Chronic glomerulonephritis associated with IgG subclass deficiency

We experienced two patients with IgG subclass deficiency who suffered from chronic glomerulonephritis (GN). Patient 1 was a 17-year-old girl with IgG subclass deficiency (combined deficiency of IgG2 and IgG4). Renal biopsy was performed when she was aged 16 years, and she was diagnosed with membranoproliferative GN. Patient 2 was a 16-year-old girl with IgG subclass deficiency (combined deficiency of IgG2, IgG3, and IgG4). Renal biopsy was performed when she was aged 15 years, and she was diagnosed with membranous nephropathy. We examined the glomerular deposition patterns of their IgG subclasses. Furthermore, we compared their clinical and laboratory findings with those of three patients with IgG subclass deficiency without GN. Patients with GN suffered infections more frequently than those without GN. The serum levels of IgG (especially IgG1) and IgM were higher in patients with GN than in those without GN. In patient 1 IgG1 and IgG3 were deposited in a mesangiocapillary pattern, but, in patient 2, only IgG1 was deposited in a capillary pattern. Thus, the different patterns of IgG subclass deficiency between the two patients may be responsible for their different glomerular pathologies. To the best of our knowledge, this is the first report of chronic GN in patients with IgG subclass deficiency.     

IgG, IgA and IgM rheumatoid factors in patients with glomerulonephritis

Rheumatoid factors (RF), autoantibodies to IgG, have been postulated to have some pathogenetic role in the development of some types of glomerulonephritis. A simple and sensitive solid-phase fluorescence immunoassay was employed to determine whether IgG, IgA and IgM RF were detectable in sera from patients with various types of glomerulonephritis, rheumatoid arthritis (RA) and those with various streptococcal infections. IgG, IgA and IgM RF were significantly increased in the majority of patients with RA, lupus nephritis (SLE), acute poststreptococcal glomerulonephritis (APSGN) and various streptococcal infections. The titers of IgG and IgA RF were significantly higher in patients with APSGN than in those with simple pharyngitis. IgM RF was increated in patients with IgA nephropathy (IgA-N) and in those with membranoproliferative glomerulonephritis type I (MPGN). No significantly high RF was observed in membranous nephropathy (MN) or chronic mesangial proliferative glomerulonephritis without IgA deposition (PGN). It is suggested that some autologous immune mechanisms may be involved in the pathogenesis of some types of glomerulonephritis.     

Circulating immune complexes in glomerulonephritis: a longitudinal study

A longitudinal study of circulating immune complexes (CIC) was performed in 121 patients with biopsy verified glomerulonephritis (GN). 1286 blood samples were obtained during a mean observation period of 21 months. Two methods for detection of CIC were used, the Clq-binding activity and a PEG precipitation test. CIC were detected by both tests in 21% of all blood samples and detected in at least one blood sample from 57 patients. The presence of CIC was found to be either transient (34 patients), intermittent (11 patients) or permanent (12 patients). CIC were found transiently at the time of renal biopsy and disappeared within months in patients with idiopathic extracapillary GN (7 of 9 patients), endocapillary GN (2/2) and GN associated with polyarteritis nodosa (5/6), Wegener's granulomatosis (3/3) and Henoch-Schoenlein syndrome (3/6). CIC were detected either transiently, intermittently or permanently for years after renal biopsy in patients with SLE (12/14) and membranoproliferative GN type I (7/12). CIC were only occasionally detected in patients with minor change nephropathy (1/9), membranoproliferative GN type II (0/2), IgA nephropathy (6/17), focal segmental sclerosis (1/8) and membranous GN (2/11). In these patients CIC were often transiently present without apparent relationship to time since renal biopsy. Overall, a relationship was found between the presence of CIC and decreasing serum creatinine, but there was no correlation with changes in proteinuria or with increasing blood pressure. Serial measurements of CIC showed correlations with clinical events only in individual patients, but not in the population as a whole.     

Distribution of glomerular IgG subclass deposits in malignancy-associated membranous nephropathy.

