ArticleJournal of the American Society of Nephrology : JASN2020
Cellular and Molecular Mechanisms of Kidney Injury in 2,8-Dihydroxyadenine Nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 86 citations in OpenAlex.
- Polydatin alleviates adenine-induced nephropathy in mice.Renal failure · 2026Article
- Animal models of anemia of inflammation: Methodological advances, limitations, and translational applications.Animal models and experimental medicine · 2026Review
- Adenine phosphoribosyltransferase deficiency and 2,8-dihydroxyadeninuria.Pediatric nephrology (Berlin, Germany) · 2026Review
- A novel mouse model of adenine-supplemented high-fat diet induced cardiovascular-kidney-metabolic syndrome.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Inhibition of (interstitial) P2YPflugers Archiv : European journal of physiology · 2026Article
- Plasma Metabolomics Reveals a Shared Metabolomic Profile in Experimental and Human Chronic Kidney Disease.Toxins · 2026Article
- Heat-KilledJournal of microbiology and biotechnology · 2026Article
- Lactulose, a Disaccharide Prebiotic, Improves the Gut-Kidney Axis via Enhancement of Akkermansia Muciniphila Production.Kidney360 · 2026Article
- Inhibition of (interstitial) P2YResearch square · 2026Article
- Stroke in persistent chronic kidney disease condition alters innate-immunity to escalate mitochondrial dysfunction and aging.npj aging · 2026Article
- Inhibition of (interstitial) P2YbioRxiv : the preprint server for biology · 2026Article
- 2,8-Dihydroxyadenine disrupts epithelial integrity and alters kidney cell phenotype in vitro.Journal of molecular medicine (Berlin, Germany) · 2026Article
- C-C motif receptor 2 is a core profibrotic factor in uremic cardiomyopathy.Disease models & mechanisms · 2026Article
- Evaluation of Feline Exosome Mediated Renal Regeneration in Adenine-Induced Chronic Kidney Disease.Biomolecules · 2025Article
- Renal Denervation Improves Uremic Cardiomyopathy in Rats With Chronic Kidney Disease.Journal of the American Heart Association · 2025Article
- Adenine phosphoribosyltransferase (APRT) deficiency: an increasingly recognized disease.International urology and nephrology · 2025Review
- Gavage versus dietary adenine administration is more effective for the female mouse model of chronic kidney disease.Scientific reports · 2025Article
- Modulation of Sel1L can alleviate altered ER homeostasis towards white matter damage in CKD-stroke complex.Communications biology · 2025Article
- Metabolomic profiling of adenine-induced CKD: pathway interconnections and kidney injury.Toxicology research · 2025Article
- Targeted Polymer-Peptide Conjugates for E-Selectin Blockade in Renal Injury.Pharmaceutics · 2025Article
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 4 countries.
Funding
Abstract
backgroundHereditary deficiency of adenine phosphoribosyltransferase causes 2,8-dihydroxyadenine (2,8-DHA) nephropathy, a rare condition characterized by formation of 2,8-DHA crystals within renal tubules. Clinical relevance of rodent models of 2,8-DHA crystal nephropathy induced by excessive adenine intake is unknown.
methodsUsing animal models and patient kidney biopsies, we assessed the pathogenic sequelae of 2,8-DHA crystal-induced kidney damage. We also used knockout mice to investigate the role of TNF receptors 1 and 2 (TNFR1 and TNFR2), CD44, or alpha2-HS glycoprotein (AHSG), all of which are involved in the pathogenesis of other types of crystal-induced nephropathies.
resultsAdenine-enriched diet in mice induced 2,8-DHA nephropathy, leading to progressive kidney disease, characterized by crystal deposits, tubular injury, inflammation, and fibrosis. Kidney injury depended on crystal size. The smallest crystals were endocytosed by tubular epithelial cells. Crystals of variable size were excreted in urine. Large crystals obstructed whole tubules. Medium-sized crystals induced a particular reparative process that we term
conclusionsRodent models of the cellular and molecular mechanisms of 2,8-DHA nephropathy and crystal clearance have clinical relevance and offer insight into potential future targets for therapeutic interventions.
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