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Clinical Advances in Lupus Nephritis
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Clinical Advances in Lupus Nephritis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Nephrology & Urology".

Deadline for manuscript submissions: closed (25 March 2022) | Viewed by 12090

Special Issue Editor

Dr. Roberta Fenoglio

E-Mail Website
Guest Editor
Department of Clinical and Biological Sciences, Center of Research of Immunopathology and Rare Diseases-Nephrology and Dialysis S. Giovanni Bosco Hospital, University of Turin, Turin, Italy
Interests: glomerulonephritis; vasculitis; lupus nephritis; autoimmunity;

Special Issue Information

Dear Colleagues,

Systemic lupus erythematosus (SLE) is the prototype of autoimmune conditions characterised by an abnormal autoimmune response associated with a loss of tolerance to endogenous nuclear antigens leading to inflammation in various tissues. Lupus nephritis (LN) can occur in up to 60% of patients with SLE and represents a major cause of morbidity and mortality. A growing body of recent insights into the genetic and molecular mechanisms in SLE and LN has triggered the development of novel therapies for these patients. The B-cell-centred approaches have been paralleled by the identification of additional multiple extrarenal and intrarenal pathways contributing to kidney-specific autoimmunity leading to the investigation of novel therapeutic strategies. The formerly induction-maintenance treatment approaches were recently challenged by the promising results obtained from trials that evaluated add-on therapy with voclosporin, belimumab, or obinutuzumab. The scope of this Special Issue is to provide a critical insight into the current knowledge of LN pathogenesis and future therapeutic strategies.

Dr. Roberta Fenoglio

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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • lupus nephritis
  • systemic lupus erythematosus
  • kidney biopsy, B-cells
  • rituximab
  • obinutuzumab
  • anifrolumab
  • belimumab
  • interferon
  • neutrophils
  • pathogenesis
  • voclosporin

Published Papers (4 papers)

