ReviewNature reviews. Nephrology2021
Randall's plaque and calcium oxalate stone formation: role for immunity and inflammation.
Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 4 of them syntheses that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
257 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- Association between the triglyceride-glucose index and kidney stone disease: a systematic review and dose-response meta-analysis.Lipids in health and disease · 2026Pooled it
- A holistic guide to effective prevention and treatment for kidney stones: a systematic review exploring anti-urolithiasis approaches.Naunyn-Schmiedeberg's archives of pharmacology · 2026Pooled it
- Plant-based therapies for urolithiasis: a systematic review of clinical and preclinical studies.International urology and nephrology · 2024Pooled it
- Vascular calcification on the risk of kidney stone: a meta-analysis.Renal failure · 2023Pooled it
- Integrative transcriptomic and single-cell analyses identify CD74 as a candidate regulator of ferroptosis in renal tubular cells during nephrolithiasis.Renal failure · 2026Article
- Novel insights into the role of the renal interstitial microenvironment in Randall's plaque formation (Review).International journal of molecular medicine · 2026Review
- SIRT5-Mediated Desuccinylation of ACAA2 Protects Against Calcium Oxalate-Induced Kidney Injury by Regulating Fatty Acid Oxidation to Suppress Mitochondrial Oxidative Injury and Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- β-carotene attenuates calcium oxalate crystal-induced renal injury through suppression of NF-κB-mediated inflammation.Urolithiasis · 2026Article
- Bronchial lesions in a high serum IgA mouse model: pulmonary venular IgA deposition and spatially distinct lymphoid cell aggregation.Journal of pathology and translational medicine · 2026Article
- Phenylalanine primes renal tubular redox vulnerability and calcium oxalate crystal retention through a PPARδ-CPT1A fatty-acid oxidation axis.Redox biology · 2026Article
- Gut Microbiota-Isoallolithocholic Acid Crosstalk Promotes Calcium Oxalate Kidney Stone Formation via PARP1-Mediated Parthanatos.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Rare Earth Element and Yttrium Fingerprints in Human Kidney Stones: Tracing Environmental Exposure and Pathological Mineralization Pathway.Biological trace element research · 2026Article
- Protective effects of Rhus coriaria L. fruit extract against experimental calcium oxalate nephrolithiasis via modulation of oxidative stress and renal injury.Urolithiasis · 2026Article
- Herba Lysimachiae Polysaccharide-Modified Selenium Nanoparticles Alleviate Oxidative Injury in Kidney Stones via TOMM22-Regulated Mitophagy Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Probucol inhibits palmitic acid-mediated renal calcium oxalate stone formation by targeting KLF5-PPARγ axis-mediated lipotoxicity.Journal of pharmaceutical analysis · 2026Article
- Lactobacillus acidophilus abolishes oxalate-mediated renal epithelial barrier disruption and calcium oxalate monohydrate crystal adhesion to renal epithelial cells.Cellular & molecular biology letters · 2026Article
- Deciphering the association between uric acid and kidney stones: insights into the mediating roles of BMI and serum iron: a cross-sectional study based on NHANES 2007-2018.International journal of surgery (London, England) · 2026Article
- Cell type-stratified immunogenetic framework reveals immune drivers and therapeutic targets in kidney stone disease.Molecular therapy. Nucleic acids · 2026Article
- Allicin inhibits kidney stone formation by suppressing the TNF/NF-κB pathway: Experimental validation through network pharmacology, in vitro, and in vivo studies.Molecular biology reports · 2026Article
- FASLG Derived from Fibroblasts in Hydroxyapatite-Rich Microenvironment Induces Urothelial Anoikis to Trigger Randall's Plaque Exposure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
197 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic calcium oxalate (CaOx) stones often develop attached to Randall's plaque present on kidney papillary surfaces. Similar to the plaques formed during vascular calcification, Randall's plaques consist of calcium phosphate crystals mixed with an organic matrix that is rich in proteins, such as inter-α-trypsin inhibitor, as well as lipids, and includes membrane-bound vesicles or exosomes, collagen fibres and other components of the extracellular matrix. Kidney tissue surrounding Randall's plaques is associated with the presence of classically activated, pro-inflammatory macrophages (also termed M1) and downregulation of alternatively activated, anti-inflammatory macrophages (also termed M2). In animal models, crystal deposition in the kidneys has been associated with the production of reactive oxygen species, inflammasome activation and increased expression of molecules implicated in the inflammatory cascade, including osteopontin, matrix Gla protein and fetuin A (also known as α2-HS-glycoprotein). Many of these molecules, including osteopontin and matrix Gla protein, are well known inhibitors of vascular calcification. We propose that conditions of urine supersaturation promote kidney damage by inducing the production of reactive oxygen species and oxidative stress, and that the ensuing inflammatory immune response promotes Randall's plaque initiation and calcium stone formation.
Indexed as
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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.