Comparative Study of IgA Nephropathy with Acute and Insidious Onset

Suzuki, Satoru; Sato, Hírokazu; Kobayashi, Hiroyuki; Takayama, Ryuichi; Maruyama, Yoshihiro; Ogino, Soujirou; Ueno, Hideki; Inomata, Akira; Nishi, Shinichi; Saito, Takao; In, Hian; Arakawa, Masaaki

doi:10.1159/000168413

Cited by 30 publications

(16 citation statements)

References 7 publications

(8 reference statements)

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“…Histopathologic findings of kidney biopsy specimens of IgAN patients were classified according to the classification described previously (Suzuki et al, 1992). A single pathologist evaluated all specimens by light microscopy in a double-blind fashion.…”

Section: Histopathological Analysismentioning

confidence: 99%

Genetic Polymorphism of NPHS1 Modifies the Clinical Manifestations of Ig A Nephropathy

Narita

Goto

Saito

et al. 2003

Laboratory Investigation

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SUMMARY:Nephrin, the molecule responsible for congenital nephrotic syndrome of Finnish type, is crucial in maintaining the glomerular filtration barrier. Recently, its complete gene structure and common gene polymorphisms in its exons have been reported, although the functional and clinical significance of these polymorphisms has not yet been elucidated. We investigated a possible association of the NPHS1 polymorphisms with the development of Ig A nephropathy (IgAN), as well as the clinical and histologic manifestations in IgAN. A total of 464 Japanese subjects, including 267 patients with histologically proven IgAN and 197 healthy controls with normal urinalysis, were genotyped for the NPHS1 G349A, G2289A, and T3315C polymorphisms. The frequencies of the genotypes, alleles, and estimated haplotypes of NPHS1 polymorphisms were no different between patients with IgAN and the controls. Within the IgAN group, patients carrying at least one G allele of G349A tended to present with more proteinuria, lower renal function, and more severe histopathologic injury than those with the AA genotype, although the time from the first urinary abnormality to the renal biopsy was no different between both groups. The logistic regression analysis indicated that even after adjusting for the effect of proteinuria and hypertension the GG genotype of NPHS1 G349A was an independent risk factor for the deteriorated renal function at the time of diagnosis. This study suggests that the NPHS1 G349A polymorphism may be associated with heavy proteinuria and a decline in renal function in patients with IgAN. (Lab Invest 2003, 83:1193-1200.

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Section: Histopathological Analysismentioning

confidence: 99%

Genetic Polymorphism of NPHS1 Modifies the Clinical Manifestations of Ig A Nephropathy

Narita

Goto

Saito

et al. 2003

Laboratory Investigation

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“…The glomerular changes, degree of proliferation of mesangial cells (C) and expansion of mesangial matrices (M), were classified into the following six categories (C0-C5, M0-M5) as previously reported [24]: grade 0 (C0, M0), no light microscopic abnormalities; grade 1 (C1, M1), segmental, mild; grade 2 (C2, M2), segmental, moderate; grade 3 (C3, M3), global, mild; grade 4 (C4, M4), global, moderate, and grade 5 (C5, M5), global, marked. Other glomerular lesions, including sclerotic lesions, adhesions, crescentic formations, exudative lesions, endocapillary proliferation, or duplications of the glomerular basement membrane (GBM), and nonglomerular changes, such as arterial or arteriolar sclerosis, or tubulointerstitial lesions, were also evaluated.…”

Section: Light Microscopic Examinationmentioning

confidence: 99%

Significance of Glomerular Deposition of C3c and C3d in IgA Nephropathy

et al. 2000

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Background: Complement activation plays an important role in the pathogenesis of IgA nephropathy. The clinico-pathological significance of the glomerular deposition of complement breakdown products, C3c and C3d in IgA nephropathy remains to be clarified. Methods: We examined the relationship between glomerular staining patterns of C3c and C3d and clinico-pathological findings with 163 patients with IgA nephropathy. Renal biopsy specimens were stained with C3c and C3d by immunofluorescence, and patients were divided into the following two groups: the intensity of C3c deposition stronger than C3d deposition, or equal to it (group A); the intensity of C3d deposition stronger than C3c deposition (group B). Results: In group A, the incidence of severe hematuria (over 20 urinary red blood cells in high-power field microscope (×400)) or of higher urinary fibrinogen degenerated products (over 0.1 μg/ml) was significantly higher than that in group B. In addition, group A showed a significant decrease in the glomerular filtration rate. Group A also showed a significantly higher incidence of glomerular endocapillary proliferation than in group B. Conclusion: These findings suggest that the glomerular deposition of C3c is associated with the inflammatory active phase of glomeruli in IgA nephropathy.

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“…Although the antigen of the deposited IgA has not been precisely determined, several bacteria probably induce antibacteria-specific IgA in IgAN patients (3 -6). The acute onset of IgAN is associated with mucosal infections, such as tonsillitis or pharyngitis (7). Consequently, tonsillectomy has been reported to be an efficient therapeutic method for IgAN (8).…”

Section: Introductionmentioning

confidence: 99%

Production of Interferon-?by Tonsillar Mononuclear Cells in IgA Nephropathy Patients

Fujieda

Sunaga²,

Yamamoto³

et al. 2000

Acta Oto-Laryngologica

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Much evidence, both in vivo and in vitro, suggests that patients with IgA nephropathy (IgAN) have enhanced IgA production. We hypothesized that Haemophilus parainfluenzae (HP) in the tonsil plays an important role in the IgA production of IgAN patients. In this study, we focused on interferon-gamma (IFN-gamma) and IgA production by tonsillar mononuclear cells (TMC) in patients with IgAN. Tonsillectomies were performed in patients with IgAN and chronic tonsillitis (CT). The induction of IFN-gamma and IgA in vitro by TMC from IgAN patients was compared with that from CT patients. In addition, we investigated whether stimulation with the outer membranes of HP (OMHP) enhanced IFN-gamma and IgA induction by TMC from patients with IgAN. Spontaneous IFN-gamma production and spontaneous total IgA production by TMC were higher in IgAN patients than in those patients with CT (p < 0.05). IFN-gamma induction by OMHP stimulation was also higher in IgAN patients than in CT patients. The stimulation of OMHP enhanced HP-specific IgA in IgAN but had no influence on the production of IFN-gamma in patients with either IgAN or CT compared with spontaneous IFN-gamma production. IFN-gamma production was positively correlated with total IgA values in both IgAN and CT patients, but not with HP-specific IgA. These results suggest that increased IFN-gamma production in patients with IgAN is not associated with HP infection but may play a role in the pathogenesis of IgAN.

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Comparative Study of IgA Nephropathy with Acute and Insidious Onset

Cited by 30 publications

References 7 publications

Genetic Polymorphism of NPHS1 Modifies the Clinical Manifestations of Ig A Nephropathy

Genetic Polymorphism of NPHS1 Modifies the Clinical Manifestations of Ig A Nephropathy

Significance of Glomerular Deposition of C3c and C3d in IgA Nephropathy

Production of Interferon-?by Tonsillar Mononuclear Cells in IgA Nephropathy Patients

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