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Infection and the Kidney 2.0
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Infection and the Kidney 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 March 2024) | Viewed by 8546

Special Issue Editor

Prof. Dr. Takashi Oda

E-Mail Website
Guest Editor
Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Tokyo 193-0998, Japan
Interests: rapidly progressive glomerulonephritis; ANCA-associated vasculitis; infection-related glomerulonephritis; post-infectious acute glomerulonephritis; renal interstitial fibrosis; renal transplantation–recurrence of glomerulonephritis; renal transplantation-infection-related complications; role of complements in renal disease; chronic kidney disease; kidney diseases caused by viral infection; kidney diseases caused by bacterial infection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Infection is known to induce kidney parenchymal injury directly or indirectly through various mechanisms in various renal diseases. For example, severe bacterial infection can cause sepsis that may involve the kidneys in the form of acute kidney injury (AKI), which is a life-threatening condition. It has also been recently revealed that severe infection with COVID-19 can frequently lead to the development of AKI. Direct infection with a virus (such as BK virus) in the parenchyma of the kidneys leads to tubulo-interstitial nephritis, which is a common, kidney-threatening condition in transplanted kidneys. On the other hand, certain infections (bacterial or viral, focal or systemic) can indirectly relate to the development of various renal diseases, such as infection-related glomerulonephritis (IRGN), IgA-dominant IRGN, IgA nephropathy, IgA vasculitis, ANCA-associated glomerulonephritis, and thrombotic microangiopathy (TMA), through various mechanisms, such as nephritogenic bacterial protein with related plasmin activity, bacterial toxin with super-antigenic property, formation of autoantibodies (ANCA, ANA, anti-DNA antibody, antibodies to complement components, etc.), bacterial neuraminidase exposing hidden antigens to naturally existing autoantibodies, and so on.

A detailed understanding of the mechanisms of the relationship between infection and the kidneys is important because it may also lead to the elucidation of the pathogenic mechanism of idiopathic renal diseases. This Special Issue, “Infection and the Kidneys”, welcomes case reports, original research and review articles in the field, with a focus on but not limited to kidney injury directly or indirectly related with infection, such as sepsis-associated AKI, AKI in COVID-19, IRGN, IgA-IRGN, IgA nephropathy, IgA vasculitis, infection-induced ANCA-associated glomerulonephritis, infection-associated TMA, and direct viral infection on transplanted kidney.

Prof. Dr. Takashi Oda
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • sepsis-associated acute kidney injury (AKI)
  • COVID-19-associated AKI
  • infection-related glomerulonephritis (IRGN)
  • IgA-dominant IRGN
  • IgA nephropathy
  • IgA vasculitis
  • autoantibody
  • ANCA-associated vasculitis
  • thrombotic microangiopathy
  • viral infection on transplanted kidneys

Published Papers (5 papers)

