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At least 19 recordsLinked to original sources
PubMed1989

Distribution of familial nephritis antigen in normal tissue and renal basement membranes of patients with homozygous and heterozygous Alport familial nephritis. Relationship of familial nephritis and Goodpasture antigens to novel collagen chains and type IV collagen.

The glomerular basement membranes (GBM) of Alport familial nephritis (FN) are laminated and split and fail to bind Goodpasture autoantibodies by indirect immunofluorescence. The Goodpasture antigen has been localized to multiple peptides of the noncollagenous C terminal (NC1) domain of type IV collagen. The principal target antigen is a 28-kDa peptide (M28) that coisolates with type IV collagen NC1 and which is derived from a larger collagenous molecule. We have shown that two novel 28-kDa peptides found in normal GBM (M28M28+) are absent from collagenase digests of X-linked dominant Alport FN GBM and that monoclonal antibodies specific for these collagen chains fail to bind to Alport GBM. In normal tissue these chains have a distribution restricted to specific basement membranes of kidney, eye, inner ear, lung, and brain, the former three of which are affected in Alport FN. Epitopes on a 26-kDa NC1 peptide identified by an antibody from a transplanted Alport patient (FN antibody) colocalized with the 28-kDa components in these tissues. The FN antibody did not bind to the GBM of homozygous Alport males. Antibodies to the 28-kDa peptides and the FN antibody colocalized in a segmental pattern in heterozygous Alport GBM by indirect immunofluorescence and were unrelated to the normal distribution of type IV collagen. Three of eight homozygous Alport FN tissues showed the presence of the 28-kDa components in Bowman's capsule in a focal distribution, and in four of eight tissues reactive antigen was present in the cytoplasm of some parietal and visceral epithelial cells. These observations support the hypothesis that the genetic abnormality in Alport FN is a defective parent chain of the 26-kDa peptide, which results in failure of normal 28-kDa collagen chain integration.

Antibodies, Monoclonal↗
PubMed2000

The outcome of acute interstitial nephritis: risk factors for the transition from acute to chronic interstitial nephritis.

BACKGROUND: Acute interstitial nephritis has been known as a complication of mainly streptococcal infection for nearly a century. With the advent of infection control, it became a complication caused by antibiotics and later by other drugs, which might have changed the outcome. To determine risk factors for the development of chronic renal insufficiency, and thus, the transition from acute to chronic interstitial nephritis, we performed a retrospective study of all cases of acute interstitial nephritis found by reviewing 1,068 renal biopsies from 1968 to 1997. METHODS: Patients with permanent and reversible renal insufficiency after acute interstitial nephritis were compared with respect to the causative event, the symptoms, and the clinical and histological findings. Differences between the groups were calculated by applying bi- and multivariate analysis. RESULTS: Acute interstitial nephritis was found in 6.5% of all biopsies (64 patients with 68 episodes of acute interstitial nephritis); it was infection-induced in 10%, idiopathic in 4%, and drug-induced in 85% of the cases (antibiotics in 13 cases, analgesics in 17, non-steroidal anti-inflammatory drugs (NSAIDs) in 16, diuretics in 5, and various other drugs in 7). Renal insufficiency was reversible in 69% and permanent in 31% (12% partially reversible, 19% irreversible). The infection-induced and idiopathic types of acute interstitial nephritis were always reversible. Drug-related acute interstitial nephritis caused permanent renal insufficiency in 36% with a maximum of 56% in NSAID-induced cases. In drug-induced cases, intake of the suspected drug for more than a month prior to diagnosis caused permanent renal insufficiency in 88% and interstitial granuloma in 31%. Multivariate analysis disclosed the following significant features separating the permanent from the reversible renal insufficiency group: patients in the first group had more tubular atrophy in their histology, more chronic use of mixed analgesics and/or NSAIDs, less oliguria or anuria as an acute symptom, fewer antibiotics as causative agents, more interstitial granuloma, more pronounced interstitial cell infiltration in their histology, and more imaging of renal shrinkage. Renal histology had the highest predictive value. CONCLUSION: Today, acute interstitial nephritis is mainly drug-induced. NSAIDs are the most frequent cause of permanent renal insufficiency after acute interstitial nephritis. Clinically, subacute symptoms, a prolonged intake of the suspect drug, and chronic analgesic or NSAID use are related to a more chronic course of interstitial nephritis. In histology, tubular atrophy, interstitial granuloma, and pronounced interstitial cell infiltration indicate chronicity.

