased amount of PMN localized in glomeruli in patients with IgA nephropathy using immunofluorescence of monoclonal anti-PMN antibody. It appeared that the increased renal infiltration of PMN which have a high potential for production of reactive oxygen species might induce the glomerular injuries in patients with IgA nephropathy.     

Autoimmunity to glomerular antigens in Henoch-Schoenlein nephritis.

1. Henoch-Schoenlein nephritis and IgA nephropathy share clinical and immunological features, but the pathogenesis of neither condition is established. We have recently described IgG autoantibodies to glomerular components in active IgA nephropathy and have now sought evidence for a similar autoimmune component in Henoch-Schoenlein purpura. 2. Sera from 26 patients with Henoch-Schoenlein nephritis and six patients with Henoch-Schoenlein purpura without accompanying nephritis were studied and compared with sera from 20 patients with other forms of glomerulonephritis and 40 normal subjects. E.l.i.s.a.s were developed to detect IgA and IgG binding to the ligand from whole human glomeruli previously described, laminin, DNA, cardiolipin (diphosphatidylglycerol) and a panel of dietary constituents (BSA, alpha-caesin, beta-lactoglobulin, ovalbumin and wheat gliadin). 3. Sera from 16 of the 26 patients with Henoch-Schoenlein nephritis displayed increased IgG binding to the human glomerular extract compared with the normal control group (P < 0.001), whereas IgG binding was not significantly raised in the patients with Henoch-Schoenlein purpura without evidence of renal involvement. IgA binding was not raised compared with control subjects. Serum IgA and IgG binding to other potential autoantigens or antigens present on dietary constituents was not significantly different in patients with Henoch-Schoenlein nephritis or patients with Henoch-Schoenlein purpura without nephritis compared with control subjects. 4. Western blotting of the denatured and reduced glomerular extract revealed binding of IgG, from the sera of patients with active Henoch-Schoenlein nephritis, to glomerular components of M(r) 48,000 and 58,000, similar to the M(r) of the glomerular antigens identified in IgA nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enzymolysis of glomerular immune deposits in vivo with dextranase/protease ameliorates proteinuria, hematuria, and mesangial proliferation in murine experimental IgA nephropathy.

The therapeutic effects of saccharolytic and proteolytic enzymes were investigated in models of IgA nephropathy. Mesangial glomerulonephritis was induced in mice by intravenous injection of preformed soluble immune complexes of dextran sulfate and either IgA (J 558) or IgM (MOPC 104 E) anti-dextran MAb (passive model) or by immunization with DEAE dextran (active model). In the passive model, only 30-40% of dextranase-treated mice given IgA or IgM immune complexes had mesangial Ig or dextran deposits, compared with 100% of saline-treated controls (P less than 0.01). There was no significant difference in mice given only protease. In the active model, dextranase and protease separately each reduced glomerular dextran and C3 deposits, and hematuria (P less than 0.01). Dextranase also reduced the glomerular IgA deposits (20 vs. 100% of saline-treated mice) and the frequency and severity of mesangial matrix expansion (both P less than 0.02), but did not reduce the modest IgG or IgM codeposits. Protease reduced IgG and IgM deposits, proteinuria and mesangial hypercellularity compared with saline (P less than 0.02), but did not diminish IgA, and had no effect on mesangial matrix expansion. The combination of dextranase plus protease attenuated all components of glomerular injury as judged by clinical and pathological parameters, but inactivated dextranase plus inactivated protease had no effect on any parameter. We conclude that enzymatic digestion of antigen and antibody can reduce immune deposits, mesangial proliferation, proteinuria, and hematuria in experimental glomerulonephritis.     

Circulating immune complexes in IgA nephropathy consist of IgA1 with galactose-deficient hinge region and antiglycan antibodies

