Evidence map›Paper›PMID 36615824›Full record

ReviewNutrients2022

Bone Disease in Chronic Kidney Disease and Kidney Transplant.

Ezequiel Bellorin-Font, Eudocia Rojas, Kevin J Martin

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Association between renal function and fracture incidence during treatment with teriparatide or alendronate: an exploratory subgroup analysis of the Japanese Osteoporosis Intervention Trial-05.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2024
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  16. Osteosarcopenia in Chronic Kidney Disease: An Overlooked Syndrome?Journal of cachexia, sarcopenia and muscle · 2025
    Review
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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

3 authors at 2 institutions in 2 countries.

Ezequiel Bellorin-FontDivision of Nephrology and Hypertension, Saint Louis University, Saint Louis, MO 63103, USA.
Eudocia RojasDivision of Nephrology and Kidney Transplantation, University Hospital of Caracas, Caracas 1053, Venezuela.
Kevin J MartinDivision of Nephrology and Hypertension, Saint Louis University, Saint Louis, MO 63103, USA.
Saint Louis University · USHospital Clínico Universitario de Caracas · VE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) comprises alterations in calcium, phosphorus, parathyroid hormone (PTH), Vitamin D, and fibroblast growth factor-23 (FGF-23) metabolism, abnormalities in bone turnover, mineralization, volume, linear growth or strength, and vascular calcification leading to an increase in bone fractures and vascular disease, which ultimately result in high morbidity and mortality. The bone component of CKD-MBD, referred to as renal osteodystrophy, starts early during the course of CKD as a result of the effects of progressive reduction in kidney function which modify the tight interaction between mineral, hormonal, and other biochemical mediators of cell function that ultimately lead to bone disease. In addition, other factors, such as osteoporosis not apparently dependent on the typical pathophysiologic abnormalities resulting from altered kidney function, may accompany the different varieties of renal osteodystrophy leading to an increment in the risk of bone fracture. After kidney transplantation, these bone alterations and others directly associated or not with changes in kidney function may persist, progress or transform into a different entity due to new pathogenetic mechanisms. With time, these alterations may improve or worsen depending to a large extent on the restoration of kidney function and correction of the metabolic abnormalities developed during the course of CKD. In this paper, we review the bone lesions that occur during both CKD progression and after kidney transplant and analyze the factors involved in their pathogenesis as a means to raise awareness of their complexity and interrelationship.

Indexed as

Bone DiseasesChronic Kidney Disease-Mineral and Bone DisorderFractures, BoneKidney TransplantationRenal Insufficiency, ChronicVascular CalcificationHumansParathyroid HormoneParathyroid Hormonebone diseaseCKD: chronic kidney diseaseCKD-MBDFGF-23high-turnover bone diseasehyperparathyroidismkidney transplantlow-turnover bone diseaseosteoporosisPTHrenal osteodystrophy

Identifiers

PMID36615824
PMCPMC9824497
OpenAlexW4313588101

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.