Urine macrophages reflect kidney macrophage content during acute tubular interstitial and glomerular injury

Sun, Pingping; Zhou, Xu‐jie; Su, Jincang; Wang, Chen; Yu, Xiao‐Juan; Su, Tao; Liu, Gang; Wang, Suxia; Nie, Jing; Yang, Li

doi:10.1016/j.clim.2019.06.005

Cited by 23 publications

(23 citation statements)

References 30 publications

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“…Research focus has shifted from identifying Mφ expression to analyzing Mφ function and finding triggers that alter the Mφ phenotypes to create novel therapeutic targets. However, evidence regarding Mφs in urinary sediments is scant, and the direct manipulation of Mφ phenotypes for clinical use needs to be determined ( 56 ). Future investigations should strive to establish a urinary biomarker for liquid biopsies ( 57 ), and an Mφ-specific target therapy using antibodies, vectors, and nanoparticles ( 58 , 59 ).…”

Section: Discussionmentioning

confidence: 99%

Macrophage Function in Calcium Oxalate Kidney Stone Formation: A Systematic Review of Literature

et al. 2021

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BackgroundThe global prevalence and recurrence rate of kidney stones is very high. Recent studies of Randall plaques and urinary components in vivo, and in vitro including gene manipulation, have attempted to reveal the pathogenesis of kidney stones. However, the evidence remains insufficient to facilitate the development of novel curative therapies. The involvement of renal and peripheral macrophages in inflammatory processes offers promise that might lead to the development of therapeutic targets. The present systematic literature review aimed to determine current consensus about the functions of macrophages in renal crystal development and suppression, and to synthesize evidence to provide a basis for future immunotherapy.MethodsWe systematically reviewed the literature during February 2021 according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Articles investigating the relationship between macrophages and urolithiasis, particularly calcium oxalate (CaOx) stones, were extracted from PubMed, MEDLINE, Embase, and Scopus. Study subjects, languages, and publication dates were unrestricted. Two authors searched and screened the publications.ResultsAlthough several studies have applied mixed modalities, we selected 10, 12, and seven (total, n = 29) of 380 articles that respectively described cultured cells, animal models, and human samples.The investigative trend has shifted to macrophage phenotypes and signaling pathways, including micro (m)-RNAs since the discovery of macrophage involvement in kidney stones in 1999. Earlier studies of mice-associated macrophages with the acceleration and suppression of renal crystal formation. Later studies found that pro-inflammatory M1- and anti-inflammatory M2-macrophages are involved. Studies of human-derived and other macrophages in vitro and ex vivo showed that M2-macrophages (stimulated by CSF-1, IL-4, and IL-13) can phagocytose CaOx crystals, which suppresses stone development. The signaling mechanisms that promote M2-like macrophage polarization toward CaOx nephrocalcinosis, include the NLRP3, PPARγ-miR-23-Irf1/Pknox1, miR-93-TLR4/IRF1, and miR-185-5p/CSF1 pathways.Proteomic findings have indicated that patients who form kidney stones mainly express M1-like macrophage-related proteins, which might be due to CaOx stimulation of the macrophage exosomal pathway.ConclusionsThis systematic review provides an update regarding the current status of macrophage involvement in CaOx nephrolithiasis. Targeting M2-like macrophage function might offer a therapeutic strategy with which to prevent stones via crystal phagocytosis.

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Section: Discussionmentioning

confidence: 99%

Macrophage Function in Calcium Oxalate Kidney Stone Formation: A Systematic Review of Literature

et al. 2021

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“…More recently, Sun PP et al. enrolled 205 patients with renal intrinsic AKI revealing a sharp augment of urinary sCD163 in glomerulopathy cases ( 138 ). In addition, urinary CD163 showed better diagnostic performance in differentiating disease etiologies compared to traditional urinary biomarkers of AKI (i.e.…”

Section: Systemic Biomarkers Of Iraes and Ici-induced Akimentioning

confidence: 99%

The Use of Immune Checkpoint Inhibitors in Oncology and the Occurrence of AKI: Where Do We Stand?

et al. 2020

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Immune checkpoint inhibitors (ICIs) are a novel class of immunotherapy drugs that have improved the treatment of a broad spectrum of cancers as metastatic melanoma, non-small lung cancer or renal cell carcinoma. These humanized monoclonal antibodies target inhibitory receptors (e.g. CTLA-4, PD-1, LAG-3, TIM-3) and ligands (PD-L1) expressed on T lymphocytes, antigen presenting cells and tumor cells and elicit an anti-tumor response by stimulating immune system. Nevertheless, the improved overall survival is complicated by the manifestation of Immune-related Adverse Effects (irAEs). During treatment with ICIs, the most common adverse kidney effect is represented by the development of acute kidney injury (AKI) with the acute tubulointerstitial nephritis as recurrent histological feature. The mechanisms involved in ICIs-induced AKI include the re-activation of effector T cells previously stimulated by nephrotoxic drugs (i.e. by antibiotics), the loss of tolerance versus self-renal antigens, the increased PD-L1 expression by tubular cells or the establishment of a pro-inflammatory milieu with the release of self-reactive antibodies. For renal transplant recipient treated with ICIs, the increased incidence of rejection is a serious concern. Therefore, the combination of ICIs with mTOR inhibitors represents an emerging strategy. Finally, it is relevant to anticipate which patients under ICIs would experience severe irAEs and from a kidney perspective, to predict patients with higher risk of AKI. Here, we provide a detailed overview of ICIs-related nephrotoxicity and the recently described multicenter studies. Several factors have been reported as biomarkers of ICIs-irAEs, in this review we speculate on potential biomarkers for ICIs-associated AKI.

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“…2) (84). Sun et al (85) quantified sCD163 in the urine, and measured macrophage subtypes in the urine and renal biopsies (Table I). The authors found that urinary M1 is associated with interstitial M1 infiltration, while urinary sCD163 level and M2 subtype are positively correlated with infiltrating M2 in the glomeruli.…”

Section: Macrophage-derived Mediators In Akimentioning

confidence: 99%

Major signaling pathways and key mediators of macrophages in acute kidney injury (Review)

Chen

Wang³

et al. 2021

Mol Med Rep

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Acute kidney injury (AKI) has become a global public health problem with high morbidity and mortality rates, as well as high healthcare costs. Immune cells, particularly macrophages, which regulate tissue development, destroy pathogens, control homeostasis and repair wounds, play crucial and complex roles in AKI. In various types of AKI, numerous rapidly recruited monocytes and tissue-resident macrophages act in a coordinated manner. Thus, elucidating the phenotypic and functional characteristics of macrophages in AKI is essential for identifying potential therapeutic targets. Macrophage-sensing mediators and macrophage-derived mediators participate in the major macrophage-related signaling pathways in AKI, which regulate macrophage polarization and determine disease progression. In conclusion, macrophages change their roles and regulatory mechanisms during the occurrence and development of AKI. The aim of the present review was to contribute to an improved understanding of AKI and to the identification of novel therapeutic targets for this condition.

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Urine macrophages reflect kidney macrophage content during acute tubular interstitial and glomerular injury

Cited by 23 publications

References 30 publications

Macrophage Function in Calcium Oxalate Kidney Stone Formation: A Systematic Review of Literature

Macrophage Function in Calcium Oxalate Kidney Stone Formation: A Systematic Review of Literature

The Use of Immune Checkpoint Inhibitors in Oncology and the Occurrence of AKI: Where Do We Stand?

Major signaling pathways and key mediators of macrophages in acute kidney injury (Review)

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