Circulating immune complexes (CICs) isolated from sera of patients with IgA nephropathy (IgAN) consist of undergalactosylated, mostly polymeric, and J chain-containing IgA1 and IgG antibodies specific for N-acetylgalactosamine (GalNAc) residues in O-linked glycans of the hinge region of IgA1 heavy chains. Antibodies with such specificity occur in sera of IgAN patients, and in smaller quantities in patients with non-IgA proliferative glomerulonephritis and in healthy controls; they are present mainly in the IgG (predominantly IgG2 subclass), and less frequently in the IgA1 isotype. Their specificity for GalNAc was determined by reactivity with IgA1 myeloma proteins with enzymatically removed N-acetylneuraminic acid (NeuNAc) and galactose (Gal); removal of the O-linked glycans of IgA1 resulted in significantly decreased reactivity. Furthermore, IgA2 proteins that lack the hinge region with O-linked glycans but are otherwise structurally similar to IgA1 did not react with IgG or IgA1 antibodies. The re-formation of isolated and acid-dissociated CICs was inhibited more effectively by IgA1 lacking NeuNAc and Gal than by intact IgA1. Immobilized GalNAc and asialo-ovine submaxillary mucin (rich in O-linked glycans) were also effective inhibitors. Our results suggest that the deficiency of Gal in the hinge region of IgA1 molecules results in the generation of antigenic determinants containing GalNAc residues that are recognized by naturally occurring IgG and IgA1 antibodies.     

Proliferative glomerulonephritis in rats: evidence that mononuclear phagocytes infiltrating the glomeruli stimulate the proliferation of endothelial and mesangial cells

Abstract. A proliferative, non-crescentic, glomerulonephritis (GN) was induced in rats preimmunized with rabbit IgG by injecting a sub-nephrotoxic dose of rabbit anti-GBM IgG. Control rats either received anti-GBM IgG only, or were totally irradiated (800 rads, kidneys protected) 2 days before the second injection. All the GN rats developed a severe proteinuria within 2–4 days after the injection of anti-GBM IgG, contrarily to the control rats. At the same time, many mononuclear cells, of predominantly extra-renal origin, infiltrated the glomeruli. Glomeruli were isolated from GN, normal and control rats and were cultivated in RPMI medium. In normal and control rat cultures, epithelial and mesangial cells were observed. In GN rat cultures, not only epithelial and mesangial cells, but also endothelial and macrophagic cells were identified; the outgrowth capacity of the mesangial cells was enhanced. These data were particularly evident in cultures of GN glomeruli isolated within 2–4 days after the induction of the renal disease, exactly when the glomeruli were infiltrated by a large number of mononuclear phagocytes. It is suggested that the mononuclear phagocytes infiltrating the glomeruli of rats with this model of GN stimulate the proliferation of endothelial and mesangial cells in vitro.     

Lysophosphatidic acid and mesangial cells: implications for renal diseases

The last decade has witnessed a phenomenal increase in our understanding of the biological role of lysophosphatidic acid (LPA) and has led to an appreciation of this critical serum-derived growth factor released from platelets. We herein summarize recent observations that collectively support the hypothesis that LPA may play a key role in the pathogenesis of initiation and progression of proliferative glomerulonephritis. LPA synergistically stimulates mesangial cell proliferation in combination with platelet-derived growth factor in primary culture. The mechanism of co-mitogenesis is likely to be mediated by the prolonged activation of mitogen-activated protein kinase which is stimulated by platelet-derived growth factor and LPA through different mechanisms. LPA contracts cultured mesangial cells and has properties in common with other pressor molecules including mobilization of intracellular Ca2+ and promotion of Ca2+ entry through dihydropyridine-sensitive calcium channels. LPA receptor mRNA has been identified in isolated glomeruli dissected from renal biopsy samples of patients with IgA nephropathy. All of these facts have led us to postulate that LPA is produced within glomeruli and that LPA's mitogenic as well as haemodynamic action contribute to the pathological process of mesangial proliferative glomerulonephritis. The possible production of LPA as an autocrine factor from mesangial cells themselves has also been discussed.     

Immunohistochemical study of the human glomerular C3b receptor in normal kidney and in seventy-five cases of renal diseases: loss of C3b receptor antigen in focal hyalinosis and in proliferative nephritis of systemic lupus erythematosus.

