Evidence map›Paper›PMID 37658999›Full record

ReviewOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2023

Mixed uremic osteodystrophy: an ill-described common bone pathology in patients with chronic kidney disease.

Ekbal Elkhouli, Eman Nagy, Cassia Gomes S Santos, Fellype Carvalho Barreto, Juliana Chaer, Vanda Jorgetti, Amr El-Husseini

Abstract readReview
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In one paragraph

Review in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  3. Review
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

7 authors at 4 institutions in 3 countries.

Ekbal ElkhouliMansoura pathology department, Mansoura University, Mansoura, Egypt.
Eman NagyMansoura Nephrology and Dialysis Unit, Mansoura University, Mansoura, Egypt.
Cassia Gomes S SantosDivision of Nephrology, Department of Internal Medicine, Federal University of Paraná, Curitiba, Paraná, Brazil.
Fellype Carvalho BarretoDivision of Nephrology, Department of Internal Medicine, Federal University of Paraná, Curitiba, Paraná, Brazil.
Juliana ChaerUniversity of São Paulo, Department of Internal Medicine, São Paulo, Brazil.
Vanda JorgettiUniversity of São Paulo, Department of Internal Medicine, São Paulo, Brazil.
Amr El-HusseiniDivision of Nephrology & Bone and Mineral Metabolism, University of Kentucky, Lexington, USA. amr.elhusseini@worldkidneyacademy.org.ORCID http://orcid.org/0000-0001-9072-5029
Mansoura University · EGUniversidade de São Paulo · BRUniversidade Federal do Paraná · BRUniversity of Kentucky · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal osteodystrophy (ROD) starts early and progresses with further loss of kidney function in patients with chronic kidney disease (CKD). There are four distinct types of ROD based on undecalcified bone biopsy results. Adynamic bone disease and osteomalacia are the predominant forms of low bone turnover, while hyperparathyroid bone disease and mixed uremic osteodystrophy (MUO) are typically associated with high bone turnover. MUO is a prevalent but poorly described pathology that demonstrates evidence of osteomalacia on top of the high bone formation/resorption. The prevalence of MUO ranges from 5 to 63% among different studies. The pathogenesis of MUO is multi-factorial. Altered phosphate homeostasis, hypocalcemia, vitamin D deficiency, increased FGF-23, interleukins 1 and 6, TNF-α, amyloid, and heavy metal accumulation are the main inducers of MUO. The clinical findings of MUO are usually non-specific. The use of non-invasive testing such as bone turnover markers and imaging techniques might help to suspect MUO. However, it is usually impossible to precisely diagnose this condition without performing bone biopsy. The principal management of MUO is to control the maladaptive hyperparathyroidism along with correcting any nutritional mineral deficiencies that may induce mineralization defect. MUO is a common but still poorly understood bone pathology category; it demonstrates the complexity and difficulty in understanding ROD. A large prospective bone biopsy-based studies are needed for better identification as proper diagnosis and management would improve the outcome of patients with MUO.

Indexed as

Bone Diseases, MetabolicBone ResorptionChronic Kidney Disease-Mineral and Bone DisorderOsteomalaciaRenal Insufficiency, ChronicBone and BonesHumansProspective StudiesBone pathologyCKD-MBDmanagementMixed uremic osteodystrophyrenal osteodystrophy

Identifiers

PMID37658999
OpenAlexW4386388255

What OpenQuestion holds

Textmetadata
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.