Evidence map›Paper›PMID 21514417›Full record

ArticleThe American journal of pathology2011

A murine model of phosphate nephropathy.

Philipp Eller, Kathrin Eller, Alexander H Kirsch, Josef J Patsch, Anna M Wolf, Andrea Tagwerker, Ursula Stanzl, Reinhard Kaindl, Volker Kahlenberg, Gert Mayer and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 30% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Lung-kidney interactions and their role in chronic kidney disease-associated pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Sustained Klotho delivery reduces serum phosphate in a model of diabetic nephropathy.Journal of applied physiology (Bethesda, Md. : 1985) · 2019
    Article
  16. Article
  17. High phosphate diet suppresses lipogenesis in white adipose tissue.Journal of clinical biochemistry and nutrition · 2018
    Article
  18. Article
  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

12 authors at 2 institutions in 1 country.

Philipp EllerDepartment of Internal Medicine I, Innsbruck Medical University, Innsbruck, Austria. philipp.eller@i-med.ac.at
Kathrin Eller
Alexander H Kirsch
Josef J Patsch
Anna M Wolf
Andrea Tagwerker
Ursula Stanzl
Reinhard Kaindl
Volker Kahlenberg
Gert Mayer
Josef R Patsch
Alexander R Rosenkranz
Innsbruck Medical University · ATUniversität Innsbruck · AT

Funding

Austrian Science Fund FWF P 21402
6 · The paper itself

Abstract

We established a murine model of phosphate nephropathy with secondary hyperparathyroidism. db/db mice, which develop obesity and type 2 diabetes mellitus, were uninephrectomized at the age of 6 weeks and were fed either standard chow or a phosphorus-rich diet during the next 8 weeks. Thereafter, renal cryosections showed abundant tubular casts with a strong histochemical von Kossa reaction in all db/db mice on the phosphorus-rich diet but none in the controls. X-ray diffraction and Raman spectroscopy proved that these tubular casts consist mostly of hydroxyapatite Ca₅(PO₄)₃(OH). These intraluminal precipitations were located in distal tubuli and collecting ducts and were associated with degenerative tubular changes and peritubular infiltration of T cells and macrophages. In line, kidneys of db/db mice on the phosphorus-rich diet displayed significantly increased mRNA expression of the T(H)1 cytokines interferon γ, IL-6, and tumor necrosis factor α. In addition, mice developed signs of secondary hyperparathyroidism as shown by elevated serum phosphate, decreased serum calcium, and increased parathyroid hormone, osteopontin, and fibroblast growth factor 23 levels. db/db mice on the phosphorus-rich diet also presented with significantly lower body weight, lower homeostasis model assessment of insulin resistance index, and hypertrophic cardiomyopathy. Thus, we provide a murine model of phosphate nephropathy and secondary hyperparathyroidism, which can be used for future pharmacologic and pathophysiologic studies to analyze the effect of hyperphosphatemia on renal, metabolic, and cardiovascular phenotypes.

Indexed as

Disease Models, AnimalAnimalsHyperparathyroidism, SecondaryHyperphosphatemiaKidney DiseasesMaleMiceMice, Mutant StrainsPhosphatesReceptors, LeptinReverse Transcriptase Polymerase Chain ReactionPhosphatesReceptors, Leptin

Identifiers

PMID21514417
PMCPMC3081192
OpenAlexW2091938814

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.