The presence and distribution of C3b receptors in normal human kidneys and in biopsies from 75 patients with renal disease were investigated by immunohistochemical techniques using monospecific rabbit antibody to the 205,000-mol wt glycoprotein that is the C3b receptor of human peripheral blood cells. Anti-C3b receptor bound exclusively to podocytes in normal renal cortex, and was homogeneously distributed on the plasma membrane of these cells. Biosynthesis of the receptor by the podocyte was suggested by the presence of antigenic activity in the Golgi apparatus. Although occupancy of receptor sites following the interaction of kidney sections with aggregated IgG preincubated with normal serum inhibited binding to glomeruli of C3b coated cells, the C3b receptor remained accessible to anti-C3b receptor antibody. No staining of podocytes was found in extra-capillary proliferating cells in rapidly progressive glomerulonephritis (GN). Segmental loss of staining was found in focal hyalinosis, nodular diabetic glomerulosclerosis, and amyloidosis while no detectable C3b receptor antigen was found in severe proliferative nephritis of systemic lupus erythematosus (SLE). Normal staining of podocytes was found in other nephropathies with endocapillary proliferation such as acute GN and mesangial GN and in renal diseases associated with immune deposits containing C3 such as mesangial proliferative and membranous SLE nephritis, idiopathic membranous GN, membranoproliferative GN types I and II, mesangial GN with IgA or C3 deposition and Henoch Schönlein's purpura. Loss of C3b receptor antigen in the diffuse proliferative nephritis of SLE distinguishes it both from nonproliferative lupus nephritis and other immunologically mediated proliferative GN.     

膜型IgA肾病

肾病是我国常见的肾小球疾病，病理类型很多，但膜型ＩｇＡ肾病极罕见。本文报告３例膜型ＩｇＡ肾病。病理特点是系膜增生的同时，肾小球毛细血管基底膜增厚，并有钉突形成。患者有大量蛋白尿。系膜区有大量ＩｇＡ沉积，毛细血管基底膜外侧有ＩｇＧ沉积。超微结构显示在系膜区及基底膜上皮细胞下均有电子致密物。本文通过免疫荧光和免疫电镜的研究认为，膜型ＩｇＡ肾病是膜型肾小球肾炎与系膜增生型ＩｇＡ肾病的相互重叠。     

The role of IgA1 rheumatoid factor in the formation of IgA-containing immune complexes in Henoch-Sch?nlein purpura

The present study was performed to investigate the role of IgA rheumatoid factor (RF) in the formation of IgA-containing immune complexes and to determine the IgA subclass composition of IgA RF in patients with Henoch-Sch?nlein purpura (HSP). Immune complexes were isolated from the sera of 22 children with HSP and 13 controls by means of polyethylene glycol (PEG) precipitation. The percentage of IgG, IgA, and IgM precipitated by PEG was significantly greater in HSP patients than controls (p less than 0.01). There was a strong correlation (r = 0.723, p less than 0.001) between the amount of IgG and IgA in the PEG precipitates from HSP patients, but not controls. HSP patients had significantly higher levels of IgA RF in their serum (p less than 0.05) and in their PEG precipitates (p less than 0.05) compared to controls. There was a strong correlation between IgA RF concentrations in the serum and PEG precipitates in HSP patients (r = 0.910, p less than 0.001). PEG precipitation eliminated IgA RF activity from the serum of 7 of 8 HSP patients tested, and substantially reduced the titer in the remaining patient. IgA RF was recovered in the PEG precipitates from all patients. Testing of HSP patients showed that IgA1 was the predominant IgA subclass of the serum IgA RF (p less than 0.02) and PEG precipitate IgA RF (p less than 0.01). These results indicate that IgA RF is a constituent of IgA-containing immune complexes in HSP, and that IgA RF is composed primarily of IgA1.     

Newborn humans manifest autoantibodies to defined self molecules detected by antigen microarray informatics

Autoimmune diseases are often marked by autoantibodies binding to self antigens. However, many healthy persons also manifest autoantibodies that bind to self antigens, known as natural autoantibodies. In order to characterize natural autoantibodies present at birth, we used an antigen microarray (antigen chip) to analyze informatically (with clustering algorithms and correlation mapping) the natural IgM, IgA, and IgG autoantibody repertoires present in 10 pairs of sera from healthy mothers and the cords of their newborn babies. These autoantibodies were found to bind to 305 different, mostly self, molecules. We report that in utero, humans develop IgM and IgA autoantibodies to relatively uniform sets of self molecules. The global patterns of maternal IgM autoantibodies significantly diverged from those at birth, although certain reactivities remained common to both maternal and cord samples. Because maternal IgG antibodies (unlike IgM and IgA) cross the placenta, maternal and cord IgG autoantibodies showed essentially identical reactivities. We found that some self antigens that bind cord autoantibodies were among the target self antigens associated with autoimmune diseases later in life. Thus, the obviously benign autoimmunity prevalent at birth may provide the basis for the emergence of some autoimmune diseases relatively prevalent later in life.     

