ReviewPediatric nephrology (Berlin, Germany)2010
Post-renal transplantation hypophosphatemia.
Review in Pediatric nephrology (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed, 34 citations in OpenAlex.
- Phosphate: An Anion Controlling Metabolic Functions.Nutrients · 2026Review
- An adolescent with abdominal pain and tremors: Answers.Pediatric nephrology (Berlin, Germany) · 2023Article
- Hyperparathyroidism Is an Independent Risk Factor for Allograft Dysfunction in Pediatric Kidney Transplantation.Kidney international reports · 2023Article
- What is the clinical relevance of deviant serum calcium and phosphate levels after pig-to-primate kidney xenotransplantation?Xenotransplantation · 2022Article
- Editorial: Metabolic Changes After Kidney Transplantation.Frontiers in medicine · 2021Article
- Serum Klotho in Living Kidney Donors and Kidney Transplant Recipients: A Meta-Analysis.Journal of clinical medicine · 2020Article
- Electrolyte and Acid-Base Disorders in the Renal Transplant Recipient.Frontiers in medicine · 2018Review
- Phosphate and FGF-23 homeostasis after kidney transplantation.Nature reviews. Nephrology · 2015Review
- Transplant endocrinology.Medical journal, Armed Forces IndiaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
An understanding of the pathophysiologic mechanisms of post-renal transplant (PRT) bone disease is of important clinical significance. Although bone disease occurs after all solid organ transplantation, the cumulative skeletal fracture rate remains high in PRT subjects while reaching a plateau with other transplantations. One major difference in the pathophysiology of PRT bone disease is, perhaps, due to persistent renal phosphorus (Pi) wasting. Novel phosphaturic agents have recently been suggested to participate in the development of bone disease in PRT subjects. However, it is unclear as of yet whether these factors alone or in conjunction with excess parathyroid hormone (PTH) secretion play a key role in the development of negative Pi balance and consequent bone disease in this population. In this review, I present a natural history of PRT hypophosphatemia and persistent renal Pi leak, provide pathophysiologic insight into these developments, and discuss the difficulty in diagnosing these phenotypes in both adult and pediatric populations.
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What OpenQuestion holds
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 OpenQuestion graph.