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Research

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13 pages, 2180 KiB  
Article
Serum and Urine Interferon Gamma-Induced Protein 10 (IP-10) Levels in Lupus Nephritis
by Makayla P. Brady, Saiteja Chava, Shweta Tandon, Madhavi J. Rane, Michelle T. Barati, Dawn J. Caster and David W. Powell
J. Clin. Med. 2022, 11(11), 3199; https://doi.org/10.3390/jcm11113199 - 3 Jun 2022
Cited by 3 | Viewed by 1865
Abstract
Background: Lupus nephritis (LN) is a prevalent and severe complication of systemic lupus erythematosus (SLE). Non-invasive diagnostics are limited, and current therapies have inadequate response rates. Expression of the chemokine Interferon-γ-induced protein 10 (IP-10) is regulated by Interferon-γ signaling and NF-κB, and its [...] Read more.
Background: Lupus nephritis (LN) is a prevalent and severe complication of systemic lupus erythematosus (SLE). Non-invasive diagnostics are limited, and current therapies have inadequate response rates. Expression of the chemokine Interferon-γ-induced protein 10 (IP-10) is regulated by Interferon-γ signaling and NF-κB, and its molecular activity and enhanced urine concentrations are implicated in LN, but its utility as a diagnostic marker and association with demographic, clinical, or pathologic features is not defined. Methods: 38 LN patients and 11 patients with non-LN glomerular diseases (GD) with active disease were included. Eighteen of the LN patients had achieved remission at one follow-up during the study time. Serum and urine were obtained from these samples, and the IP-10 levels were measured. Results: Serum and urine IP-10 levels are significantly enhanced in LN patients with active disease as compared with normal individuals (serum average 179.7 pg/mL vs. 7.2 pg/mL, p < 0.0001; urine average 28.7 pg/mg vs. 1.6 pg/mg, p = 0.0019) and patients with other forms of glomerular disease (serum average 179.7 pg/mL vs. 84.9 pg/mL, p = 0.0176; urine average 28.7 pg/mg vs. 0.18 pg/mg, p = 0.0011). Urine IP-10 levels are significantly higher in patients with proliferative LN (PLN) than those with membranous LN (MLN) (average 32.8 pg/mg vs. 7.6 pg/mg, p = 0.0155). Urine IP-10 levels are also higher in MLN versus primary membranous nephropathy (MN) (average 7.6 pg/mg vs. 0.2 pg/mg, p = 0.0193). Importantly, serum IP-10 levels remain elevated during active LN and LN remission, but urine IP-10 levels are decreased from active LN to remission in 72% of our patients. Lastly, serum, but not urine IP-10 levels are significantly higher in African American than White American LN patients in active LN (average 227.8 pg/mL vs. 103.4 pg/mL, p = 0.0309) and during LN remission (average 254.6 pg/mL vs. 89.2 pg/mL, p = 0.0399). Conclusions: Our findings suggest that serum and urine IP-10 measurements provide promising tests for monitoring LN activity, differentiation between classifications of LN, and differentiation between LN and other forms of glomerular disease. We also conclude that further assessment of elevated IP-10 levels in the serum and urine of high-risk populations (i.e., African American) could be beneficial in determining why many of these patients have worse outcomes and are non-responsive to standard therapeutics. Full article
(This article belongs to the Special Issue Clinical Advances in Lupus Nephritis)
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8 pages, 866 KiB  
Article
Dickkopf Homolog 3 (DKK3) as a Prognostic Marker in Lupus Nephritis: A Prospective Monocentric Experience
by Savino Sciascia, Alice Barinotti, Massimo Radin, Irene Cecchi, Elisa Menegatti, Edoardo Terzolo, Daniela Rossi, Simone Baldovino, Roberta Fenoglio and Dario Roccatello
J. Clin. Med. 2022, 11(11), 2977; https://doi.org/10.3390/jcm11112977 - 25 May 2022
Cited by 6 | Viewed by 1657
Abstract
Background: The gold standard for diagnosis of lupus nephritis (LN) is still represented by renal biopsy, and serological prognostic biomarkers are still lacking. Dickkopf homolog-3 (DKK3) has been suggested as a marker of tissue fibrosis in different conditions; however, its role in autoimmune [...] Read more.
Background: The gold standard for diagnosis of lupus nephritis (LN) is still represented by renal biopsy, and serological prognostic biomarkers are still lacking. Dickkopf homolog-3 (DKK3) has been suggested as a marker of tissue fibrosis in different conditions; however, its role in autoimmune diseases needs to be elucidated. Here, we investigated the prognostic role of DKK3 in systemic lupus erythematosus (SLE) patients with and without LN, assessing its changes in relation to kidney function, flares, and interstitial fibrosis. Methods: Overall, 132 SLE patients (57 with LN) were included and prospectively followed up for at least 36 months. DKK3 was measured in serum at baseline. Biopsies were evaluated for glomerular involvement, interstitial fibrosis, and tubular atrophy. Results: Patients with biopsy-proven LN had significantly higher levels of DKK3 than those without (median [min–max]: 215 ng/mL [81–341] vs. 21.1 ng/mL [1–69], p < 0.01). DKK3 levels were associated with prevalent chronic kidney diseases (OR: 4.31 [C.I. 2.01–6.61] per DKK3 doubling, p < 0.01), higher chronicity index at biopsy (1.75 [1.51–2.77] per DKK3 doubling, p < 0.01), and flares rate (OR: 1.45 [C.I. 1.1–5.71] per DKK3 doubling, p < 0.044). Conclusions: While kidney biopsy still represents the gold standard for diagnostic and prognostic assessment in LN, DKK3 could represent an additional prognostic tool to monitor SLE patients and guide therapeutic choices. Full article
(This article belongs to the Special Issue Clinical Advances in Lupus Nephritis)
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Review