Acute Disease↗
PubMed1981

Heymann nephritis-DOCA-NaCl hypertension in the rat. Role of nephritis, DOCA, NaCl, and vascular lesions in the development of hypertension.

In order to explore the impact of nephritis on the development of hypertension, rats with Heymann nephritis were given 0.9% NaCl to drink, in combination with or without DOCA injections, for up to 6 months. Combined nephritis-DOCA-NaCl resulted in severe hypertension and shortened life span, whereas nephritis-NaCl combination failed to induce hypertension or shorten life span. All immunized rats developed membranous glomerulonephritis but creatinine clearance did not decrease. DOCA-NaCl-treated nephritic rats had a heavier proteinuria and more marked renal lesions than NaCl-treated nephritis rats. Proliferative-sclerotic glomerular lesions were seen in the nephritis-DOCA-NaCl group only, correlating to the severity of hypertension. Other renal and extrarenal vascular lesions, increasing with time, also appeared related to the severity of hypertension. This suggests a secondary relationship of vascular damage to hypertension in this model. Appearance of proteinuria preceded the establishment of hypertension, suggesting that nephritis sensitized to the development of hypertension during DOCA-NaCl treatment. Sodium excess alone, however, did not induce hypertension in Heymann nephritic rats. The present Heymann nephritis-DOCA-NaCl hypertension model appears a useful model for the study of hypertension complicating glomerulonephritis.

Animals↗
PubMed1989

Monocyte infiltration and cross-linked fibrin deposition in IgA nephritis and Henoch-Schoenlein purpura nephritis.

To clarify the role of immune cell infiltration and fibrin deposition in glomerular injury, renal biopsy specimens taken from patients with primary IgA nephritis and Henoch-Schönlein purpura nephritis (HSPN) were evaluated using monoclonal antibodies specific to mononuclear cell surfaces and cross-linked fibrin (XFb). Monocytes/macrophages were the predominant cell type infiltrating glomeruli in IgA nephritis and HSPN. The intraglomerular monocyte population in both diseases was significantly higher than that in normals, mesangial proliferative (non-IgA) glomerulonephritis or minimal change nephrotic syndrome. In IgA nephritis, there was a clear correlation between glomerular monocyte accumulation and the degree of proteinuria. Although the monocyte influx tended to decline with time in HSPN, it remained unchanged in IgA nephritis. XFb deposition was found in the glomeruli of 27 out of 48 patients with IgA nephritis, and in 15 out of 20 with HSPN. The degree of XFb deposition in IgA nephritis correlated significantly with the degree of mesangial proliferation. These findings indicate a close relationship of monocyte/macrophage infiltration and XFb deposition with glomerular injury in IgA nephritis.

Adolescent↗
PubMed1992

[A case report of lupus nephritis associated with minimal change nephrotic syndrome--comparison of various histological types of 67 cases with lupus nephritis].

