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

Uchida, Takahiro; Oda, Takashi

doi:10.3390/ijms21072595

Cited by 24 publications

(28 citation statements)

References 37 publications

(55 reference statements)

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“…[ 14 ] We believe the Gd-IgA1 was triggered by infection, since the secondary IgAN observed (IgA of lupus nephritis, hepatic IgAN, and Gd-IgA1) did not merge. [ 9 ] Additionally, as observed in our case, the Gd-IgA1 of staphylococcus associated glomerulonephritis showed weak to strong positive results. [ 15 ] Therefore, we suggest the therapeutic usefulness of Gd-IgA to diagnosis IRGN in kidney tissues, particularly when the case presents with Full house (IgG, IgA, IgM, C1q, C3, positive immunostaining) pattern.…”

Section: Discussionsupporting

confidence: 72%

“…[ 8 ] Therefore, NAPlr and plasmin activity have been proposed as the general biomarkers of bacterial IRGN. [ 9 ] On this basis, we diagnosed our case as IRGN, however, infection was not detected clinically. Whilst no cases of IgA-dominant IRGN with positive glomerular staining for NAPlr have been published to date, Kikuchi et al have reported a case of Henoch-Schonlein purpura (IgA vasculitis) with positive staining for NAPlr and plasmin activity in kidney glomeruli.…”

Section: Discussionmentioning

confidence: 90%

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Galactose-deficient IgA1 and nephritis-associated plasmin receptors as markers for IgA-dominant infection-related glomerulonephritis

et al. 2021

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Rational: Immunoglobulin A (IgA) nephropathy is a common heterogeneous kidney disease. One of the causes of secondary immunoglobulin A nephropathy is infection-related glomerulonephritis (IRGN), however, its accurate diagnosis is difficult. Patient concerns: We report a rare case of an 82-year-old male presenting rapidly progressive glomerulonephritis. Assessment of a kidney biopsy by light microscopy revealed endocapillary glomerulonephritis with subendothelial deposits, such as wire loop lesions and cellular crescents. Immunofluorescence demonstrated strong staining for IgA and C3 along the glomerular capillary. Additional tests included positive staining for nephritis-associated plasmin receptor and positive plasmin activity in the glomeruli. Moreover, IgA and galactose-deficient IgA1 (Gd-IgA1) staining merged using immunofluorescence, followed by confirmation of high serum levels of Gd-IgA1 (9.3 μg/mL) by ELISA was observed. Diagnosis: The diagnosis of IgA-dominant IRGN was made. Interventions and outcomes: We have initiated treatment with intravenous methylprednisolone 500 mg/day for 3 days, followed by oral prednisolone 25 mg/d as rapidly progressive glomerulonephritis. However immunosuppressive therapy was halted because of a poor response, and hemodialysis was initiated. Lessons: This is a case of IgA-dominant IRGN patient exhibiting positive glomerular staining for nephritis-associated plasmin receptor accompanied with high titers of serum Gd-IgA1. Our observations suggest that serum and kidney tissue of Gd-IgA1 may be useful for the diagnosis of IgA-dominant IRGN.

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 90%

Galactose-deficient IgA1 and nephritis-associated plasmin receptors as markers for IgA-dominant infection-related glomerulonephritis

et al. 2021

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“…In fact, the preceding infection might be an infection other than GAS, because the GAPDH of various bacteria show cross-immunoreactivity to the anti-NAPlr antibody, and simultaneously show plasmin-binding function [ 32 , 33 , 34 ]. From these results, NAPlr and associated plasmin activity are presently considered as general biomarkers of IRGN [ 35 ]. Positive glomerular staining of these markers usually disappears within 30 days after the onset of PSAGN [ 25 ].…”

Section: Persistent Infection As a Possible Cause Of The Progressimentioning

confidence: 99%

Factors Affecting the Progression of Infection-Related Glomerulonephritis to Chronic Kidney Disease

Oda

Yoshizawa

2021

IJMS

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Acute glomerulonephritis (AGN) triggered by infection is still one of the major causes of acute kidney injury. During the previous two decades, there has been a major paradigm shift in the epidemiology of AGN. The incidence of poststreptococcal acute glomerulonephritis (PSAGN), which develops after the cure of group A Streptococcus infection in children has decreased, whereas adult AGN cases have been increasing, and those associated with nonstreptococcal infections, particularly infections by Staphylococcus, are now as common as PSAGN. In adult AGN patients, particularly older patients with comorbidities, infections are usually ongoing at the time when glomerulonephritis is diagnosed; thus, the term “infection-related glomerulonephritis (IRGN)” has recently been popularly used instead of “post-infectious AGN”. The prognosis of children with PSAGN is generally considered excellent compared with that of adult IRGN cases. However, long-term epidemiological analysis demonstrated that an episode of PSAGN in childhood is a strong risk factor for chronic kidney disease (CKD), even after the complete remission of PSAGN. Although the precise mechanism of the transition from IRGN to CKD remains unknown, its clarification is important as it will lead to the prevention of CKD. In this review, we therefore focus on the possible factors that may contribute to the progression of IRGN into CKD. Four factors, namely, persistent infection, genetic background of the host’s complement system, tubulointerstitial changes, and pre-existing histological damage, are discussed.

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“…Nephritis-associated plasmin receptor (NAPlr) was isolated from the cytoplasmic fraction of group A streptococcus (GAS), and its deposition was reported to be observed in the glomeruli of patients with post-streptococcal acute glomerulonephritis (PSAGN) [6,7]. In addition, recently, glomerular NAPlr deposition was reported to be observed in not only patients with PSAGN but also those with other glomerular diseases, in whom a preceding bacterial infection had been suggested [8]. These findings indicate that glomerular NAPlr deposition can aid in making a diagnosis and reveal the pathogenesis of IRGN in patients with CGN.…”

Section: Introductionmentioning

confidence: 99%

A man with immunoglobulin A nephropathy complicated by infection-related glomerulonephritis with glomerular depositions of nephritis-associated plasmin receptor

et al. 2021

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A 27-year-old man who developed heavy proteinuria with hematuria and acute kidney injury 2 weeks after a fever was referred to our hospital. Because he had low complements without autoantibodies, we clinically diagnosed him with infectionrelated glomerulonephritis. The proliferation of mesangial cells and endothelial cells with glomerular deposits of immunoglobulin A and complement 3 was found. Deposition of glomerular nephritis-associated plasmin receptor, a marker of infection-related glomerulonephritis, was also found. In addition, the distribution of nephritis-associated plasmin receptor deposition almost perfectly matched the plasmin activity-positive region. Over 3 months later, his symptoms were resolved, although moderate proteinuria and active urine sediment were persistent. He underwent a second renal biopsy, and the histological findings revealed that he had immunoglobulin A nephropathy. Therefore, we diagnosed him with infection-related glomerulonephritis superimposed on immunoglobulin A nephropathy at the first renal biopsy. The glomerular deposition of nephritis-associated plasmin receptor is a useful marker and may cause worsening urinalysis findings after bacterial infection in cases of chronic glomerulonephritis.

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

Cited by 24 publications

References 37 publications

Galactose-deficient IgA1 and nephritis-associated plasmin receptors as markers for IgA-dominant infection-related glomerulonephritis

Galactose-deficient IgA1 and nephritis-associated plasmin receptors as markers for IgA-dominant infection-related glomerulonephritis

Factors Affecting the Progression of Infection-Related Glomerulonephritis to Chronic Kidney Disease

A man with immunoglobulin A nephropathy complicated by infection-related glomerulonephritis with glomerular depositions of nephritis-associated plasmin receptor

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