BACKGROUND: Several studies have shown a predominant glomerular deposition of IgG4 in patients with idiopathic membranous nephropathy (MN), whereas significant depositions of other IgG subclasses have been shown in patients with lupus-associated MN and bucillamine-induced MN. METHODS: We examined the distribution patterns of glomerular IgG subclass deposits in 10 patients with malignancy-associated MN (M-MN) and in 15 patients with idiopathic MN by immunofluorescence (IF) microscopy. RESULTS: The glomerular IF intensities of IgG1 and IgG2 were significantly stronger in the malignancy group than in the idiopathic group (P<0.05). In contrast, there were no differences in glomerular IF intensities of IgG3 and IgG4 between the two groups. CONCLUSION: Our findings suggest that the distribution patterns of glomerular IgG subclass deposits are different in idiopathic MN and M-MN. The strong IF intensity of glomerular IgG1 and IgG2 in M-MN may provide a possible predictor for this condition.     

Complement Receptor (CR1) and IgG or IgA on Erythrocytes and in Circulating Immune Complexes in Patients with Glomerulonephritis

This study reports the quantitative analysis of complement receptor(CR1) molecules on erythrocyte surface, the amount of immunoglobulin-containingmaterial (IgG-IC and IgA1-IM) on the erythrocyte surface, andthe concentrations of circulating immune complexes (IgG-CICand IgA-CIC); also reported are the HLA phenotypes of 44 patientsaffected by various forms of glomerulonephritis (including 20primary IgA nephropathy, 11 membranous glomerulonephritis, 9lupus nephritis and 4 renal vasculitis). Erythrocyte CR1 molecules were found to be decreased (P<0.02)and erythrocyte IgG-IC were less than in controls (P<0.025)in lupus nephritis patients, whereas IgG-CIC were significantlygreater (P<0.02). In patients affected by primary IgA nephropathy, mean erythrocyteCR1 concentrations were significantly decreased (P<0.02).Patients with impaired renal function had mean erythrocyte CR1values significantly greater than those with normal renal function(P<0.002). Immunoglobulin-containing material on the erythrocytesurface was not significantly increased, whereas the serum concentrationsof both IgA-CIC and IgG-CIC were significantly increased (P<0.02). In membranous nephropathy erythrocyte CR1 molecules were quantitativelysimilar to control data and no increase in CIC was observed.Conversely, erythrocyte IgG-IC were significantly increased(P<0.01). No significant relationship among erythrocyte CR1 molecules,erythrocyte surface-associated immunoglobulins, CIC, and HLAphenotype was observed in any patient group.     

Anti -PLA2R autoantibodies in serum and IgG subclass deposits on glomeruli in undetermined atypical membranous nephropathy

ObjectiveTo investigate the characteristic of autoantibodies of M – type phospholipase A2 receptor (PLA2R) in serum and the glomerular IgG subclass deposits in undetermined atypical membranous nephropathy (MN) patients. MethodsFrom Feb 2004 to Nov 2011, 53 cases diagnosed as MN by kidney puncture biopsy in our hospital were included into the study. There were 20 undetermined atypical membranous nephropathy (UAMN), 20 idiopathic membranous nephropathy (IMN) and 13 secondary membranous nephropathy (SMN) which were composed of lupus membranous nephropathy (LMN) and HBV related membranous nephropathy (HBV-MN). Clinlical and pathological characteristics were analyzed. The autoantibodies of PLA2R in serum were detected and the glomerular IgG subclass deposits were observed. Results(1) The average age underwent renal biopsy was (37.9±3.8) years of UAMN, (50.1±3.0) years of IMN and (49.5±4.5) years of SMN. The difference in onset average age at disease was significant between UAMN and IMN (P＝0.0178). The female/male ratio (F/M) in UAMN, IMN and SMN was 0.8∶1, 0.7∶1 and 0.6∶1(P＞0.05). (2) Compared with SMN, the level of 24-hours urinary protein excretion (3.47 g vs 7.89 g, P＝0.023), the ratio of amount urinary protein patients (50.0% vs 84.6%, P＝0.043), the level of serum IgG [(8.40±3.58) g/L vs (10.09±4.69) g/L, P＝0.025] and the positive rate of ANA in serum (10.0% vs 53.8%, P＝0.006) in UAMN were all much lower. There were no significant statistical differences in serum albumin, serum creatinine, eGFR, positive rate of HBsAg, HBeAg or HCV, as well as the ratio of hypo - albuminemia and nephritic syndrome among the three groups. (3) IF positive rate of IgA, IgM and C1q in UAMN were all significantly higher than that in IMN (P＜0.01). There were no significant differences in IF positive rate of IgA, IgM, C1q, IgG and C3 between UAMN and SMN. The IF strength of IgA, IgG, IgM, C3 and C1q in UAMN showed no significant differences between UAMN and SMN. (4) The serum autoantibodies of PLA2R were only detected in 10 cases of IMN group (50%) with all the other cases negative. This detection rate of serum autoantibodies of PLA2R showed significant statistical differences among the three groups (P＜0.01), but no differences between UAMN and SMN (the detection rate in both groups were 0%). (5) IgG1 deposits was the dominant IgG on the glomeruli in UAMN group (40%), as well as in SMN group (76.9%). IgG4 deposits was the dominant IgG on the glomeruli in IMN group (60%). The positive rate of IgG1 and IgG3 in UAMN showed no significant statistical differences when compared with IMN or SMN. The positive rate of IgG2 in UAMN was significantly lower than in SMN（30.0% vs 69.2%, P＜0.05). The positive rate of IgG4 in UAMN was significantly lower than in IMN (20% vs 60%, P＜0.05). The positive rate of IgG1, IgG2 and IgG3 in SMN were all significantly higher than in IMN. ConclusionsNone of the UAMN group had autoantibodies of PLA2R in serum, and IgG1 deposits was the dominant IgG subclass on the glomeruli which indicated the similarity with the SMN group. At the same time, UAMN was significantly different from SMN in clinical manifestations.     

