ReviewNature reviews. Nephrology2017
Crystal nephropathies: mechanisms of crystal-induced kidney injury.
Review in Nature reviews. Nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 213 citations in OpenAlex.
- The hippo-YAP1/TEAD1-SLC7A5 axis: uncovering a novel therapeutic target for oxalate-induced renal tubular ferroptosis.Redox report : communications in free radical research · 2026Article
- Beyond the stone: nephrolithiasis as a metabolic sentinel in upper tract urothelial carcinoma and papillary renal cell carcinoma: toward a risk-stratified management framework.International urology and nephrology · 2026Review
- Neutrophil Secretory Proteins Inhibit Calcium Oxalate Crystallisation and Crystal Growth, but Promote Crystal Aggregation.Immunology · 2026Article
- Gut Microbiota-Isoallolithocholic Acid Crosstalk Promotes Calcium Oxalate Kidney Stone Formation via PARP1-Mediated Parthanatos.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- EP3 receptor mediates calcium oxalate kidney stone formation via Ca²⁺/AKT and necroinflammation.Urolithiasis · 2026Article
- Sequential changes in urinary crystal morphology in ethylene glycol poisoning: first human LV-SEM characterization of recovery-phase crystals.CEN case reports · 2026Article
- Gouty kidney disease: a tubulointerstitial paradigm reimagined-early detection, precision stratification, and targeted intervention.Rheumatology international · 2026Review
- Overexpression of SIRT3 ameliorates calcium oxalate crystal-induced renal necroptosis by suppressing the TNF-α/RIPK3/P-MLKL pathway.Translational andrology and urology · 2026Article
- NINJ1 ubiquitination by TRIM72 protects against plasma membrane rupture and AKI-CKD progression.Cell death and differentiation · 2026Article
- Heat-KilledJournal of microbiology and biotechnology · 2026Article
- A nonsense mutation in the Mocos gene induces xanthinuria, obstructive nephropathy, and anemia in rats.Experimental animals · 2026Article
- Research Prospects for Necroptosis in Inflammatory Diseases: A Bibliometric Analysis.Current medicinal chemistry · 2026Review
- ER stress induced extracellular vesicles secretion from macrophages promotes calcium oxalate crystals formation in kidney.Molecular biomedicine · 2025Article
- Linoelaidic acid alleviates COM-induced kidney injury and crystal deposition via the PPARγ/MAPK signaling pathway.Urolithiasis · 2025Article
- A novel synbiotic formulation prevents calcium oxalate stones by restoring gut microbiota homeostasis.BMC microbiology · 2025Article
- Sirtuin1 mitigation of calcium oxalate nephropathy via enhancing itaconate abundance through reduction of histone trimethylation.Clinical and translational medicine · 2025Article
- NLRP3 inflammasome activation and macrophage distribution in kidney tissues from patients with acute oxalate nephropathy.Kidney research and clinical practice · 2025Article
- Roles of ACSL4/GPX4 and FSP1 in oxalate-induced acute kidney injury.Cell death discovery · 2025Article
- Kidney immunology from pathophysiology to clinical translation.Nature reviews. Immunology · 2025Review
- Gasdermin D deficiency aggravates nephrocalcinosis-related chronic kidney disease with rendering macrophages vulnerable to necroptosis.Cell death & disease · 2025Article
48 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Crystals can trigger a wide range of kidney injuries that can lead to acute kidney injury, chronic kidney disease, renal colic or nephrocalcinosis, depending on the localization and dynamics of crystal deposition. Studies of the biology of crystal handling by the kidney have shown that the formation of different crystals and other microparticles and the associated mechanisms of renal damage share molecular mechanisms, such as stimulation of the NLRP3 inflammasome or direct cytotoxicity through activation of the necroptosis signalling pathway. By contrast, crystal granuloma formation is limited to chronic crystallopathies that lead to chronic kidney disease and renal fibrosis. Here, we discuss current understanding of the pathomechanisms underlying the different types of crystal-induced kidney injury and propose a classification of crystal nephropathies based on the localization of crystal deposits in the renal vasculature (type 1), the nephron (type 2), or the draining urinary tract (type 3). Further exploration of the molecular mechanisms of crystal-induced kidney injury and renal remodelling might aid the development of innovative cures for these diseases.
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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.