A 22 year old male of lupus nephritis associated with minimal change nephrotic syndrome was described. The patient was well until 4 years earlier, when Raynaud's phenomenon and photosensitivity developed. One week before admission, edema appeared suddenly and proteinuria was pointed out on July 28, 1990. On admission, his legs, ankles, and eyelids were edematous. There was no sclerodactylia, although Raynaud's phenomenon was positive when his hand disclosed to the cold. Urinalysis showed heavy albuminuria (10.4g/day), but urinary sediment showed no abnormality. Immunological examination showed positive antinuclear antibody, determination at a titer of 1: 160 with a speckled pattern. Anti-RNP and anti-Sm antibody were positive. However, neither anti-DNA antibody nor hypocomplementemia was detected. There was high concentration of serum IgE (2564IU/ml). Renal biopsy was performed. Light microscopic study showed slight increase of mesangial cells and matrix. Immunofluorescence study showed mesangial localization of IgG and C3. Electron microscopic study showed electron dense deposits only in the mesangial area. The diagnosis of lupus nephritis associated with minimal change nephrotic syndrome (MCNS) was made and administration of PSL was started. Proteinuria disappeared after 3 weeks and nephrotic syndrome remitted completely. The case of lupus nephritis associated with MCNS is very rare. Therefore, the relationship between amounts of proteinuria and various histological types of 67 cases with lupus nephritis which we experienced at our hospital was evaluated. Results showed that nephrotic range proteinuria was not present in mesangial lupus nephritis. So, it was concluded that if heavy albuminuria was found in mesangial lupus nephritis, we should consider the possibility of lupus nephritis associated with MCNS.

Adult↗
PubMed1990

Idiotypic characteristics of immunoglobulins associated with human systemic lupus erythematosus. Association of high serum levels of IdGN2 with nephritis but not with HLA class II genes predisposing to nephritis.

Serum levels of IdGN2 (an idiotype enriched in nephritogenic antibodies), IdX (an idiotype not enriched in nephritogenic antibodies), IgG, and anti-DNA were measured in 23 Caucasian patients with lupus nephritis, in age- and sex-matched lupus patients without nephritis, and in similarly matched healthy individuals. Serum levels of IdGN2 were significantly higher in the patients with lupus nephritis than in those without, and they were higher in all lupus patients compared with the healthy control subjects. However, the same observations were true for serum levels of IdX. There were significant positive correlations between the serum levels of IgG, IdGN2, IdX, and anti-DNA. HLA typing at the DR and DQ loci was performed in 105 lupus patients of different races (Caucasian, black, and Asian/Polynesian/Filipino). Serum levels of IdGN2 in 83 of these individuals did not correlate with any of the HLA class II haplotypes currently known to predispose to lupus nephritis. We conclude that the high serum levels of IdGN2, which are characteristic of some patients with lupus nephritis, may often result from polyclonal B cell activation rather than from idiotype-specific upregulation associated with one or more of the class II genes that predispose to nephritis in this disease.

Genes, MHC Class II↗
PubMed2002

Induction of nephrotoxic serum nephritis in inbred mice and suppressive effect of colchicine on the development of this nephritis.

Accelerated nephrotoxic serum (NTS) nephritis is successfully produced in C57BL/6 mice, using anti-murine glomerular basement membrane (GBM) rabbit antiserum. Anti-murine GBM rabbits antiserum was obtained by immunization of New Zealand white rabbit with trypsinized GBM antigen from normal C57BL/6 mice. Preimmunization with normal rabbit IgG and injection with 150 microl of NTS induced typical NTS nephritis with cellular proliferation in glomeruli, occlusion of glomerular loops, crescents, tubulointerstitial changes and hyperazotemia within 14 days. Polymorphonuclear leucocytes (PMN) have an important role in induction and development of NTS nephritis. Furthermore, clinically used colchicine is thought to suppress functions of PMN. Therefore, the therapeutic effect of colchicine on NTS nephritis was examined. The histological score (HS) of the group treated with 60 microg kg (-1) of colchicine (2.8 +/- 0.5) was significantly lower than that of positive control group (4.03 +/- 0.3).The direct immunofluorescent microscopic study revealed that there is no quantitative difference in the deposition of rabbit IgG, mouse IgG and C3 in GBM between these two groups. Urinary protein excretion and hyperazotemia were significantly suppressed by treatment with 60 microg kg (-1) of colchicine. A NTS nephritis model was established, it was found that colchicine may have a suppressive effect on the development of glomerular nephritis.