Estimation of circulating immune complexes following oral challenge with cow's milk in patients with IgA nephropathy

We recently reported on an experimentally induced model of IgA nephropathy in mice by long-term oral immunization under the reticuloendothelial dysfunction, which was found to be effectively inhibited by the administration of the antiallergic agent sodium cromoglycate (SCG). On the basis of these findings, we investigated the participation of food antigens in patients with IgA nephropathy. We studied 24 patients with IgA nephropathy, 11 patients with primary glomerulonephritis (PGN) except IgA nephropathy and 11 healthy controls. Serum levels of immunoglobulins (IgG, IgA, IgE) and circulating immune complexes containing IgG (IgG-CIC) or IgA (IgA-CIC) were measured in the fasting state and 30, 60, 120 or 180 min after oral challenging with cow's milk (400 ml). After the oral challenge IgA-CIC levels remained within the normal range in healthy controls and in patients with PGN, while 3 out of the 24 patients with IgA nephropathy showed a transient elevation and 2 cases showed a significant rise of IgA-CIC levels. The levels of IgG, IgA, IgE and IgG-CIC remained uninfluenced by the challenge test in all subjects. In addition, we carried out the same challenge test under SCG administration. These cases indicating an oral-challenge-induced IgA-CIC elevation demonstrated an inhibition of this elevation, and in 3 out 7 patients who showed hyper-IgA-CIC-emia before and after oral challenge IgA-CIC levels returned to the normal range through SCG administration. These results suggest that food antigens participate strongly in the pathogenesis of some patients with IgA nephropathy, and that SCG is an effective agent for such patients.     

Studies on circulating immune complexes. II: Circulating immune complexes in primary IgA nephropathy and membranoproliferative glomerulonephritis

A study of circulating immune complexes (CIC) was undertaken in 25 patients with primary IgA nephropathy and 13 patients with membranoproliferative glomerulonephritis (MPGN). Clinically, the 25 patients with IgA nephropathy were divided into two groups: the latent type, characterized by chance proteinuria and/or hematuria; and the acute onset type, revealing acute nephritic syndrome. Both the IgG class of CIC (IgG-IC) and the IgA class of CIC (IgA-IC) were measured by conglutinin binding enzyme immunoassay (C-assay). IgG-IC were found to be positive in 32% of the patients with IgA nephropathy, and in 77% of those with MPGN. IgA-IC were positive in 72% of the patients with IgA nephropathy, and in 54% of those with MPGN. Concerning the acute onset type of IgA nephropathy, IgG-IC and IgA-IC were found in 71% and 86% of the patients, respectively, which was more frequent than in the latent type group. Simultaneous presence of IgA-IC and glomerular IgA deposits detected by an immunofluorescence study was noted in 75% of the patients with IgA nephropathy. On the other hand, 78% of the patients with MPGN revealed IgG-IC and glomerular IgG deposits simultaneously. Thus, IgG-IC and IgA-IC appear to play important roles in the pathogenesis of MPGN and IgA nephropathy, respectively.     

