ArticleThe Journal of urology2016
Calcium Oxalate Stone Fragment and Crystal Phagocytosis by Human Macrophages.
Article in The Journal of urology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 3 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 3 syntheses or guidelines pooled it, 124 citations in OpenAlex.
- Metabolic changes in kidney stone disease.Frontiers in immunology · 2023Pooled it
- The role of autophagy in calcium oxalate kidney stone: A systematic review of the literature.Frontiers in physiology · 2022Pooled it
- Macrophage Function in Calcium Oxalate Kidney Stone Formation: A Systematic Review of Literature.Frontiers in immunology · 2021Pooled it
- Keratoconjunctivitis Caused By Dieffenbachia Plant Sap: A Case Series.The American journal of case reports · 2026Article
- Cell type-stratified immunogenetic framework reveals immune drivers and therapeutic targets in kidney stone disease.Molecular therapy. Nucleic acids · 2026Article
- Inducing bacterial calcification for systematic treatment and immunomodulation against methicillin-resistant Staphylococcus aureus.Nature biotechnology · 2026Article
- Oxalate as an Emerging Contributor to Cardiovascular Disease: Links to Inflammation, Immunity, and Oxidative Stress.Nutrients · 2026Review
- Steroid hormones and nephrolithiasis: regulation of urine components metabolism and inflammation.Biology of sex differences · 2026Review
- M2 Macrophages Attenuate AQP2Research (Washington, D.C.) · 2026Article
- Regulated Cell Death in Calcium Oxalate Stone Disease: From Tubular Epithelial Injury to Inflammatory Amplification.Journal of inflammation research · 2026Review
- Genetically predicted Circulating inflammatory proteins mediate the association between plasma lipidome and kidney stones: A Mendelian randomization study.Urolithiasis · 2025Article
- The effects of immune cells and blood metabolites on kidney stones: a bidirectional two-sample Mendelian randomization study and mediation analysis.International urology and nephrology · 2025Article
- Role of UropathogenicPathogens (Basel, Switzerland) · 2025Review
- Sirtuin1 mitigation of calcium oxalate nephropathy via enhancing itaconate abundance through reduction of histone trimethylation.Clinical and translational medicine · 2025Article
- Macrophage Reprogramming: Emerging Molecular Therapeutic Strategies for Nephrolithiasis.Biomolecules · 2025Review
- Differences in macrophage pyroptosis and polarization induced by nano-/micro-calcium oxalate crystals.Journal of nanobiotechnology · 2025Article
- Clinical manifestations and renal pathology of ethylene glycol.CEN case reports · 2025Article
- CREB1/CRTC2 regulated tubular epithelial-derived exosomal miR-93-3p promotes kidney injury induced by calcium oxalate via activating M1 polarization and macrophage extracellular trap formation.Journal of nanobiotechnology · 2025Article
- Associations between multiple inflammatory biomarkers and the risk of developing kidney stones.BMC urology · 2025Article
- Premature renal epithelial cell senescence promoted by LXN/Rps3/p53 signaling pathway activation increases calcium oxalate crystal deposition by altering macrophage polarization.Frontiers in immunology · 2025Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeIn murine and human hyperoxaluric conditions macrophages can be seen surrounding renal calcium oxalate crystal deposits. We hypothesized that macrophages have a role in degrading and destroying these deposits. We investigated the inflammatory response and phagocytic mechanisms when macrophages were exposed to human kidney stones and inorganic crystals. MATERIALS AND
methodsHuman monocytes were differentiated into resting, fully differentiated macrophages by treatment with recombinant human macrophage colony-stimulating factor (M-CSF) or GM-CSF (granulocyte M-CSF) for 6 days. After confirming phenotype by flow cytometry the macrophages were exposed for 20 hours to fragments of sterile human calcium oxalate stones or calcium oxalate crystals. Crystal uptake was determined, and supernatant cytokine and chemokine profiles were analyzed using antibody arrays. Quantitative reverse transcriptase-polymerase chain reaction was done to validate mRNA profile expression.
resultsUnder direct vision fluorescence microscopy activated human macrophages were noted to surround stone fragments and synthesized crystals, and destroy them in a step-by-step process that involved clathrin mediated endocytosis and phagocytosis. An inflammatory cascade was released by macrophages, including the chemokines chemokine ligand (CCL)2, CCL3, interleukin (IL)-1 receptor antagonist (IL-1ra), complement component C5/C5a and IL-8. Response patterns to stone and crystal material depended on macrophage phenotype and activation status.
conclusionsIn our in vitro study macrophages differentiated with M-CSF showed greater ability to phagocytize crystal deposits than those treated with GM-CSF. Following clathrin mediated endocytosis macrophages released a number of cytokines that are crucial for the inflammatory immune response. This suggests that tissue macrophages have an important role in preventing kidney stone disease by removing and digesting interstitial renal crystal deposits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.