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30 pages, 474 KiB  
Review
Current Insights on Biomarkers in Lupus Nephritis: A Systematic Review of the Literature
by Leonardo Palazzo, Julius Lindblom, Chandra Mohan and Ioannis Parodis
J. Clin. Med. 2022, 11(19), 5759; https://doi.org/10.3390/jcm11195759 - 28 Sep 2022
Cited by 15 | Viewed by 4669
Abstract
Lupus nephritis (LN) is a major cause of morbidity and mortality among patients with systemic lupus erythematosus (SLE). However, promising emerging biomarkers pave the way toward an improved management of patients with LN. We have reviewed the literature over the past decade, and [...] Read more.
Lupus nephritis (LN) is a major cause of morbidity and mortality among patients with systemic lupus erythematosus (SLE). However, promising emerging biomarkers pave the way toward an improved management of patients with LN. We have reviewed the literature over the past decade, and we herein summarise the most relevant biomarkers for diagnosis, monitoring, and prognosis in LN. An initial systematic search of Medline was conducted to identify pertinent articles. A total of 104 studies were selected to be included in this review. Several diagnostic biomarkers, including MCP-1, TWEAK, NGAL, and uric acid, exhibited good ability to differentiate LN patients from non-renal SLE patients. Several cytokines and chemokines, including IL-10, IL-17, MCP-1, and IP-10, hold promise for assessing LN disease activity, as do cell adhesion molecules (CAMs). Angiogenesis-related and haemostasis-related proteins have also displayed potential for monitoring disease activity. Biomarkers of responses to therapy include Axl, CD163, and BAFF, whereas VCAM-1, ALCAM, and ANCAs have been reported as prognostic markers, along with traditional markers. In addition, novel renal tissue biomarkers may prove to be a useful complement to histological evaluations. The overall heterogeneity of the inclusion criteria and outcome measures across different studies, along with a lack of validation in multi-centre cohorts, call for future collaborative efforts. Nevertheless, we foresee that several biomarkers hold promise toward optimisation of the management of LN, with the use of integrated omics and panels of less invasive biomarkers paving the way towards personalised medicine. Full article
(This article belongs to the Special Issue Clinical Advances in Lupus Nephritis)
15 pages, 792 KiB  
Review
Old and New Calcineurin Inhibitors in Lupus Nephritis
by Claudio Ponticelli, Francesco Reggiani and Gabriella Moroni
J. Clin. Med. 2021, 10(21), 4832; https://doi.org/10.3390/jcm10214832 - 21 Oct 2021
Cited by 12 | Viewed by 7917
Abstract
Calcineurin inhibitors (CNIs) are drugs that inhibit calcineurin, a key phosphatase that dephosphorylates a transcription factor called the nuclear factor of activated T cells (NFAT), allowing its translocation into the nucleus of quiescent T cells. In the nucleus, NFAT activates interleukin 2, which [...] Read more.
Calcineurin inhibitors (CNIs) are drugs that inhibit calcineurin, a key phosphatase that dephosphorylates a transcription factor called the nuclear factor of activated T cells (NFAT), allowing its translocation into the nucleus of quiescent T cells. In the nucleus, NFAT activates interleukin 2, which stimulates the proliferation and differentiation of T-cells. CNIs can also stabilize the actin cytoskeleton of podocytes reducing proteinuria. Thanks to these characteristics, CNIs have been often used in the treatment of autoimmune diseases. However, the therapeutic index of CNIs is narrow, and their interactions with other drugs can increase toxicity or reduce efficacy. In lupus nephritis, cyclosporine and tacrolimus have been used both in induction and maintenance therapies. Observational studies and randomized controlled trials showed that both cyclosporine and tacrolimus can increase efficacy. Tolerance is satisfactory if low doses are used and the patient is carefully monitored. More recently, a new CNI, called voclosporin (VCS), has been approved by the Food and Drug Administration for use in lupus nephritis. VCS offers potential advantages over other CNIs. In two large multiethnic trials, VCS was not associated with adverse renal and metabolic events and obtained positive results despite a novel and rapid corticosteroid tapering regime. Full article
(This article belongs to the Special Issue Clinical Advances in Lupus Nephritis)
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