Glomerular proliferating cell kinetics in acute post-streptococcal glomerulonephritis (APSGN)

Oda, Takashi; Yoshizawa, Nobuyuki; Takeuchi, Akihiko; Nakabayashi, Iwao; Nishiyama, Junichiro; Ishida, Aki; Tazawa, Keiji; Murayama, Masahiro; Hasegawa, Osamu; Taguma, Yoshio

doi:10.1002/(sici)1096-9896(199711)183:3<359::aid-path939>3.0.co;2-b

Cited by 23 publications

(16 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, NAPlr as well as complement components are associated with APSGN (22)(23)(24). In the study presented here, the deposition of C3 without IgG in glomeruli in 9 of 25 patients 1 to 14 d after APSGN onset and the lack of circulating anti-NAPlr antibody in 4 of 50 patients suggest that complement components are associated with the initial inflammatory reaction (25)(26)(27). In addition, NAPlr cleaved C3 to C3b in human serum in vitro.…”

Section: Discussionmentioning

confidence: 52%

Nephritis-Associated Plasmin Receptor and Acute Poststreptococcal Glomerulonephritis

Yoshizawa¹,

Yamakami²,

Fujino³

et al. 2004

Journal of the American Society of Nephrology

117

View full text Add to dashboard Cite

Abstract. The role of nephritis-associated antigen as a virulence factor for acute poststreptococcal glomerulonephritis (APSGN) remains to be fully clarified. Nephritis-associated plasmin receptor (NAPlr) was previously isolated from group A streptococcus (GAS) and shown to bind plasmin(ogen). The nucleotide sequence of the naplr gene from GAS isolates obtained from patients with APSGN was determined. The sequence of the putative open reading frame (1011 bp) showed 99.8% identity among isolated strains. Homology screen revealed an exact match with streptococcal glyceraldehyde-3-phosphate dehydrogenase (GAPDH). NAPlr exhibited GAPDH activity in zymography, and it activated the complement pathway in vitro. In APSGN kidney biopsy specimens, NAPlr was observed mainly in the early stage of the disease (1 to 14 d after onset) but was not colocalized with either C3 or IgG as assessed by double immunofluorescence staining. Sera of patients with APSGN, patients with GAS infection without renal involvement, nonrenal pediatric patients, and healthy adults as controls were assayed for antiNAPlr antibody titers. Anti-NAPlr antibodies were present most frequently in APSGN sera, and antibody titers were also significantly higher than in patients with GAS infection alone or in other control patients. Moreover, antibody titers remained elevated during the entire 10-yr follow-up period.

show abstract

Section: Discussionmentioning

confidence: 52%

Nephritis-Associated Plasmin Receptor and Acute Poststreptococcal Glomerulonephritis

Yoshizawa¹,

Yamakami²,

Fujino³

et al. 2004

Journal of the American Society of Nephrology

117

View full text Add to dashboard Cite

show abstract

“…Interstitial macrophages, myofibroblasts and proliferating cells in paraffin-embedded sections of kidneys of UUO-R mice treated with MC-1 were evaluated by immunoperoxidase staining for macrophages, a-SMA and proliferating cell nuclear antigen (PCNA) as described previously. 23,26 Cryostat sections (5-mm thick) of fresh frozen kidney were used for IF staining. Kidney sections from sham-operated, UUO and UUO-R mice were used for epimorphin staining, and kidney sections from MC-1-treated UUO-R mice were used for E-cadherin staining.…”