Detection of activated platelets in urinary sediments by immunofluorescence using monoclonal antibody to human platelet GMP-140 in patients with IgA nephropathy

The presence of activated platelets in the urinary sediments was studied by indirect immunofluorescence using monoclonal antigranular membrane protein (GMP)-140 antibody. GMP-140 is generally expressed on the activated-platelets and -vascular endothelial cells. The purpose of the present study was to determine if the presence of activated platelets in the urinary sediments is correlated with glomerular injuries in patients with IgA nephropathy. Fourteen patients with IgA nephropathy and 11 patients with diffuse mesangial proliferative glomerulonephritis without glomerular IgA deposition (PGN) were examined. The number of activated platelets in the urinary sediments was markedly increased in patients in the advanced stage of IgA nephropathy. The ratio of activated platelets to total platelets in the urinary sediments was also increased in such patients. It appears that the detection of activated platelets in the urinary sediments is useful in determining the degree of histological changes in IgA nephropathy. © 1993 Wiley-Liss, Inc.     

In vitro fixation of guinea pig complement by renal biopsies.

The in vitro fixation of heterologous complement by cryostat sections of human renal biopsy material was studied to determine the mechanism of complement activation. Various types of guinea pig sera with different parts of the complement system inhibited were used, the fixation of complement being detected by direct immunofluorescence. Cases of idiopathic focal nephritis with mesangial IgA (mesangial IgA disease), Henoch-Sch?nlein purpura (HSP) and mesangio-capillary glomerulonephritis (MCGN) fixed complement by the alternative pathway alone and in systemic lupus erythematosus (SLE) both the classical and alternative pathways were involved. Only one of the seven cases of membranous glomerulonephritis fixed complement and this was by the classical pathway. After prior treatment with C3b inactivator, the in vitro complement fixation in mesangial IgA disease, HSP and MCGN was greatly reduced. In SLE it was slightly reduced and in membranous glomerulonephritis there was no change. This is a convenient method of studying the biological properties of complexes which is believed to reflect the in vivo behaviour of the tissue deposited complex.     

IgA肾病患者扁桃体切除前后血、尿IL-2、IL-6的变化

目的检测IgA肾病患者扁桃体切除前后患者的血、尿IL-2、IL-6的水平,以探讨其变化规律和临床意义。方法选取经肾活检诊断为IgA肾病的患者76例,并排除肝硬化等继发性IgA肾病,并根据系膜增生程度分为轻度系膜增生组(A组)62例,中度系膜增生组(B组)5例,中度系膜增生伴新月体形成(C组)5例、局灶节段硬化组(D组)4例,同时选取健康查体10人作正常对照组(E组),观察患者扁桃体切除术前、术后6个月时患者的血尿IL-2、IL-6的水平。结果轻、中度系膜增生组扁桃体切除半年后尿IL-2、血IL-6、尿IL-6含量明显低于扁桃体切除前,结果有显著性差异(T=1.9624-9.6436、P0.05),而中度系膜增生伴新月体形成组和局灶节段硬化组两组患者扁桃体切除前和切除半年后血清及尿IL-2、IL-6较前下降,但无统计学意义(t=0.3221-1.0914)。无论扁桃体切除前后C、D两组患者的尿IL-2、IL-6水平均明显高于A、B组患者,二者有统计学差异(T2.235 5,P0.01)。结论轻、中度系膜增生性IgA肾病患者行扁桃体切除能改善患者的炎症因子的产生,降低患者尿IL-2、IL-6水平,而对于中度系膜增生伴新月体形成和局灶节段硬化的患者来说,扁桃体切除意义不大;对于尿液中IL-2、IL-6水平持续处于高水平的患者,提示病理损伤较重,扁桃体切除的意义不大。     

