Special Issue "Role of Innate Immunity in Chronic Kidney Diseases"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (16 August 2023) | Viewed by 3324

Special Issue Editor

Katz Family Division of Nephrology and Hypertension, University of Miami Miller School of Medicine, Miami, FL, USA
Interests: kidney; podocytes; lipids; lipid droplet; sphingolipids; innate immunity; diabetic kidney disease; focal segmental glomerulosclerosis
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Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) is a worldwide health problem, with a global estimated prevalence of 16% and costs of USD 7.1 million for renal replacement therapy for patients with end-stage kidney disease. Among the multiple pathogenic mechanisms responsible for CKD, deregulated inflammation, oxidative stress, and immune system activation have deserved significant attention in recent years. More precisely, sterile inflammation triggered by the activation of the innate immune system has been shown to be an important driver of CKD. While our understanding of the innate immune system’s components and ligands, as well as its activation and regulation, has substantially improved in recent years, finding new drug targets and implementations of anti-inflammatory treatments for patients with CKD remains a challenge. This Special Issue will focus on different aspects of innate immunity involvement in CKD development and progression, including molecular, biochemical, and physiological mechanisms. We welcome original basic research and clinical manuscripts, reports on new technologies, methodological reports, and review articles related to the role of innate immunity in CKD.

Dr. Alla Mitrofanova
Guest Editor

Manuscript Submission Information

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Keywords

  • CKD
  • glomeruli
  • tubules
  • sterile inflammation
  • innate immunity
  • pattern recognition receptors (PRRs)
  • damage-associated molecular patterns (DAMPs)
  • STING
  • Toll-like receptors
  • RIG-I
  • NLRP

Published Papers (3 papers)

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Research

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Article
Expression of Interferon Regulatory Factor 8 (IRF8) and Its Association with Infections in Dialysis Patients
Cells 2023, 12(14), 1892; https://doi.org/10.3390/cells12141892 - 19 Jul 2023
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Abstract
Patients on dialysis have dysfunctions of innate and adaptive immune system responses. The transcriptional factor IRF8 (interferon regulatory factor 8) is primarily expressed in plasmacytoid cells (pDCs) and myeloid dendritic cells (mDCs), playing a crucial role in the maturation of dendritic cells, monocytes, [...] Read more.
Patients on dialysis have dysfunctions of innate and adaptive immune system responses. The transcriptional factor IRF8 (interferon regulatory factor 8) is primarily expressed in plasmacytoid cells (pDCs) and myeloid dendritic cells (mDCs), playing a crucial role in the maturation of dendritic cells, monocytes, and macrophages, and contributing to protection against bacterial infections. The current study analyzed the expression patterns of IRF8 and assessed its association with the risk of infections in 79 dialysis patients compared to 44 healthy controls. Different subsets of leukocytes and the intracellular expression of IRF8 were measured using flow cytometry. Compared to the healthy controls, the dialysis patients showed significantly reduced numbers of pDCs and significantly increased numbers of natural killer cells and classical and intermediate monocytes. The dialysis patients exhibited decreased numbers of IRF8-positive dendritic cells (pDC p < 0.001, mDC1 p < 0.001, mDC2 p = 0.005) and increased numbers of IRF8-positive monocytes (p < 0.001). IRF8 expression in pDC, mDC, and classical monocytes was lower in the dialysis patients than in the controls. Dialysis patients who required hospitalization due to infections within one year of follow-up displayed significantly reduced IRF8 expression levels in pDCs compared to patients without such infections (p = 0.04). Our results suggest that reduced IRF8 expression in pDCs is a potential risk factor predisposing dialysis patients to serious infections. Full article
(This article belongs to the Special Issue Role of Innate Immunity in Chronic Kidney Diseases)
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Article
Diagnostic and Prognostic Comparison of Immune-Complex-Mediated Membranoproliferative Glomerulonephritis and C3 Glomerulopathy
Cells 2023, 12(5), 712; https://doi.org/10.3390/cells12050712 - 23 Feb 2023
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Abstract
Membranoproliferative glomerulonephritis (MPGN) is subdivided into immune-complex-mediated glomerulonephritis (IC-MPGN) and C3 glomerulopathy (C3G). Classically, MPGN has a membranoproliferative-type pattern, but other morphologies have also been described depending on the time course and phase of the disease. Our aim was to explore whether the [...] Read more.
Membranoproliferative glomerulonephritis (MPGN) is subdivided into immune-complex-mediated glomerulonephritis (IC-MPGN) and C3 glomerulopathy (C3G). Classically, MPGN has a membranoproliferative-type pattern, but other morphologies have also been described depending on the time course and phase of the disease. Our aim was to explore whether the two diseases are truly different, or merely represent the same disease process. All 60 eligible adult MPGN patients diagnosed between 2006 and 2017 in the Helsinki University Hospital district, Finland, were reviewed retrospectively and asked for a follow-up outpatient visit for extensive laboratory analyses. Thirty-seven (62%) had IC-MPGN and 23 (38%) C3G (including one patient with dense deposit disease, DDD). EGFR was below normal (≤60 mL/min/1.73 m2) in 67% of the entire study population, 58% had nephrotic range proteinuria, and a significant proportion had paraproteins in their serum or urine. A classical MPGN-type pattern was seen in only 34% of the whole study population and histological features were similarly distributed. Treatments at baseline or during follow-up did not differ between the groups, nor were there significant differences observed in complement activity or component levels at the follow-up visit. The risk of end-stage kidney disease and survival probability were similar in the groups. IC-MPGN and C3G have surprisingly similar characteristics, kidney and overall survival, which suggests that the current subdivision of MPGN does not add substantial clinical value to the assessment of renal prognosis. The high proportion of paraproteins in patient sera or in urine suggests their involvement in disease development. Full article
(This article belongs to the Special Issue Role of Innate Immunity in Chronic Kidney Diseases)
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Review

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Review
The Role of Inflammation in CKD
Cells 2023, 12(12), 1581; https://doi.org/10.3390/cells12121581 - 07 Jun 2023
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Abstract
Chronic kidney disease (CKD) affects many adults worldwide. Persistent low-grade inflammation is a substantial factor in its development and progression and has correlated with increased mortality and cardiovascular problems. This low-grade inflammation is a product of dysregulation of the normal balance between pro- [...] Read more.
Chronic kidney disease (CKD) affects many adults worldwide. Persistent low-grade inflammation is a substantial factor in its development and progression and has correlated with increased mortality and cardiovascular problems. This low-grade inflammation is a product of dysregulation of the normal balance between pro- and anti-inflammatory markers. Various factors such as increased innate immune system activation, reactive oxygen species production, periodontal disease, dysregulation of anti-inflammatory systems and intestinal dysbiosis result in the dysregulation of this balance. Furthermore, this low-grade inflammation has down-effects such as hypertension, renal fibrosis and acceleration of renal function decline. Moreover, low-grade inflammation over time has been linked to malignancy in CKD. As CKD progresses, many patients require dialysis, which has a negative bidirectional relationship with persistent inflammation. Treatment options for inflammation in CKD are vast, including cytokine inhibitors, statins and diets. However, more research is needed to create a standardized management plan. In this review, we will examine the normal physiology of the kidney and its relationship with the immune system. We will then delve into the pathology behind persistent inflammation, the various causes of inflammation, the downstream effects of inflammation, dialysis and potential treatments for inflammation in CKD. Full article
(This article belongs to the Special Issue Role of Innate Immunity in Chronic Kidney Diseases)
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