ArticleThe Journal of clinical investigation2021
A generic crystallopathic model for chronic kidney disease progression.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Risk analysis and nomogram-based prediction for Double-J stent encrustation: accounting for chronic kidney disease.Clinical and experimental nephrology · 2026Observational
- Renal tubular calcium phosphate microcrystallopathy and age-related kidney function decline: The Aging Kidney Study.Clinical kidney journal · 2026Article
- The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026Review
- Calcium Phosphate-Induced Injury in Kidney Tubular Cells-Supersaturated Solution vs Preformed Crystals.Journal of biochemical and molecular toxicology · 2025Article
- Ten tips on how to care for your CKD patients in episodes of extreme heat.Clinical kidney journal · 2024Review
- Uric Acid and Chronic Kidney Disease: Still More to Do.Kidney international reports · 2023Review
- Nephrocalcinosis: unveiling renal tubulopathies in the genomic era.Jornal brasileiro de nefrologiaArticle
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Abstract
Chronic kidney disease (CKD) has reached epidemic proportions globally. The natural course of chronic kidney disease is almost uniformly progressive, albeit at different rates in different individuals. The downhill course appears to pervade kidney diseases of all etiologies and seems to spiral down a self-perpetuating vortex, even if the original insult is ameliorated or controlled. In this issue of the JCI, Shiizaki, Tsubouchi, and colleagues proposed a model of renal tubule luminal calcium phosphate crystallopathy that accounts for renal function demise. Calcium phosphate crystals attached to TLR4 and underwent endocytosis at the brush border, triggering inflammation and fibrosis. This mechanism might operate in different kinds of kidney disease, with a theoretical phosphate concentration threshold in the proximal tubular lumen, beyond which is triggered undesirable downstream effects that eventuate in loss of renal function. If this model parallels human CKD, clinicians may focus efforts on determining phosphate exposure in the proximal tubular lumen.
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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.