SAIMSARA Journal

Machine Generated Science • ISSN 3054-3991

Chronic Kidney Disease and Vascular Calcification: Scoping Review with ☸️SAIMSARA.

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Vascular Health

Issue 1, Volume 1, 2026

Editorial note
• Last update: 2026-03-22 14:13:40
What is this paper about
This paper shows that vascular calcification in CKD is not a passive byproduct of renal failure, but an active, biologically driven process fueled by phosphate burden, uremic toxins, inflammation, and VSMC transdifferentiation. The full paper is worth reading because it maps where the strongest mechanistic and clinical signals converge across 1,230 original studies, and highlights which biomarkers and interventions may actually become actionable in routine CKD care.


DOI: 10.62487/saimsara449d96eb

Abstract: The aim of this paper is to comprehensively synthesize the current understanding of chronic kidney disease and vascular calcification by integrating findings from diverse study designs, including human cohorts, animal models, and in vitro experimental studies, to identify key mechanisms, diagnostic markers, and therapeutic targets. The review utilises 1230 original studies with 405323 total participants (topic deduplicated ΣN). This scoping review maps a large and rapidly expanding evidence base linking CKD with vascular calcification and highlights a prominent signal that uremic-toxin exposure, inflammation/oxidative stress, and VSMC osteochondrogenic transdifferentiation converge to accelerate medial calcification in the uremic milieu. Across topics, the evidence consistently emphasizes mineral dysregulation (particularly phosphate burden), CPP biology, and inflammatory signaling (including NLRP3/NF-κB) as recurrent mechanistic themes, alongside emerging roles for non-coding RNAs, exosome-mediated crosstalk, and progenitor-cell contributions. Clinically, the map supports practical focus on risk stratification and modifiable drivers (dialysis-related calcium/alkali loading, phosphate control, and magnesium/CPP modulation) while recognizing that several biomarker and therapeutic signals remain largely preclinical or early-phase. Interpretation is tempered by the scoping design and LLM-assisted classification workflow, which prioritize coverage over causal inference and may affect reproducibility. Future work should therefore concentrate on longitudinal validation of promising biomarkers and well-designed trials of mechanistically targeted interventions to determine which pathways are most actionable in routine CKD care.

Keywords: Chronic kidney disease; Vascular calcification; Vascular smooth muscle cells; Calciprotein particles; Uremic toxins; Biomarkers; Inflammation; Runx2; Magnesium; MicroRNAs

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