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Research

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16 pages, 8288 KiB  
Article
Investigation of Clinical Features and Association between Vascular Endothelial Injury Markers and Cytomegalovirus Infection Associated with Thrombotic Microangiopathy in Patients with Anti-Neutrophil Cytoplasmic Antibody (ANCA)-Associated Vasculitis: Case-Based Research
by Takayuki Nimura, Daiki Aomura, Makoto Harada, Akinori Yamaguchi, Kosuke Yamaka, Takero Nakajima, Naoki Tanaka, Takashi Ehara, Koji Hashimoto and Yuji Kamijo
Int. J. Mol. Sci. 2024, 25(2), 812; https://doi.org/10.3390/ijms25020812 - 09 Jan 2024
Viewed by 847
Abstract
Anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) can occasionally trigger thrombotic microangiopathy (TMA). Cytomegalovirus (CMV) may be reactivated during intensive immunosuppressive therapy for AAV and cause TMA. Therefore, we aimed to evaluate the clinical features of and the association between vascular endothelial injury markers and [...] Read more.
Anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) can occasionally trigger thrombotic microangiopathy (TMA). Cytomegalovirus (CMV) may be reactivated during intensive immunosuppressive therapy for AAV and cause TMA. Therefore, we aimed to evaluate the clinical features of and the association between vascular endothelial injury markers and TMA due to CMV in patients with AAV. A 61-year-old female was diagnosed with AAV and severe kidney injury. Immunosuppressive therapy gradually improved her symptoms and laboratory findings. However, 2 weeks after induction therapy initiation, she exhibited altered consciousness, a significant decrease in platelet count, and hemolytic anemia, resulting in a TMA diagnosis. Plasma exchange did not improve TMA findings and routine screening test revealed CMV infection. Ganciclovir injection improved the infection and TMA findings. Consequently, we diagnosed her with CMV-induced TMA. Both AAV and CMV may induce severe vascular endothelial injury, potentially leading to TMA development. CMV-induced TMA should be considered when TMA develops during induction therapy against AAV. Moreover, of the three serum markers of vascular injury—serum sulfatides, soluble thrombomodulin, and pentraxin 3—serum sulfatides may be associated with the development of TMA, and a high level of soluble thrombomodulin may be associated with the development of CMV viremia during the clinical course of AAV. Full article
(This article belongs to the Special Issue Infection and the Kidney 2.0)
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12 pages, 2018 KiB  
Article
Pre-Existing Intrarenal Parvovirus B19 Infection May Relate to Antibody-Mediated Rejection in Pediatric Kidney Transplant Patients
by Nicola Bertazza Partigiani, Susanna Negrisolo, Andrea Carraro, Diana Marzenta, Elisabetta Manaresi, Giorgio Gallinella, Luisa Barzon and Elisa Benetti
Int. J. Mol. Sci. 2023, 24(11), 9147; https://doi.org/10.3390/ijms24119147 - 23 May 2023
Cited by 1 | Viewed by 1245
Abstract
Viral infections can lead to transplant dysfunction, and their possible role in rejection is described. In total, 218 protocol biopsies performed in 106 children at 6, 12 and 24 months after transplantation were analyzed according to Banff ’15. RT-PCR for cytomegalovirus, Epstein-Barr virus, [...] Read more.
Viral infections can lead to transplant dysfunction, and their possible role in rejection is described. In total, 218 protocol biopsies performed in 106 children at 6, 12 and 24 months after transplantation were analyzed according to Banff ’15. RT-PCR for cytomegalovirus, Epstein-Barr virus, BK virus and Parvovirus B19 was performed on blood and bioptic samples at the time of transplant and each protocol biopsy. The prevalence of intrarenal viral infection increases between 6 and 12 months after transplantation (24% vs. 44%, p = 0.007). Intrarenal Parvovirus B19 infection is also associated with antibody-mediated rejection (ABMR) (50% ABMR vs. 19% T-cell-mediated rejection, p = 0.04). Moreover, Parvovirus infection is higher at 12 months of follow-up and it decreases at 48 months (40.4% vs. 14%, p = 0.02), while in 24% of grafts, Parvovirus is already detectable at the moment of transplantation. Intrarenal Parvovirus B19 infection seems to be related to ABMR in pediatric kidney recipients. The graft itself may be the way of transmission for Parvovirus, so performance of a PCR test for Parvovirus B19 should be considered to identify high-risk patients. Intrarenal Parvovirus infection presents mainly during the first-year post-transplantation; thus, we recommend an active surveillance of donor-specific antibodies (DSA) in patients with intrarenal Parvovirus B19 infection during this period. Indeed, it should be considered a treatment with intravenous immunoglobulins in patients with intrarenal Parvovirus B19 infection and DSA positivity, even in the absence of ABMR criteria for kidney biopsy. Full article
(This article belongs to the Special Issue Infection and the Kidney 2.0)
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Review

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14 pages, 1652 KiB  
Review
Clinico-Pathogenic Similarities and Differences between Infection-Related Glomerulonephritis and C3 Glomerulopathy
by Yukihiro Wada, Mariko Kamata, Ryoma Miyasaka, Tetsuya Abe, Sayumi Kawamura, Kazuhiro Takeuchi, Togo Aoyama, Takashi Oda and Yasuo Takeuchi
Int. J. Mol. Sci. 2023, 24(9), 8432; https://doi.org/10.3390/ijms24098432 - 08 May 2023
Cited by 5 | Viewed by 3292
Abstract
Recently, the comprehensive concept of “infection-related glomerulonephritis (IRGN)” has replaced that of postinfectious glomerulonephritis (PIGN) because of the diverse infection patterns, epidemiology, clinical features, and pathogenesis. In addition to evidence of infection, hypocomplementemia particularly depresses serum complement 3 (C3), with endocapillary proliferative and [...] Read more.
Recently, the comprehensive concept of “infection-related glomerulonephritis (IRGN)” has replaced that of postinfectious glomerulonephritis (PIGN) because of the diverse infection patterns, epidemiology, clinical features, and pathogenesis. In addition to evidence of infection, hypocomplementemia particularly depresses serum complement 3 (C3), with endocapillary proliferative and exudative GN developing into membranoproliferative glomerulonephritis (MPGN); also, C3-dominant or co-dominant glomerular immunofluorescence staining is central for diagnosing IRGN. Moreover, nephritis-associated plasmin receptor (NAPlr), originally isolated from the cytoplasmic fraction of group A Streptococci, is vital as an essential inducer of C3-dominant glomerular injury and is a key diagnostic biomarker for IRGN. Meanwhile, “C3 glomerulopathy (C3G)”, also showing a histological pattern of MPGN due to acquired or genetic dysregulation of the complement alternative pathway (AP), mimics C3-dominant IRGN. Initially, C3G was characterized by intensive “isolated C3” deposition on glomeruli. However, updated definitions allow for glomerular deposition of other complement factors or immunoglobulins if C3 positivity is dominant and at least two orders of magnitude greater than any other immunoreactant, which makes it challenging to quickly distinguish pathomorphological findings between IRGN and C3G. As for NAPlr, it was demonstrated to induce complement AP activation directly in vitro, and it aggravates glomerular injury in the development of IRGN. A recent report identified anti-factor B autoantibodies as a contributing factor for complement AP activation in pediatric patients with PIGN. Moreover, C3G with glomerular NAPlr deposition without evidence of infection was reported. Taken together, the clinico-pathogenic features of IRGN overlap considerably with those of C3G. In this review, similarities and differences between the two diseases are highlighted. Full article
(This article belongs to the Special Issue Infection and the Kidney 2.0)
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Other