Treatment of lupus nephritis and primary glomerulonephritis with enteric-coated mycophenolate sodium

AIMS: Mycophenolate mofetil is an effective therapy for lupus nephritis (LN) and other glomerulonephritis (GN). However, gastrointestinal (GI) complications can limit its use. Enteric-coated mycophenolate sodium (EC-MPS) has been designed to reduce GI adverse events, but it has not been fully investigated in the treatment of GN. METHODS: Patients with LN and primary GN who had received EC-MPS were studied for effects on renal function. RESULTS: 30 subjects (17 LN, 13 primary GN) were studied. EC-MPS decreased proteinuria in both LN and GN. In LN, 16 patients had EC-MPS as induction therapy. Of these, 8 patients achieved complete remission (CR), 4 had partial remission (PR) and 1 improved renal function. In primary GN, CR was achieved in 4 out of 5 with minimal change disease, but only 1 did not relapse. PR was achieved in 1 of 4 patients with membranous glomerulopathy, 2 out of 2 patients with focal segmental glomerulosclerosis and 1 out of 2 patients with IgA nephropathy. Infections, anemia and alopecia were observed, but no patient had GI side effects. CONCLUSIONS: EC-MPS is effective in LN, but not as effective in primary GN. The risk of GI side effects appears to be low, but other side effects can still occur.     

Studies on circulating immune complexes. I: Circulating immune complexes in various types of glomerulonephritis and collagen disease: a comparative study employing conglutinin solid phase radioimmunoassay and raji cell radioimmunoassay

A study was undertaken to examine the differences in serum levels of circulating immune complexes (CIC) detected by different methods in various types of collagen disease and primary glomerulonephritis. The subjects used were 16 patients with SLE, 22 with IgA nephropathy, 8 with membranoproliferative glomerulonephritis, 8 with membranous nephropathy, 6 with minimal change nephrotic syndrome, and 2 each with RA, PSS, DM, Sj?gren syndrome, PN, MCTD and overlap syndrome, respectively. CIC were measured by two assays, namely, bovine conglutinin solid phase radioimmunoassay (C-assay) and Raji cell radioimmunoassay (R-assay). In SLE, the incidence and amounts of CIC detected were higher in R-assay than in C-assay. Similar results were obtained for the other types of collagen diseases. Furthermore, a discrepancy in the incidence of CIC detected by the two assays was found in 30% of patients with collagen diseases. Concerning the detection of CIC in primary glomerulonephritis, the sensitivity of C-assay was higher than that of R-assay. This discrepancy appears to reflect the different sensitivities of the two assays. No significant correlation was found between the CIC level and the intensity of IgG deposits in various types of glomerulonephritis. These results suggest that the R-assay was better for the detection of CIC in collagen diseases, and that the C-assay was suitable for that in primary glomerulonephritis.     

IgG subclass composition of monomeric and polymeric IgG in the serum of patients with nephrotic syndrome

The serum levels of immunoglobulins G, A and M and of the four subclasses of IgG have been measured in 54 patients with the nephrotic syndrome; 27 had minimal change disease (MCD), 9 membranous glomerulopathy (MGN), 5 focal glomerulosclerosis (FGS), 5 proliferative glomerulonephritis (PGN) and 8 miscellaneous forms of nephrotic syndrome (Table 1). Low levels of IgG and A, previously described in MCD, were found in all histological diagnoses; only about half the cases of MCD showed a high IgM. Measurement of the subclasses IgG 1-4 showed all to be depressed. Proportionately, however, the IgG2 was most affected (8.8% total IgG, cf 18.3% controls). Urinary protein loss, either total or IgG, only partially correlated with IgG suppression, while IgG2 in the urine usually comprised an even lower proportion of total IgG than in serum. The polyethylene glycol (PEG) 6,000 precipitate from serum at 4% concentration was also examined for IgG and subclasses in MCD (27 cases), MGN (9 cases) and PGN (3 cases). Raised levels above those of 14 normal controls were found in nearly all cases of MCD, even in remission, but in no cases of MGN. In MCD no IgG4 was found in any of the precipitates, while IgG2 was proportionately raised (22% of total) in the precipitate as compared with whole serum (8.8%). Serial studies on 9 adults (3 MCD, 3 MGN, 1 FGS, 1 PGN, 1 IgA nephropathy) showed only that the low levels of IgG and subclasses were associated with relapses and reverted toward normal in remission.     

