Evidence map›Paper›PMID 23716689›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Sulfatides are required for renal adaptation to chronic metabolic acidosis.

Paula Stettner, Soline Bourgeois, Christian Marsching, Milena Traykova-Brauch, Stefan Porubsky, Viola Nordström, Carsten Hopf, Robert Koesters, Robert Kösters, Roger Sandhoff and 4 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Functions of Sulfatide in the Nervous, Immune, and Urinary Systems.Advances in experimental medicine and biology · 2026
    Review
  4. Review
  5. A lipid atlas of the human kidney.Science advances · 2025
    Article
  6. Article
  7. Review
  8. State of knowledge on ammonia handling by the kidney.Pflugers Archiv : European journal of physiology · 2024
    Review
  9. Metabolic acidosis in chronic kidney disease: mere consequence or also culprit?Pflugers Archiv : European journal of physiology · 2024
    Review
  10. Article
  11. Article
  12. Kidney metabolism and acid-base control: back to the basics.Pflugers Archiv : European journal of physiology · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Zeta-crystallin: a moonlighting player in cancer.Cellular and molecular life sciences : CMLS · 2020
    Review
  18. Review
  19. Article
  20. Renal Tubular Acidosis: HAdvances in chronic kidney disease · 2018
    Review
4 · The record

Corrections and comments

  • Erratum issued
    Kösters, Robert [corrected to Koesters, Robert]
5 · Who and what money

Authors and funding

14 authors at 4 institutions in 3 countries.

Paula StettnerDepartment of Cellular and Molecular Pathology, German Cancer Research Center, D-69120 Heidelberg, Germany.
Soline Bourgeois
Christian Marsching
Milena Traykova-Brauch
Stefan Porubsky
Viola Nordström
Carsten Hopf
Robert Koesters
Robert Kösters
Roger Sandhoff
Herbert Wiegandt
Carsten A Wagner
Hermann-Josef Gröne
Richard Jennemann
German Cancer Research Center · DETechnische Hochschule Mannheim · DEUniversity of Zurich · CHInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Urinary ammonium excretion by the kidney is essential for renal excretion of sufficient amounts of protons and to maintain stable blood pH. Ammonium secretion by the collecting duct epithelia accounts for the majority of urinary ammonium; it is driven by an interstitium-to-lumen NH3 gradient due to the accumulation of ammonium in the medullary and papillary interstitium. Here, we demonstrate that sulfatides, highly charged anionic glycosphingolipids, are important for maintaining high papillary ammonium concentration and increased urinary acid elimination during metabolic acidosis. We disrupted sulfatide synthesis by a genetic approach along the entire renal tubule. Renal sulfatide-deficient mice had lower urinary pH accompanied by lower ammonium excretion. Upon acid diet, they showed impaired ammonuria, decreased ammonium accumulation in the papilla, and chronic hyperchloremic metabolic acidosis. Expression levels of ammoniagenic enzymes and Na(+)-K(+)/NH4(+)-2Cl(-) cotransporter 2 were higher, and transepithelial NH3 transport, examined by in vitro microperfusion of cortical and outer medullary collecting ducts, was unaffected in mutant mice. We therefore suggest that sulfatides act as counterions for interstitial ammonium facilitating its retention in the papilla. This study points to a seminal role of sulfatides in renal ammonium handling, urinary acidification, and acid-base homeostasis.

Indexed as

AcidosisAmmoniaAnimalsBlotting, WesternFemaleGlucosyltransferasesHomeostasisHydrogen-Ion ConcentrationKidneyKidney TubulesMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicSulfoglycosphingolipidsAmmoniaceramide glucosyltransferasegalactosylceramide sulfotransferaseGlucosyltransferasesSulfoglycosphingolipidsSulfotransferasesSymporters

Identifiers

PMID23716689
PMCPMC3683795
OpenAlexW1963902911

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.