Evidence map›Paper›PMID 33765230›Full record

ReviewCalcified tissue international2021

Bone Mineral Disease After Kidney Transplantation.

Josep-Vicent Torregrosa, Ana Carina Ferreira, David Cucchiari, Aníbal Ferreira

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Calcified tissue international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Bone Fusion in the Cervical Spine: Where Are We Now?Bioengineering (Basel, Switzerland) · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Bone health and fracture prevention after kidney transplantation.Journal of clinical & translational endocrinology · 2024
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Risk Factors for First and Recurrent Fractures among Kidney Transplant Recipients.Progress in transplantation (Aliso Viejo, Calif.) · 2023
    Article
  20. 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

4 authors at 2 institutions in 2 countries.

Josep-Vicent TorregrosaNephrology & Renal Transplant Department - Hospital Clínic, Barcelona, Spain. vtorre@clinic.cat.ORCID 0000-0001-5160-3248
Ana Carina FerreiraNephrology Department, Centro Hospitalare, Universitário de Lisboa Central, Lisbon, Portugal.ORCID 0000-0002-1323-5293
David CucchiariNephrology & Renal Transplant Department - Hospital Clínic, Barcelona, Spain.
Aníbal FerreiraNephrology Department, Centro Hospitalare, Universitário de Lisboa Central, Lisbon, Portugal.ORCID 0000-0002-3300-6033
Hospital Clínic de Barcelona · ESUnidade Local de Saúde de São José · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease-mineral bone disorder (CKD-MBD) after kidney transplantation is a mix of pre-existing disorders and new alterations. The final consequences are reflected fundamentally as abnormal mineral metabolism (hypercalcemia, hypophosphatemia) and bone alterations [high or low bone turnover disease (as fibrous osteitis or adynamic bone disease), an eventual compromise of bone mineralization, decrease bone mineral density and bone fractures]. The major cause of post-transplantation hypercalcemia is the persistence of severe secondary hyperparathyroidism, and treatment options include calcimimetics or parathyroidectomy. On turn, hypophosphatemia is caused by both the persistence of high blood levels of PTH and/or high blood levels of FGF23, with its correction being very difficult to achieve. The most frequent bone morphology alteration is low bone turnover disease, while high-turnover osteopathy decreases in frequency after transplantation. Although the pathogenic mechanisms of these abnormalities have not been fully clarified, the available evidence suggests that there are a number of factors that play a very important role, such as immunosuppressive treatment, persistently high levels of PTH, vitamin D deficiency and hypophosphatemia. Fracture risk is four-fold higher in transplanted patients compared to general population. The most relevant risk factors for fracture in the kidney transplant population are diabetes mellitus, female sex, advanced age (especially > 65 years), dialysis vintage, high PTH levels and low phosphate levels, osteoporosis, pre-transplant stress fracture and high doses or prolonged steroids therapy. Treatment alternatives for CKD-MBD after transplantation include minimization of corticosteroids, use of calcium and vitamin D supplements, antiresorptives (bisphosphonates or Denosumab) and osteoformers (synthetic parathyroid hormone). As both mineral metabolism and bone disorders lead to increased morbidity and mortality, the presence of these changes after transplantation has to be prevented (if possible), minimized, diagnosed, and treated as soon as possible.

Indexed as

Bone DiseasesHyperparathyroidism, SecondaryKidney TransplantationVitamin D DeficiencyBone DensityFemaleFibroblast Growth Factor-23HumansInfant, NewbornMineralsParathyroid HormoneFGF23 protein, humanFibroblast Growth Factor-23MineralsParathyroid HormoneBone diseaseFracturesMineral metabolismRenal transplantation

Identifiers

PMID33765230
OpenAlexW3136864388

What Socratic 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 Socratic graph.