Evidence map›Paper›PMID 22350303›Full record

ReviewPediatric nephrology (Berlin, Germany)2012

Genetic disorders of phosphate regulation.

Jyothsna Gattineni, Michel Baum

Open access · bronzeAbstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. The PTH-Vitamin D-FGF23 axis.Reviews in endocrine & metabolic disorders · 2015
    Review
  16. Review
  17. Alpha Klotho and phosphate homeostasis.Journal of endocrinological investigation · 2014
    Review
  18. Article
  19. Review
  20. FGF23 associated bone diseases.Frontiers of medicine · 2013
    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

2 authors at 2 institutions in 1 country.

Jyothsna GattineniDepartment of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75235-9063, USA. Jyothsna.Gattineni@UTSouthwestern.edu
Michel Baum
Southwestern Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

UT Southwestern O'Brien Kidney Research Core CenterP30DK079328 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 2007 to 2021
$16.9M
RENAL CONTROL OF BODY COMPOSITION AND BLOOD PRESSURET32DK007257 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL GERARD, MOE, ORSON W · 1986 to 2021
$5.0M
Neonatal Proximal Tubule AcidificationR01DK041612 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL GERARD, MOE, ORSON W · 1991 to 2013
$2.7M
Effect of Prenatal Programming on Renal Tubular TransportR01DK078596 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL GERARD · 2009 to 2012
$1.3M
Fibroblast Growth Factor 23 (FGF23) and It's ReceptorsK08DK089295 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI GATTINENI, JYOTHSNA · 2010 to 2014
$726k
NIDDK NIH HHS DK078596NIDDK NIH HHS DK41612NIDDK NIH HHS K08 DK089295NIDDK NIH HHS K08DK089295-01NIDDK NIH HHS P30 DK079328NIDDK NIH HHS P30DK079328NIDDK NIH HHS R01 DK041612NIDDK NIH HHS R01 DK078596NIDDK NIH HHS T32 DK007257NIDDK NIH HHS T32 DK07257
6 · The paper itself

Abstract

Regulation of phosphate homeostasis is critical for many biological processes, and both hypophosphatemia and hyperphosphatemia can have adverse clinical consequences. Only a very small percentage (1%) of total body phosphate is present in the extracellular fluid, which is measured by routine laboratory assays and does not reflect total body phosphate stores. Phosphate is absorbed from the gastrointestinal tract via the transcellular route [sodium phosphate cotransporter 2b (NaPi2b)] and across the paracellular pathway. Approximately 85% of the filtered phosphate is reabsorbed from the kidney, predominantly in the proximal tubule, by NaPi2a and NaPi2c, which are present on the brush border membrane. Renal phosphate transport is tightly regulated. Dietary phosphate intake, parathyroid hormone (PTH), 1,25 (OH)2 vitamin D3, and fibroblast growth factor 23 (FGF23) are the principal regulators of phosphate reabsorption from the kidney. Recent advances in genetic techniques and animal models have identified many genetic disorders of phosphate homeostasis. Mutations in NaPi2a and NaPi2c; and hormonal dysregulation of PTH, FGF23, and Klotho, are primarily responsible for most genetic disorders of phosphate transport. The main focus of this educational review article is to discuss the genetic and clinical features of phosphate regulation disorders and provide understanding and treatment options.

Indexed as

AnimalsFibroblast Growth Factor-23HomeostasisHumansHyperphosphatemiaHypophosphatemia, FamilialMetabolism, Inborn ErrorsPhosphatesSodium-Phosphate Cotransporter Proteins, Type IIFGF23 protein, humanFibroblast Growth Factor-23PhosphatesSodium-Phosphate Cotransporter Proteins, Type II

Identifiers

PMID22350303
PMCPMC3407352
OpenAlexW2108037207

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.