ArticleThe Journal of clinical investigation2013
Calcium oxalate crystals induce renal inflammation by NLRP3-mediated IL-1β secretion.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 273 papers, 2 of them syntheses that pooled it.
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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
273 citing papers in PubMed, 2 syntheses or guidelines pooled it, 451 citations in OpenAlex.
- Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.Frontiers in immunology · 2022Pooled it
- Systematic Overview of Solid Particles and Their Host Responses.Frontiers in immunology · 2018Pooled it
- ePHex: a phase 3, double-blind, placebo-controlled, randomized study to evaluate long-term efficacy and safety of Oxalobacter formigenes in patients with primary hyperoxaluria.Pediatric nephrology (Berlin, Germany) · 2023Trial
- Gut microbiota: a novel key player in urinary stone formation - from oxalate metabolism to systemic regulation.Gut microbes · 2026Review
- Adenine phosphoribosyltransferase deficiency and 2,8-dihydroxyadeninuria.Pediatric nephrology (Berlin, Germany) · 2026Review
- Oridonin Protects Mice Against Cadmium-induced Kidney Injury by Inhibiting Ferroptosis via SIRT1 Regulation.Biological trace element research · 2026Article
- Gut Dysbiosis, Uremic Toxins, and NLRP3 Signaling in Chronic Kidney Disease: From Mechanistic Evidence to Clinical Biomarker Evaluation.Diagnostics (Basel, Switzerland) · 2026Review
- Animal Models of Hyperoxaluria and Their Relevance for Fundamental Research and Clinical Practice.International journal of molecular sciences · 2026Review
- Neutrophil Secretory Proteins Inhibit Calcium Oxalate Crystallisation and Crystal Growth, but Promote Crystal Aggregation.Immunology · 2026Article
- Article
- Bionic black phosphorus nanosheets confer dual protection against nephrocalcinosis-induced kidney injury via ROS scavenging and NETosis inhibition.Materials today. Bio · 2026Article
- Purine-Metabolism Reprogramming Associated with Failed-Repair Proximal Tubule States in the AKI-to-CKD Transition.Metabolites · 2026Article
- Multi-omics and genetic prioritization identify candidate molecular links between micro- and nanoplastics-associated signatures and chronic kidney disease.Molecular diversity · 2026Article
- Cell type-stratified immunogenetic framework reveals immune drivers and therapeutic targets in kidney stone disease.Molecular therapy. Nucleic acids · 2026Article
- Positive association between serum calcium-phosphorus ratio and kidney stone prevalence: Analysis of NHANES data (2007-2020).Medicine · 2026Article
- Oxalate as an Emerging Contributor to Cardiovascular Disease: Links to Inflammation, Immunity, and Oxidative Stress.Nutrients · 2026Review
- The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026Review
- Integration of network pharmacology and transcriptomics to reveal the ROS/NLRP3/Caspase-1/GSDMD-mediated mechanism of baicalin in alleviating contrast-induced acute kidney injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Clinical Approaches and Emerging Therapeutic Horizons in Primary Hyperoxaluria.Journal of clinical medicine · 2026Review
- 2,8-Dihydroxyadenine disrupts epithelial integrity and alters kidney cell phenotype in vitro.Journal of molecular medicine (Berlin, Germany) · 2026Article
213 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Nephrocalcinosis, acute calcium oxalate (CaOx) nephropathy, and renal stone disease can lead to inflammation and subsequent renal failure, but the underlying pathological mechanisms remain elusive. Other crystallopathies, such as gout, atherosclerosis, and asbestosis, trigger inflammation and tissue remodeling by inducing IL-1β secretion, leading us to hypothesize that CaOx crystals may induce inflammation in a similar manner. In mice, intrarenal CaOx deposition induced tubular damage, cytokine expression, neutrophil recruitment, and renal failure. We found that CaOx crystals activated murine renal DCs to secrete IL-1β through a pathway that included NLRP3, ASC, and caspase-1. Despite a similar amount of crystal deposits, intrarenal inflammation, tubular damage, and renal dysfunction were abrogated in mice deficient in MyD88; NLRP3, ASC, and caspase-1; IL-1R; or IL-18. Nephropathy was attenuated by DC depletion, ATP depletion, or therapeutic IL-1 antagonism. These data demonstrated that CaOx crystals trigger IL-1β-dependent innate immunity via the NLRP3/ASC/caspase-1 axis in intrarenal mononuclear phagocytes and directly damage tubular cells, leading to the release of the NLRP3 agonist ATP. Furthermore, these results suggest that IL-1β blockade may prevent renal damage in nephrocalcinosis.
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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.