Animals↗
PubMed1992

Role of antibodies to tubulointerstitial nephritis antigen in human anti-tubular basement membrane nephritis associated with membranous nephropathy.

We report three patients, from two unrelated families, with anti-tubular basement membrane (TBM) antibody nephritis associated with membranous nephropathy. This rare disorder is characterized by nephrotic syndrome, tubular dysfunction, and progression to renal failure. Direct immunofluorescent studies in these patients revealed linear IgG deposition along the proximal TBM, while circulating antibodies reacting with proximal TBM but not with glomerular basement membrane were identified by indirect immunofluorescence. Sera from all three patients reacted by enzyme-linked immunosorbent assay and Western immunoblotting with purified 58-kd tubulointerstitial nephritis (TIN) antigen isolated from TBM. Additional reactivity with a 175-kd component, which may be a higher-molecular-weight form of TIN antigen, was observed by immunoblotting. Since recurrent Fanconi syndrome was seen after transplantation in one patient, anti-TBM antibodies were removed by plasmapheresis prior to kidney transplantation in the other two patients. Neither patient has clinical evidence of recurrent anti-TBM nephritis in the allograft despite the posttransplantation reappearance of anti-TBM antibodies in the serum of one patient. Serologic and molecular HLA class I and class II polymorphism analysis has identified the presence of both HLA-B7 and -DRw8 antigens in two unrelated affected individuals (0.3% expected frequency in the white population). We conclude that sera from patients with anti-TBM nephritis associated with membranous nephropathy react with 58-kd TIN antigen previously implicated in the pathogenesis of primary anti-TBM nephritis. This rare autoimmune disorder may be HLA associated with B7 and/or DRw8, providing susceptibility to the disease. Further investigation is needed to understand the pathogenesis of recurrent anti-TBM nephritis in the renal allograft.

Antibodies, Anti-Idiotypic↗
PubMed1990

FK506, a novel immunosuppressive agent, induces antigen-specific immunotolerance in active Heymann's nephritis and in the autologous phase of Masugi nephritis.

FK506 is a new drug which has potent immunosuppressive activity. We studied its immunosuppressive effects on active Heymann's nephritis and the autologous phase of Masugi nephritis. The induction of active Heymann's nephritis was completely suppressed by FK506 injected simultaneously with the antigen (day 1) and then daily for 14 days at a dose of 0.64 mg/kg per day or more. With a lower dosage of this agent, antibody production and immune deposits in the glomerular basement membrane occurred despite the suppression of proteinuria. Similar results were obtained in rats on other treatment schedules (1-7 days or day 8-14 days duration). Rats that were prevented from developing Heymann's nephritis or the autologous phase of nephrotoxic antiserum nephritis by FK506 treatment exhibited a suppressed immune response to a second immunization of the same antigen even 4 weeks after cessation of drug administration: however, they developed antibodies when inoculated with other antigens. Rat peripheral leucocyte counts and serum creatinin were not remarkably influenced by the administration of FK506. These results indicate that FK506 has potent immunosuppressive activity, and it is suggested that it is able to induce an antigen-specific immunotolerance.

Animals↗
PubMed1991

Tubulointerstitial nephritis during the heterologous phase of nephrotoxic serum nephritis.