Effect of cyclosporine a on circulating immune complexes in IgA nephropathy

This work was undertaken to examine the effect of cyclosporine A (CyA) on the serum concentration of circulating immune complexes in 22 patients with IgA nephropathy during an infection-free period. They were randomly divided into 2 groups: 11 patients received oral cyclosporine A (5 mg/kg/day) for 12 weeks and 11 patients received placebo (0.05 ml/kg/day). A significant reduction of proteinuria was observed in patients on CyA therapy but not in those receiving placebo. IgG-circulating immune complexes (CIC) were determined by solid phase Clq enzyme immunoassay (Clq EIA) and radial immunodiffusion (RID) and IgA-CIC were determined by solid phase anti-C3 enzyme immunoassay (anti-C3 EIA) and radial immunodiffusion. There was no change in IgA-CIC measured by RID and anti-C3 EIA after 12 weeks of CyA therapy. Similarly, changes in IgG-CIC were not demonstrated with CyA therapy. No apparent decrease in IgG-CIC or IgA-CIC was observed with placebo treatment. Our study suggests that immunomodulation by CyA therapy does not affect the IgA-CIC and IgG-CIC levels in patients with IgA nephropathy.     

Mouse model of membranous nephropathy induced by cationic bovine serum albumin: antigen dose-response relations and strain differences.

BACKGROUND: Few well-characterized animal models have been developed to study the pathogenesis of membranous nephropathy (MN). We have developed a mouse model of MN induced by cationic bovine serum albumin (cBSA), and examined the role of genetic background on disease induction by assessing different mouse strains. METHODS: cBSA in an optimum dose was given intravenously to 8-week-old female ICR, BALB/c and C57BL/6 mice for 4 weeks. The disease state was verified by renal histopathology as well as by serum and urine metabolic profiles. Serum concentrations of anti-cBSA immunoglobulins (Igs) and circulating immune complex (CIC) were assayed to study the mechanisms of initiation and progression. T-helper (Th) cell subsets in peripheral blood were examined using flow cytometry, and the Th1/Th2 subset distribution was determined by comparing the serum concentrations of IgG1 and IgG2a, using quantitative heterologous interpolation enzyme-linked immunosorbent assays. RESULTS: Only ICR and BALB/c mice developed the typical clinical and pathological patterns of MN in response to an optimum dose of cBSA. Disease induction was dose related and strain specific. The serum concentrations of anti-cBSA were significantly higher in the strains that developed MN, but there were no differences in CIC concentrations. This suggests that in situ immune-complex glomerulonephritis may be involved in the development of MN. The Th2 type immune response may predominate in the ICR and BALB/c mice models, as the serum concentration of IgG1 was higher than that of IgG2a; moreover Th2 type strain specificity was necessary for the development of MN. CONCLUSIONS: This improved mouse model of MN induced by cBSA more closely duplicates human MN than the other available models. Disease generation is antigen dose related and strain specific.     

Monoclonal antibody analysis of glomerular, tubulo-interstitial infiltrating immune cells in various glomerulonephritis

