Evidence map›Paper›PMID 30446806›Full record

ReviewUrolithiasis2019

Calcium-sensing receptor: evidence and hypothesis for its role in nephrolithiasis.

Giuseppe Vezzoli, Lorenza Macrina, Giulia Magni, Teresa Arcidiacono

Abstract readReview
PubMed Publisher
In one paragraph

Review in Urolithiasis, 2019. 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
2.4field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Metabolic changes in kidney stone disease.Frontiers in immunology · 2023
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Pre-clinical evaluation of dual targeting of the GPCRs CaSR and V2R as therapeutic strategy for autosomal dominant polycystic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  14. Recent advances on the mechanisms of kidney stone formation (Review).International journal of molecular medicine · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Renal CaInternational journal of molecular sciences · 2019
    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

4 authors at 1 institution in 1 country.

Giuseppe VezzoliNephrology and Dialysis Unit, Postgraduate School of Nephrology, IRCCS San Raffaele Scientific Institute, Vita Salute University, 20132, Milan, Italy. vezzoli.giuseppe@hsr.it.ORCID http://orcid.org/0000-0003-4481-5693
Lorenza MacrinaNephrology and Dialysis Unit, Postgraduate School of Nephrology, IRCCS San Raffaele Scientific Institute, Vita Salute University, 20132, Milan, Italy.
Giulia MagniNephrology and Dialysis Unit, Postgraduate School of Nephrology, IRCCS San Raffaele Scientific Institute, Vita Salute University, 20132, Milan, Italy.
Teresa ArcidiaconoNephrology and Dialysis Unit, Postgraduate School of Nephrology, IRCCS San Raffaele Scientific Institute, Vita Salute University, 20132, Milan, Italy.
Vita-Salute San Raffaele University · IT

Funding

No funding to declare 000
6 · The paper itself

Abstract

Calcium-sensing receptor (CaSR) is a plasma-membrane G protein-coupled receptor activated by extracellular calcium and expressed in kidney tubular cells. It inhibits calcium reabsorption in the ascending limb and distal convoluted tubule when stimulated by the increase of serum calcium levels; therefore, these tubular segments are enabled by CaSR to play a substantial role in the regulation of serum calcium levels. In addition, CaSR increases water and proton excretion in the collecting duct and promotes phosphate reabsorption and citrate excretion in the proximal tubule. These CaSR activities form a network in which they are integrated to protect the kidney against the negative effects of high calcium concentrations and calcium precipitates in urine. Therefore, the CaSR gene has been considered as a candidate to explain calcium nephrolithiasis. Epidemiological studies observed that calcium nephrolithiasis was associated with polymorphisms of the CaSR gene regulatory region, rs6776158, located within the promoter-1, rs1501899 located in the intron 1, and rs7652589 in the 5'-untranslated region. These polymorphisms were found to reduce the transcriptional activity of promoter-1. Activating rs1042636 polymorphism located in exon 7 was associated with calcium nephrolithiasis and hypercalciuria. Genetic polymorphisms decreasing CaSR expression could predispose individuals to stones because they may impair CaSR protective effects against precipitation of calcium phosphate and oxalate. Activating polymorphisms rs1042636 could predispose to calcium stones by increasing calcium excretion. These findings suggest that CaSR may play a complex role in lithogenesis through different pathways having different relevance under different clinical conditions.

Indexed as

Genetic Predisposition to Disease5' Untranslated RegionsCalciumGenotypeHumansIntronsKidney TubulesNephrolithiasisPolymorphism, Single NucleotidePromoter Regions, GeneticReceptors, Calcium-SensingRenal EliminationRenal Reabsorption5' Untranslated RegionsCalciumReceptors, Calcium-SensingCalcium nephrolithiasisCalcium-sensing receptorCalcium stonesClaudin-14Claudin-16Gene polymorphismHypercalciuriaRandall’s plaque

Identifiers

PMID30446806
OpenAlexW2901162877

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.