Evidence map›Paper›PMID 27452364›Full record

ReviewNature reviews. Nephrology2016

Idiopathic hypercalciuria and formation of calcium renal stones.

Fredric L Coe, Elaine M Worcester, Andrew P Evan

Abstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 3 pooled it
15.1field-weighted citation impact, top 1% 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

133 citing papers in PubMed, 3 syntheses or guidelines pooled it, 249 citations in OpenAlex.

  1. Pooled it
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  15. Article
  16. A Multiomics Study of Circulating Proteins and Kidney Stone Risk.Journal of the American Society of Nephrology : JASN · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. Understanding Renal Tubular Function: Key Mechanisms, Clinical Relevance, and Comprehensive Urine Assessment.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review

73 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Fredric L CoeNephrology Section MC 5100, University of Chicago Medicine, 5841 S. Maryland Avenue, Chicago, Illinois, 60637 USA.
Elaine M WorcesterNephrology Section MC 5100, University of Chicago Medicine, 5841 S. Maryland Avenue, Chicago, Illinois, 60637 USA.
Andrew P EvanDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, 635 Barnhill Drive, MS 5055, Indianapolis, IN 46220, Indiana, USA.
University of Chicago · USIndiana University – Purdue University Indianapolis · US

Funding

STONE FORMATION IN GENETIC HYPERCALCIURIAP01DK056788 · NIDDK · UNIVERSITY OF CHICAGO · PI WORCESTER, ELAINE M · 2000 to 2021
$22.5M
NIDDK NIH HHS P01 DK056788
6 · The paper itself

Abstract

The most common presentation of nephrolithiasis is idiopathic calcium stones in patients without systemic disease. Most stones are primarily composed of calcium oxalate and form on a base of interstitial apatite deposits, known as Randall's plaque. By contrast some stones are composed largely of calcium phosphate, as either hydroxyapatite or brushite (calcium monohydrogen phosphate), and are usually accompanied by deposits of calcium phosphate in the Bellini ducts. These deposits result in local tissue damage and might serve as a site of mineral overgrowth. Stone formation is driven by supersaturation of urine with calcium oxalate and brushite. The level of supersaturation is related to fluid intake as well as to the levels of urinary citrate and calcium. Risk of stone formation is increased when urine citrate excretion is <400 mg per day, and treatment with potassium citrate has been used to prevent stones. Urine calcium levels >200 mg per day also increase stone risk and often result in negative calcium balance. Reduced renal calcium reabsorption has a role in idiopathic hypercalciuria. Low sodium diets and thiazide-type diuretics lower urine calcium levels and potentially reduce the risk of stone recurrence and bone disease.

Indexed as

ApatitesCalciumHumansHypercalciuriaKidney CalculiApatitesCalcium

Identifiers

PMID27452364
PMCPMC5837277
OpenAlexW2499126920

What OpenQuestion holds

Textmetadata
LicenceTDM
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.