To investigate the role of cell-mediated immunity (CMI) in glomerulonephritis (GN), we identified the infiltrating immune cells both within the glomerulus and in the interstitium. Frozen sections from 103 patients with various forms of GN: 10 with minor glomerular abnormality (MGA) as control, 10 with minimal change nephrotic syndrome (MCNS), 10 with membranous nephropathy (MN), 9 with focal glomerulosclerosis (FGS), 30 with IgA nephropathy (IgAN), 22 with acute post streptococcal glomerulonephritis (APSGN), and 2 with rapidly progressive glomerulonephritis (RPGN) were examined using monoclonal antibodies (MoAb) by indirect immunoalkaline-phosphatase labelling. In most glomerulonephritis, monocyte/M phi and helper/inducer T cells were predominantly infiltrating in the interstitium, but intraglomerular infiltration was rare, except for APSGN. This interstitial infiltration increased proportionally to the level of serum creatinine, and was most prominent in RPGN. Apparently different distribution was seen in APSGN, that is, prominent increase in total number of intra-glomerular monocyte/M phi infiltration with slightly increased T cells. The change was correlated with time after onset; namely the more leucocytic infiltration was observed when the tissue was taken earlier. These data suggest that in APSGN, monocyte/M phi accumulate in glomeruli via cell mediated immunity in addition to humoral immune mechanism resulting in glomerular hypercellularity, whereas in most chronic glomerulonephritis interstitial leucocyte infiltration, particularly helper T cells and monocyte/M phi may play an important role in the progression of glomerulonephritis.     

Evolution of antiglomerular basement membrane glomerulonephritis into membranous glomerulonephritis

Antiglomerular basement membrane glomerulonephritis (anti-GBM GN) is a rare disease characterized by autoantibodies to the alpha 3 chain of type IV collagen in the GBM. It is also known as Goodpasture’s syndrome when associated with pulmonary hemorrhage due to autoantibodies to the alpha 3 chain of type IV collagen also present in pulmonary alveoli. Even more rare is the evolution of anti-GBM GN into membranous nephropathy (MN). We report the management of a 9-year-old Caucasian girl with anti-GBM GN that evolved into MN and briefly review the literature.     

The spectrum of children's kidney diseases—9925 renal biopsy-proven cases from a single center of China between 2004 and 2017

Objective To analyze the spectrum of children's kidney pathology by renal biopsy. Methods The clinical and pathological data of the cases in Jinling Hospital involving the patients younger than 18 years old who received renal biopsy from April 1st, 2004 to December 31th, 2017 were retrospectively collected, and compared with the renal pathological data of 1611 children aged 0-18 years from June 1982 to March 2004. Results This study included 9925 cases of kidney diseases proven by renal biopsy. The ratio of male to female was 1.79∶1. Primary glomerulonephritis (PGN) accounted for 66.14%, and secondary glomerulonephritis (SGN) accounted for 28.00%. Top five of the PGN were IgA nephropathy (IgAN, 19.11%), mesangial proliferative glomerulonephritis (MsPGN, 16.07%), minimal change disease (MCD, 14.20%), focal segmental glomerulosclerosis (FSGS, 6.19%) and membranous nephropathy (MN, 4.70%) in whole children, IgAN (13.12%), MsPGN (11.20%), MCD(10.63%), FSGS (4.55%) and MN (2.54%) in males, and IgAN (5.99%), MsPGN (4.87%), MCD (3.57%), MN (2.16%) and FSGS (1.63%) in females. Top three of the SGN were Henoch-Schonlein purpura nephritis (HSPN, 17.74%), lupus nephritis (LN, 8.23%) and vasculitis nephropathy (1.82%). The male was in a dominant position in all kinds of pathologic types than female except LN. HSPN was the most frequent type in adolescents between 6-13 years old. LN was the commonest one in 14-18-year-old girls, while IgAN was the the most common in 14-18-year-old boys. Post infective nephritis was the most popular in 12-14-year-old teenagers. It was also found that MN ascended in female. When compared with the data before 2004, HSPN and LN accounted for a greater proportion in SGN, post infective nephritis displayed a smaller proportion. Conclusions PGN is the mainly kind of glomerular disease as before, and immune disorder related to glomerular diseases increase and post infective nephritis decreases in proportion. This study provides the reference and epidemic data for diagnosis, treatment and prevention of children's renal diseases.     

Mucosal immunity in primary glomerulonephritis: II. Study of the serum IgA subclass repertoire to food and airborne antigens.