This study was designed to characterize the immunopathology of acute tubulointerstitial disease in nephrotoxic serum nephritis in nonsensitized rats. Groups of Lewis rats were studied at 12 time periods ranging from 10 min to 28 days after nephrotoxic serum injection. Nephritic rats developed interstitial nephritis during the acute heterologous phase of renal injury. Coincident with the focal deposition of nephrotoxic antibodies along tubular basement membranes at 24 h, an influx of polymorphonuclear cells and macrophages was evident. The most prominent infiltrate, present between days 3 and 7, was dominated by macrophages with smaller numbers of lymphocytes that were mainly cytotoxic T cells. Dual-labeling studies demonstrated the colocalization of linear tubular basement membrane deposits of the nephrotoxic antibody with focal clusters of interstitial lymphohemopoietic cells. Increased complement deposition was not evident along the tubular basement membranes; moreover, C3 depletion with cobra venom factor failed to attenuate the interstitial inflammation. During the late autologous phase of glomerulonephritis, tubular basement membrane deposits of rat IgG did not appear and the interstitial disease resolved. The results of this study demonstrate that the heterologous phase of nephrotoxic serum nephritis is an antibody-mediated disease directed against the basement membranes not only of the glomeruli but also of some tubules. Antibody deposition is followed by an acute influx of phagocytic cells to both regions of the kidney. These cells may play an important role in the genesis of acute interstitial injury and chronic interstitial fibrosis associated with antiglomerular basement membrane nephritis.

Albuminuria↗
PubMed1996

[Henoch-Schoenlein purpura-nephritis followed by IgA-nephritis in 3 children].

In three patients, two boys of 7 and 10 and a girl of 9 years old, a kidney disease was diagnosed which evolved from Schönlein-Henoch nephritis to IgA nephropathy or Berger's disease. These two kidney diseases show striking similarities in pathological and immunological respects. Several patients have been described in the literature who suffered from both clinical pictures consecutively and of families in which different members showed either one or the other disease. A remarkable finding was the persistence of an elevated IgA serum level in all three children after the Schönlein-Henoch nephritis had subsided. These cases show the importance of long-term follow up of patients who had Schönlein-Henoch nephritis, in order to diagnose late renal complications at an early stage. They also give more evidence in favour of the assumption that Schönlein-Henoch nephritis and IgA nephropathy have a common aetiology.

Child↗
PubMed1987

Nonfamilial hematuria associated with glomerular basement membrane alterations characteristic of hereditary nephritis: comparison with hereditary nephritis.

Characteristic ultrastructural alterations of the glomerular basement membrane (GBM) have been reported in hereditary nephritis and in children without a family history of renal disease. The clinical features, renal biopsy findings, and subsequent course were studied retrospectively in 48 children with such GBM changes to compare findings in those with and without a family history of nephritis and to determine the significance of the GBM changes in patients with nonfamilial disease. All 48 patients had hematuria. For 30, there was hematuria in at least one other member of the family (familial hematuria group); for 18, there was no familial incidence. There were no differences between the two groups with regard to clinical and pathologic findings. At the latest follow-up six boys with familial hematuria and three boys with nonfamilial hematuria had reduced renal function, and nine boys with familial hematuria and four boys and one girl with nonfamilial hematuria had neurosensory deafness. Our study results show that children with these GBM changes, with or without a family history of hematuria, tend to have a progressive course, with frequent occurrence of neurosensory deafness, and that the prognosis is more severe in boys. These observations suggest that such GBM changes in patients with nonfamilial hematuria may represent new mutations for hereditary nephritis.

Basement Membrane↗
PubMed1996

Pan-nephritis (glomerulonephritis, arteriolitis, and tubulointerstitial nephritis) associated with predominant mesangial C1q deposition and hypocomplementemia: a variant type of C1q nephropathy?

