A case of idiopathic membranoproliferative glomerulonephritis with a transient glomerular deposition of nephritis-associated plasmin receptor antigen

Okabe, Masahiro; Tsuboi, Nobuyuki; Yokoo, Takashi; Miyazaki, Yoichi; Utsunomiya, Yasunori; Hosoya, Tatsuo

doi:10.1007/s10157-011-0570-6

Cited by 9 publications

(10 citation statements)

References 14 publications

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“…The unique glomerular staining patterns of NAPlr and plasmin activity were found not only in patients with PSAGN but also in some patients with other glomerular diseases, such as C3 glomerulopathy [18,19], membranoproliferative glomerulonephritis (MPGN) type I [20,21], antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (both ANCA positive [22] and negative [23]), and IgA vasculitis [24], in which a preceding streptococcal infection is suggested by serological markers, and these cases are referred to as SIRN [2,25]. Although prominent endocapillary proliferation is a common histological feature, the differences in immune responses of the affected hosts may affect the specific histology.…”

Section: Streptococcal Infection-related Nephritis (Sirn): Glomerularmentioning

confidence: 99%

Glomerular Deposition of Nephritis-Associated Plasmin Receptor (NAPlr) and Related Plasmin Activity: Key Diagnostic Biomarkers of Bacterial Infection-related Glomerulonephritis

Uchida

Oda

2020

IJMS

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It is widely known that glomerulonephritis (GN) often develops after the curing of an infection, a typical example of which is GN in children following streptococcal infections (poststreptococcal acute glomerulonephritis; PSAGN). On the other hand, the term “infection-related glomerulonephritis (IRGN)” has recently been proposed, because infections are usually ongoing at the time of GN onset in adult patients, particularly in older patients with comorbidities. However, there has been no specific diagnostic biomarker for IRGN, and diagnosis is based on the collection of several clinical and pathological findings and the exclusion of differential diagnoses. Nephritis-associated plasmin receptor (NAPlr) was originally isolated from the cytoplasmic fraction of group A streptococcus as a candidate nephritogenic protein for PSAGN and was found to be the same molecule as streptococcal glyceraldehyde-3-phosphate dehydrogenase and plasmin receptor. NAPlr deposition and related plasmin activity were observed with a similar distribution pattern in the glomeruli of patients with PSAGN. However, glomerular NAPlr deposition and plasmin activity could be observed not only in patients with PSAGN but also in patients with other glomerular diseases, in whom a preceding streptococcal infection was suggested. Furthermore, such glomerular staining patterns have been demonstrated in patients with IRGN induced by bacteria other than streptococci. This review discusses the recent advances in our understanding of the pathogenesis of bacterial IRGN, which is characterized by NAPlr and plasmin as key biomarkers.

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Section: Streptococcal Infection-related Nephritis (Sirn): Glomerularmentioning

confidence: 99%

Glomerular Deposition of Nephritis-Associated Plasmin Receptor (NAPlr) and Related Plasmin Activity: Key Diagnostic Biomarkers of Bacterial Infection-related Glomerulonephritis

Uchida

Oda

2020

IJMS

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“…Sethi et al described that most of the cases with biopsy-proven PIGN presenting persistent hematuria and proteinuria had underlying defects with genetic mutations and/or auto-antibodies affecting regulation of the alternative complement pathway [ 9 ]. In addition, several reports have demonstrated the presence of nephritis-associated plasmin receptor (known as NAPlr), a nephritogenic antigen for post-streptococcal acute glomerulonephritis, in cases with C3G [ 65 , 69 , 70 ]. These findings indicate that glomerular injuries initiated by infection may transfer to C3G by switching activation of the alternative complement pathway.…”

Section: Introductionmentioning

confidence: 99%

C3 glomerulopathy and current dilemmas

2016

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C3 glomerulopathy (C3G) is a recently identified disease entity caused by dysregulation of the alternative complement pathway, and dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) are its components. Because laboratory detection of complement dysregulation is still uncommon in practice, “dominant C3 deposition by two orders greater than that of immunoglobulins in the glomeruli by immunofluorescence”, as stated in the consensus report, defines C3G. However, this morphological definition possibly includes the cases with glomerular diseases of different mechanisms such as post-infectious glomerulonephritis. In addition, the differential diagnosis between DDD and C3GN is often difficult because the distinction between these two diseases is based solely on electron microscopic features. Recent molecular and genetic advances provide information to characterize C3G. Some C3G cases are found with genetic abnormalities in complement regulatory factors, but majority of cases seem to be associated with acquired factors that dysregulate the alternative complement pathway. Because clinical courses and prognoses among glomerular diseases with dominant C3 deposition differ, further understanding the background mechanism, particularly complement dysregulation in C3G, is needed. This may resolve current dilemmas in practice and shed light on novel targeted therapies to remedy the dysregulated alternative complement pathway in C3G.

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“…A renal biopsy showed membranoproliferative glomerulonephritis (MPGN) type I accompanied by the deposition of NAPlr. To the best of our knowledge, only a small number of reports have described MPGN type I as a renal pathological finding of SIRN (7,8). We herein discuss the pathogenesis of this case.…”

Section: Introductionmentioning

confidence: 92%

Streptococcal Infection-related Nephritis (SIRN) Manifesting Membranoproliferative Glomerulonephritis Type I

et al. 2016

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We herein report the case of an 18-year-old boy who developed nephrotic syndrome and hypertension after upper airway inflammation. Post-streptococcal acute glomerulonephritis was diagnosed on the basis of a high antistreptolysin O titer, hypocomplementemia, proteinuria, and microscopic hematuria. A renal biopsy was performed due to persistent proteinuria, and the pathological diagnosis was membranoproliferative glomerulonephritis (MPGN) type I. Glomeruli showed positive staining for nephritis-associated plasmin receptor (NAPlr), a nephritogenic group A streptococcal antigen, and plasmin activity was found in a similar distribution as NAPlr deposition. This rare case of streptococcal infection-related nephritis (SIRN) manifesting MPGN type I supports the histological diversity of SIRN.

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A case of idiopathic membranoproliferative glomerulonephritis with a transient glomerular deposition of nephritis-associated plasmin receptor antigen

Cited by 9 publications

References 14 publications

Glomerular Deposition of Nephritis-Associated Plasmin Receptor (NAPlr) and Related Plasmin Activity: Key Diagnostic Biomarkers of Bacterial Infection-related Glomerulonephritis

Glomerular Deposition of Nephritis-Associated Plasmin Receptor (NAPlr) and Related Plasmin Activity: Key Diagnostic Biomarkers of Bacterial Infection-related Glomerulonephritis

C3 glomerulopathy and current dilemmas

Streptococcal Infection-related Nephritis (SIRN) Manifesting Membranoproliferative Glomerulonephritis Type I

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