IgA specific for 7 food and 6 airborne antigens were sought in the serum of 30 adult patients with IgA mesangial nephropathy (IgA GN), 23 with membranous nephropathy (MGN), 20 with idiopathic nephrotic syndrome (INS), 11 with membranoproliferative GN (MPGN) and 22 healthy controls by means of an enzyme-linked immunoassay. The IgA subclass was determined using monoclonal antibodies. Increased levels of IgA specific for gliadin, bovine serum albumin (BSA), ovalbumin, lysozyme and alpha-lactalbumin were found in IgA GN, while increased levels of IgA to BSA, ovalbumin, lysozyme and alpha-lactalbumin were observed in MGN; IgA specific for alpha-lactalbumin were increased in INS, and MPGN patients had reduced levels of IgA to BSA and increased levels of IgA to beta-lactoglobulin and alpha-lactalbumin. These specific IgA to food antigens were restricted to the IgA1 subclass. Patients with IgA GN had significantly increased levels of IgA specific for Dermatophagoides pteronyssinus (DP) and Dactil while the MGN group showed increased levels of IgA specific for DP, feathers, Dactil and mold. INS patients had increased levels of IgA specific for DP, feathers, Dactil, mold and dog hairs, while MPGN patients had increased levels of IgA specific for feathers, Dactil, dog hairs and mold. All these specific IgA to airborne antigens were restricted to the IgA1 subclass. Patients with the four types of primary glomerulonephritis had decreased IgA specific for cat hairs which were of both the IgA1 and IgA2 subclasses. We conclude that anomalies of the IgA repertoire to environmental antigens are also encountered in primary glomerulonephritis other than IgA GN.     

Analysis of 4931 renal biopsy data in central China from 1994 to 2014

The purpose of this study is to investigate the changing spectrum and clinicopathologic correlation of biopsy-proven renal diseases in central China. We retrospectively analyzed data of 4931 patients who underwent renal biopsy in ten hospitals between September 1994 and December 2014. Among them, 81.55% were primary glomerular diseases (GD), and 13.02% were secondary GD. IgA nephropathy (IgAN) was the most common primary GD (43.45%), followed by focal glomerulonephritis (16.79%), mesangial proliferative glomerulonephritis (MsPGN, 14.35%), and membranous nephropathy (MN, 13.28%). IgAN was leading primary GD in patients under 60 years old, while MN was the leading one over 60 years old. The most frequent secondary GD was lupus nephritis (LN) (47.35%). The prevalence of IgAN, MN and minimal change disease was found to increase significantly (p?<?0.001, p?<?0.001, and p?<?0.01, respectively), while that of MsPGN, membranoproliferative glomerulonephritis and LN decreased significantly (p?<?0.001, p?<?0.001, and p?<?0.05, respectively). The main indication for renal biopsy was proteinuria and hematuria (49.03%), followed by nephrotic syndrome (NS, 20.36%). IgAN was the most common cause in patients with proteinuria and hematuria, chronic-progressive kidney injury, hematuria and acute kidney injury; and MN was the leading cause of NS. Primary GD remained the predominant renal disease in central China. IgAN and LN were the most prevalent histopathologic lesions of primary and secondary GD, respectively. The spectrum of biopsy-proven renal disease had a great change in the past two decades. Proteinuria and hematuria was the main indication for renal biopsy.     

De novo glomerulonephritis in renal allografts with hepatitis C virus infection

The purpose of this study was to examine the influence of hepatitis C virus (HCV) infection on the occurrence of posttransplant de novo glomerulonephritis (GN). Of 165 patients selected for the study, 44 were HCV positive and 121 HCV negative. Light and immunofluorescence microscopy were performed on all biopsies and clinical and laboratory findings reviewed. Fifteen (34%) of the 44 HCV positive patients showed de novo GN (4 membranous, 11 membranoproliferative) at a mean of 47 +/- 22 months. But only 8 (6.6%) of 121 HCV negative patients showed de novo GN (5 anti-glomerular basement membrane nephritis in recipients with Alport's disease, 2 membranous GN, 1 membranoproliferative GN) at a mean of 60 +/- 39 months. The risk of development of de novo GN was higher among patients with HCV infection (P < .001). The presence of de novo GN in HCV positive patients impaired graft survival compared with HCV positive patients without de novo GN (P < .01). The incidence of recurrence of primary disease, mainly focal segmental glomerulosclerosis, membranous glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy, was higher in HCV negative patients (29%) compared with HCV positive patients (6.8%; P = .001), namely, 50%, 57.6%, 25%, and 69%, respectively. In conclusion, HCV infection showed a strong influence on the development of de novo GN. For this reason, it is important to follow HCV positive recipients with a renal biopsy even when there are no significant clinical or laboratory findings.