Evidence map›Paper›PMID 34907378›Full record

ReviewNature reviews. Nephrology2022

The genetics of kidney stone disease and nephrocalcinosis.

Prince Singh, Peter C Harris, David J Sas, John C Lieske

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 9 pooled it
18.3field-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

145 citing papers in PubMed, 9 syntheses or guidelines pooled it, 210 citations in OpenAlex.

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85 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

4 authors at 1 institution in 1 country.

Prince SinghDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.ORCID http://orcid.org/0000-0002-9486-6002
Peter C HarrisDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
David J SasDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
John C LieskeDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA. lieske.john@mayo.edu.ORCID http://orcid.org/0000-0002-0202-5944
Mayo Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidney stones (also known as urinary stones or nephrolithiasis) are highly prevalent, affecting approximately 10% of adults worldwide, and the incidence of stone disease is increasing. Kidney stone formation results from an imbalance of inhibitors and promoters of crystallization, and calcium-containing calculi account for over 80% of stones. In most patients, the underlying aetiology is thought to be multifactorial, with environmental, dietary, hormonal and genetic components. The advent of high-throughput sequencing techniques has enabled a monogenic cause of kidney stones to be identified in up to 30% of children and 10% of adults who form stones, with ~35 different genes implicated. In addition, genome-wide association studies have implicated a series of genes involved in renal tubular handling of lithogenic substrates and of inhibitors of crystallization in stone disease in the general population. Such findings will likely lead to the identification of additional treatment targets involving underlying enzymatic or protein defects, including but not limited to those that alter urinary biochemistry.

Indexed as

Kidney CalculiNephrocalcinosisAdultChildFemaleGenome-Wide Association StudyHumansIncidenceKidney TubulesMale

Identifiers

PMID34907378
OpenAlexW4200124674

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.