A 35-year-old man showed acute nephritic syndrome manifested as proteinuria, hematuria, and hypocomplementemia after upper respiratory infection. A renal biopsy showed mild to moderate mesangial proliferative glomerulonephritis with an accumulation of mononuclear cells in the capillary loop and with the deposition of C1q (graded as 3+), immunoglobulin (Ig) G, C3 (2+), IgA, IgM, and fibrinogen (weak to 1+), and mononuclear cell infiltration of the glomerular hilus, arterioles, and proximal tubules, which was a peculiar form of renal lesion. The mesangial deposition of C1q has been well documented in lupus nephritis, membranoproliferative glomerulonephritis, and endocapillary glomerulonephritis. The clinical signs and laboratory data in our patient ruled out these diseases. Although an immunofluorescence study showed these similarities to Clq nephropathy, the histopathological features of the peculiar arteriolitis and tubulointerstitial nephritis and laboratory findings of hypocomplementemia, as well as the good response to oral steroid therapy, differed from typical C1q nephropathy. The current patient appears to be a very rare phenotype of nephritis, being the only 1 case in almost 2,800 renal biopsies.

Adult↗
PubMed1991

Circulatory antigen of Heymann nephritis. III. Presence of the 70-kD circulatory protein in the immune deposits of Heymann nephritis.

An antigen of 70 kD size has been isolated previously from normal rat serum which has immunological cross-reactivity to the Heymann nephritis antigen, F x 1A. Its role in the pathogenesis of Heymann's nephritis was unknown. In this investigation we tested for the presence of 70-kD circulatory antigen in the glomerular immune deposits of Heymann's nephritis. Further, its presence was correlated with severity of disease. It was observed that the presence of the 70-kD antigen strongly correlated with the existence of electron-dense deposits in the lamina rara externa (LRE) of the glomerular capillary wall and with pathologic proteinuria. Temporally, the presence of the 70-kD antigen in the immune deposits was followed by large electron-dense deposits, enhanced complement activity and proteinuria. The data suggest that in the growing immune complex lattice in the LRE, the 70-kD circulatory antigen by virtue of its small size, mobility and antigen cross-reactivity facilitates cross linking and coalescence of immune complexes, resulting in electron-dense immune deposits (EDD) formation which initiates complement activation and consequent proteinuria.

Animals↗
PubMed1994

The significance of tubulointerstitial nephritis in IgA nephritis.

The occurrence of significant tubulointerstitial nephritis (TIN) was observed in 6 (18.3%) of 32 patients with IgA nephritis registered in 1991. T lymphocytes and macrophages in the interstitium were seen to invade the tubulus through injured tubular basement membrane (TBM), then were seen in the intercellular spaces of tubular cells which showed degeneration, single cell necrosis or detachment. Thus some tubular components were seen destroyed and had disappeared resulting in interstitial fibrosis, and others showed a regeneration process forming a renewed TBM on the innerside of the original TBM. However the recurrence of cellular inflammation was again observed in these regenerated tubuli. Thus the progression of nephron loss by TIN was seen to be independent of the glomerular changes and TIN is considered to be one of the important factors in predicting the prognosis of IgA nephritis.

Adolescent↗
PubMed1994

[Effects of cyclosporin A on experimental nephritis in rats (2): Cyclosporin A suppresses the development of accelerated passive Heymann nephritis].

We investigated the effects of cyclosporin A (CyA) on accelerated passive Heymann nephritis, an experimental model of membranous nephropathy, that is characterized by immune complex deposition on the glomerular basement membrane. The nephritis was induced in rats by injection of antiserum against the antigen located in the renal tubular brush border membrane and sensitization with rabbit gamma-globulin. CyA was administered p.o. at the dose of 2.5, 10 or 20 mg/kg/day for 40 days after the injection of the antiserum. The administration of CyA resulted in marked suppression of proteinuria and hypercholesterolemia in the nephritic rats. In light microscopy, nephritic control rats showed thickening of the glomerular basement membrane and spike formation in the glomeruli. CyA significantly reduced the appearance of the glomerular alteration. The production of antibody was dramatically attenuated by CyA administration. However, CyA did not decrease the number of circulating white blood cells and platelets below the normal level. In conclusion, CyA suppressed the progress of accelerated passive Heymann nephritis in a dose-dependent manner. The effect of CyA is likely attributable to the powerful depression of antibody production.

Animals↗