Evidence map›Paper›PMID 37258233›Full record

ReviewJournal of atherosclerosis and thrombosis2023

Role of Chronic Kidney Disease (CKD)-Mineral and Bone Disorder (MBD) in the Pathogenesis of Cardiovascular Disease in CKD.

Shunsuke Yamada, Toshiaki Nakano

Registry-linked trialOpen access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of atherosclerosis and thrombosis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07654231 (Reducing Inflammation to Improve Vascular and Bone Outcomes With Low-dose Colchicine in CKD), which is not on this map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
14.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

NCT07654231 phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Reducing Inflammation to Improve Vascular and Bone Outcomes With Low-dose Colchicine in CKD: A Pilot Randomized Open-Label Trial (RESOLVE-CKD Trial)

TypeinterventionalSponsorUniversity of Texas Southwestern Medical CenterRan2026 to 2027Enrolled60ConditionsChronic Kidney Disease Mineral and Bone Disorder, Hypertension, Diabetes, DyslipidemiaArmsLow-dose Colchicine at 0.5mg daily, Usual Care
3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  12. High-potency statins are associated with reduced osteoporosis but increased fracture risk in CKD patients: a multi-center retrospective study.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
    Observational
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Shunsuke YamadaDepartment of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University.
Toshiaki NakanoDepartment of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University.
Kyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) is the leading cause of death in patients with chronic kidney disease (CKD). Multiple factors account for the increased incidence of cardiovascular morbidity and mortality in patients with CKD. Traditional risk factors for atherosclerosis and arteriosclerosis, including age, hypertension, dyslipidemia, diabetes mellitus, and smoking, are also risk factors for CKD. Non-traditional risk factors specific for CKD are also involved in CVD pathogenesis in patients with CKD. Recently, CKD-mineral and bone disorder (CKD-MBD) has emerged as a key player in CVD pathogenesis in the context of CKD. CKD-MBD manifests as hypocalcemia and hyperphosphatemia in the later stages of CKD; however, it initially develops much earlier in disease course. The initial step in CKD-MBD involves decreased phosphate excretion in the urine, followed by increased circulating concentrations of fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH), which increase urinary phosphate excretion. Simultaneously, the serum calcitriol concentration decreases as a result of FGF23 elevation. Importantly, FGF23 and PTH cause left ventricular hypertrophy, arrhythmia, and cardiovascular calcification. More recently, calciprotein particles, which are nanoparticles composed of calcium, phosphate, and fetuin-A, among other components, have been reported to cause inflammation, cardiovascular calcification, and other clinically relevant outcomes. CKD-MBD has become one of the critical therapeutic targets for the prevention of cardiovascular events and is another link between cardiology and nephrology. In this review, we describe the role of CKD-MBD in the pathogenesis of cardiovascular disorders and present the current treatment strategies for CKD-MBD.

Indexed as

AtherosclerosisCardiovascular DiseasesChronic Kidney Disease-Mineral and Bone DisorderRenal Insufficiency, ChronicDisease ProgressionHumansMineralsParathyroid HormonePhosphatesMineralsParathyroid HormonePhosphatesCalciumCardiovascular diseaseCKDCKD–MBDPhosphate

Identifiers

PMID37258233
PMCPMC10406631
OpenAlexW4378637425

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

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 Socratic graph.