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8 pages, 954 KiB  
Brief Report
Involvement of Innate Immune System in the Pathogenesis of Sepsis-Associated Acute Kidney Injury
by Takahiro Uchida, Muneharu Yamada, Dan Inoue, Tadasu Kojima, Noriko Yoshikawa, Shingo Suda, Hidenobu Kamohara and Takashi Oda
Int. J. Mol. Sci. 2023, 24(15), 12465; https://doi.org/10.3390/ijms241512465 - 05 Aug 2023
Cited by 1 | Viewed by 964
Abstract
Although experimental models have shown that the innate immune system is a main contributor to acute kidney injury (AKI), its involvement in human sepsis-associated AKI (SA-AKI) remains unclear. We retrospectively evaluated 19 patients with SA-AKI who were treated with continuous renal replacement therapy [...] Read more.
Although experimental models have shown that the innate immune system is a main contributor to acute kidney injury (AKI), its involvement in human sepsis-associated AKI (SA-AKI) remains unclear. We retrospectively evaluated 19 patients with SA-AKI who were treated with continuous renal replacement therapy (CRRT). Serum cytokine, complement components, and the proportion and functions of innate immune cells, such as CD56+ T cells, CD56+ natural killer (NK) cells, and monocytes, were analyzed. There were no differences in the proportions of CD56+ T and NK cells between patients with SA-AKI and healthy controls. In patients with SA-AKI, fas ligand (FasL) expression in CD56+ T cells was significantly upregulated, and the proportion of perforin-positive CD56+ T cells tended to be higher than that in healthy controls. The positive rate of both FasL and perforin of CD56+ T cells was significantly higher than that of CD56- T cells, which include cytotoxic T cells. Antigen-presenting capacity and phagocytic activity of monocytes in patients with SA-AKI were significantly decreased compared to those of healthy controls and did not recover soon after the initiation of CRRT. CD56+ T cells are involved in the disease processes of human SA-AKI through effector molecules such as FasL or perforin. Full article
(This article belongs to the Special Issue Infection and the Kidney 2.0)
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6 pages, 3174 KiB  
Case Report
Infection-Related Cryoglobulinemic Glomerulonephritis with Serum Anti-Factor B Antibodies Identified and Staining for NAPlr/Plasmin Activity Due to Infective Endocarditis
by Takumi Toishi, Takashi Oda, Atsuro Hamano, Shinnosuke Sugihara, Tomohiko Inoue, Atsuro Kawaji, Kanako Nagaoka, Masatoshi Matsunami, Junko Fukuda, Mamiko Ohara and Tomo Suzuki
Int. J. Mol. Sci. 2023, 24(11), 9369; https://doi.org/10.3390/ijms24119369 - 27 May 2023
Viewed by 1509
Abstract
In this rare case of infection-related cryoglobulinemic glomerulonephritis with infective endocarditis, a 78-year-old male presented with an acute onset of fever and rapidly progressive glomerulonephritis. His blood culture results were positive for Cutibacterium modestum, and transesophageal echocardiography showed vegetation. He was diagnosed [...] Read more.
In this rare case of infection-related cryoglobulinemic glomerulonephritis with infective endocarditis, a 78-year-old male presented with an acute onset of fever and rapidly progressive glomerulonephritis. His blood culture results were positive for Cutibacterium modestum, and transesophageal echocardiography showed vegetation. He was diagnosed with endocarditis. His serum immunoglobulin M, IgM-cryoglobulin, and proteinase-3-anti-neutrophil cytoplasmic antibody levels were elevated, and his serum complement 3 (C3) and C4 levels were decreased. Renal biopsy results showed endocapillary proliferation, mesangial cell proliferation, and no necrotizing lesions on light microscopy, with strong positive staining for IgM, C3, and C1q in the capillary wall. Electron microscopy showed deposits in the mesangial area in the form of fibrous structures without any humps. Histological examination confirmed a diagnosis of cryoglobulinemic glomerulonephritis. Further examination showed the presence of serum anti-factor B antibodies and positive staining for nephritis-associated plasmin receptor and plasmin activity in the glomeruli, suggesting infective endocarditis-induced cryoglobulinemic glomerulonephritis. Full article
(This article belongs to the Special Issue Infection and the Kidney 2.0)
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