Section: Uuo Model and Uuo-r Modelmentioning

confidence: 99%

Involvement of epimorphin in the repair of experimental renal fibrosis in mice

Yamada¹,

Oda²,

Higashi³

et al. 2010

Laboratory Investigation

Self Cite

View full text Add to dashboard Cite

Interaction between epithelial cells and mesenchymal cells is essential in normal organ morphogenesis and in tissue repair after injury. Epimorphin, a mesenchymal protein that regulates epithelial morphogenesis through epithelialmesenchymal interactions, has recently attracted attention as an important modulator of tissue repair. In this study we analyzed the role of epimorphin in renal fibrosis. We first found a progressive increase in epimorphin expression corresponding to the progression of renal fibrosis in mice with unilateral ureteral obstruction (UUO). To determine whether this expression has a role in the repair or progression of renal fibrosis, we analyzed a model of renal fibrosis repair, the UUO-release (UUO-R) model. Epimorphin expression was increased at 3 and 7 days after the UUO-R rather than on the day of release, but was decreased at 21 days after the release. Inhibition of endogenous epimorphin with antiepimorphin antibody (MC-1) significantly delayed the repair of fibrosis. When compared with normal-IgG-injected mice, MC-1-injected mice showed significantly decreased renal matrix metalloproteinase (MMP)-2 and MMP-9 expressions by western blotting and increased expression of TGF-b and collagen-I mRNA by real-time RT-PCR. Recombinant epimorphin induced prominent increases in MMP-2 and MMP-9 activities in the culture media of renal interstitial fibroblasts in vitro. These findings indicate that epimorphin has a pivotal role in the repair of renal fibrosis by modulating both extracellular matrix (ECM) degradation and its production.

show abstract

“…The present evidence suggests that immune complexes are formed with streptococcal antigens, localize on the glomerular capillary wall, and initiate a proliferative and inflammatory response. The mechanisms of renal injury remain to be elucidated [9,10,11,12].…”

Section: Introductionmentioning

confidence: 99%

Post-streptococcal acute glomerulonephritis in Chile?20�years of experience

Berríos

Lagomarsino

Solar

et al. 2004

Pediatric Nephrology

View full text Add to dashboard Cite

In order to characterize the epidemiological and clinical picture of post-streptococcal acute glomerulonephritis (PSAGN), a prospective study was designed to investigate all admissions to a general hospital of a local health service in Chile. The protocol included the investigation of previous streptococcal infections (SI), clinical symptoms and signs, socioeconomic situation (SES), throat and skin swabs for the isolation of group A beta-hemolytic streptococci, sequential determination of serum antistreptolysin O (ASO) titer, anti-DNAase B antibodies, and C3. During the 20 years studied, 926 cases were admitted (56% males). Incidence showed an endemic period (EP) 1980-1983, an epidemic outbreak (EO) 1984-1989, and a late period (LP) 1990-1999, with a rate per 100,000 inhabitants of 6.2, 13.2, and 1.7, respectively. The clinical picture was similar in the three periods. SES was homogeneous, with 80% of the population in low and middle-low categories. The average size of the family was 6.9 compared with 4.8 in the general population. Pyoderma was more frequent than pharyngeal infection, and more so during the EO. The isolation rate of group A beta-hemolytic streptococci from the pharynx was 20% compared with 60% from skin swabs. During EP, the most prevalent serotypes were T14-M0 and T1-M1 from the pharynx and TImp19-M0 from the skin. During EO, T14-M0 was more prevalent (30%). M or T classification was possible in EP and EO in 80%-85% of all strains isolated from the two locations. Significant titers for ASO and anti-DNAase B were found on admission: 55% and 75%, respectively. Both tests allowed identification of 100% of previous SI. In conclusion, the incidence of PSAGN had an uneven trend during the observed period. EO was mainly due to skin infection and a predominance of one serotype, T14-MO, was observed. After the EO, the yearly rate gradually decreased from 13.2 in 1988 to 0.0 in 1999, a rate similar to that of industrialized nations.

show abstract

Glomerular proliferating cell kinetics in acute post-streptococcal glomerulonephritis (APSGN)

Cited by 23 publications

References 22 publications

Nephritis-Associated Plasmin Receptor and Acute Poststreptococcal Glomerulonephritis

Nephritis-Associated Plasmin Receptor and Acute Poststreptococcal Glomerulonephritis

Involvement of epimorphin in the repair of experimental renal fibrosis in mice

Post-streptococcal acute glomerulonephritis in Chile?20�years of experience

Contact Info

Product

Resources

About