123例老年肾脏病患者的肾病理和临床特征分析

目的：探讨老年人原发性肾小球疾病及继发性肾脏疾病肾活检病理类型及临床特点。方法：回顾分析2003年—2005年123例年龄≥65岁,资料完整,并经临床和肾活检确诊为原发性肾小球疾病或继发性肾脏疾病患者的肾脏活组织病理和临床资料,并与同期367例中青年患者的肾脏活组织检查和临床资料进行对比。结果：①老年患者原发性肾小球疾病中膜性肾病最为常见,占原发肾脏疾病的31.46%,其次为IgA肾病（25.84%）。中青年患者原发肾脏疾病中以IgA肾病最为常见,占39.49%,其次为系膜增生性肾小球肾炎,占22.88%。②老年IgA肾病患者病理以局灶节段性肾小球硬化（FSGS）为主,占21.74%,而中青年患者以弥漫系膜增生为主,占30.95%。③糖尿病肾病是老年人最常见的继发性肾脏疾病,占32.35%,狼疮性肾炎是中青年患者最常见的继发性肾脏疾病,占58.33%。④老年肾脏疾病患者尿蛋白定量（3.60±0.78g.24h^-1）显著高于中青年组（2.19±0.68g.24h^-1）,P〈0.05。高血压的发生率显著增高（73.98%比30.51%,P〈0.01）。结论：老年患者肾脏病理类型与中青年患者不一致,老年原发性肾小球疾病以膜性肾病为主,IgA肾病的病理类型以FSGS为主;中青年患者原发性肾小球疾病以IgA肾病为主,IgA肾病的病理类型以弥漫系膜增生为主。老年患者继发性肾脏疾病的发生率高,以糖尿病肾病最为常见。肾脏病理类型的不同,是老年肾脏病患者临床表现中尿蛋白多和高血压的发生率增高的原因之一。     

小儿常见肾脏疾病尿电导率的变化分析

目的：检测小儿常见肾脏疾病尿电导率的变化,探讨该指标的临床意义。方法选择2011年3月至2012年3月本院小儿肾脏内科收治的首次诊断为肾脏疾病患儿986例及同期健康体检儿童350例的尿液,利用 Sysmex 公司的全自动尿液分析仪 UF-1000i 分别测定其尿电导率的变化。根据临床诊断将肾脏疾病患儿分为肾病综合征组、肾小球肾炎组、肾功能不全组、紫癜性肾炎组和狼疮性肾炎组。其中216例进行肾穿刺活检。根据肾穿刺活检病理诊断结果将患儿分为系膜增生性肾小球肾炎组、毛细血管内增生性肾小球肾炎组、膜性肾病组、IgA 肾病组、IgM 肾病组、过敏性紫癜性肾炎组和狼疮性肾炎组。结果1．肾病综合征组、肾小球肾炎组、肾功能不全组、紫癜性肾炎组、狼疮性肾炎组患儿的尿电导率明显低于健康对照组,差异具有统计学意义（P ＜0．05）。2．系膜增生性肾小球肾炎组、毛细血管内增生性肾小球肾炎组、膜性肾病组、IgA 肾病组、过敏性紫癜性肾炎组和狼疮性肾炎组患儿尿电导率明显低于健康对照组,差异具有统计学意义（P ＜0．05）。3．IgM 肾病组与健康对照组相比,尿电导率差异无统计学意义（P ＞0.05）。结论尿电导率可以作为小儿肾脏功能和尿液浓缩功能的重要指标。     

Deposits of IgD in Renal Disease. Immunohistological Study of 180 Renal Biopsies

Abstract. IgD deposits have been investigated by an indirect immunofluorescence technique in 180 renal biopsies carried out on patients with various renal diseases.
IgD was not present in nephrotic syndrome with minimal changes or focal glomerulosclerosis, in mesangial proliferative glomerulonephritis, in chronic advanced glomerulonephritis, in rheumatoid purpura and in other various nephropathies with predominant non-glomerulor lesions.
Significant deposits of IgD were identified in 12 out of 16 cases of membranoproliferative glomerulonephritis, in 15 out of 23 cases of membranous nephropathy, in 11 out of 21 cases of focal proliferative glomerulonephritis with mesangial IgA deposits, in 2 out of 5 cases of proliferative glomerulonephritis with crescents and in 1 out of 6 cases of proliferative exudative glomerulonephritis.
All cases of lupus nephritis and nephritis associated with mixed cryoglobulinaemia Bhowed IgD deposits.
In diabetic glomerulosclerosis, IgD was found in 1 out of 4 biopsies and only in the exudative lesions.
In 5 out of 8 cases of amyloidosis anti-IgD serum stained the amyloid substance irregularly. In such cases IgD was found in association with other immunoglobulins and complement with the same localization. These findings suggest that IgD may participate in the immunological processes which lead to the development of glomerular deposits, mainly in cases of chronic glomerular diseases.