Evidence map›Paper›PMID 24262791›Full record

ArticleJournal of the American Society of Nephrology : JASN2014

Hepatectomy-related hypophosphatemia: a novel phosphaturic factor in the liver-kidney axis.

Kengo Nomura, Sawako Tatsumi, Atsumi Miyagawa, Yuji Shiozaki, Shohei Sasaki, Ichiro Kaneko, Mikiko Ito, Shinsuke Kido, Hiroko Segawa, Mitsue Sano and 3 more

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Emerging role of liver-bone axis in osteoporosis.Journal of orthopaedic translation · 2024
    Review
  7. Ability of NAD and Sirt1 to epigenetically suppress albuminuria.Clinical and experimental nephrology · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Mechanisms of phosphate transport.Nature reviews. Nephrology · 2019
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

13 authors at 2 institutions in 1 country.

Kengo NomuraDepartment of Molecular Nutrition Institution of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan; and.
Sawako Tatsumi
Atsumi Miyagawa
Yuji Shiozaki
Shohei Sasaki
Ichiro Kaneko
Mikiko Ito
Shinsuke Kido
Hiroko Segawa
Mitsue Sano
Tsutomu Fukuwatari
Katsumi Shibata
Ken-ichi Miyamoto
Tokushima University · JPUniversity of Shiga Prefecture · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Marked hypophosphatemia is common after major hepatic resection, but the pathophysiologic mechanism remains unknown. We used a partial hepatectomy (PH) rat model to investigate the molecular basis of hypophosphatemia. PH rats exhibited hypophosphatemia and hyperphosphaturia. In renal and intestinal brush-border membrane vesicles isolated from PH rats, Na(+)-dependent phosphate (Pi) uptake decreased by 50%-60%. PH rats also exhibited significantly decreased levels of renal and intestinal Na(+)-dependent Pi transporter proteins (NaPi-IIa [NaPi-4], NaPi-IIb, and NaPi-IIc). Parathyroid hormone was elevated at 6 hours after PH. Hyperphosphaturia persisted, however, even after thyroparathyroidectomy in PH rats. Moreover, DNA microarray data revealed elevated levels of nicotinamide phosphoribosyltransferase (Nampt) mRNA in the kidney after PH, and Nampt protein levels and total NAD concentration increased significantly in the proximal tubules. PH rats also exhibited markedly increased levels of the Nampt substrate, urinary nicotinamide (NAM), and NAM catabolites. In vitro analyses using opossum kidney cells revealed that NAM alone did not affect endogenous NaPi-4 levels. However, in cells overexpressing Nampt, the addition of NAM led to a marked decrease in cell surface expression of NaPi-4 that was blocked by treatment with FK866, a specific Nampt inhibitor. Furthermore, FK866-treated mice showed elevated renal Pi reabsorption and hypophosphaturia. These findings indicate that hepatectomy-induced hypophosphatemia is due to abnormal NAM metabolism, including Nampt activation in renal proximal tubular cells.

Indexed as

AcrylamidesAnimalsHepatectomyHypophosphatemiaKidneyMaleMiceMice, Inbred C57BLNADNiacinamideNicotinamide PhosphoribosyltransferaseParathyroidectomyPiperidinesRatsRats, WistarSodium-Phosphate Cotransporter ProteinsAcrylamidesN-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamideNADNiacinamideNicotinamide PhosphoribosyltransferasePiperidinesSodium-Phosphate Cotransporter ProteinsSodium-Phosphate Cotransporter Proteins, Type IIa

Identifiers

PMID24262791
PMCPMC3968501
OpenAlexW2096749163

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.