Evidence map›Paper›PMID 22763847›Full record

ReviewPediatric nephrology (Berlin, Germany)2013

The molecular basis of blood pressure variation.

Hakan R Toka, Jacob M Koshy, Ali Hariri

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

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

  1. Pooled it
  2. Pseudohypoaldosteronism type II: The Relevance of A Challenging Diagnosis.European journal of case reports in internal medicine · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Gordon Syndrome: a continuing story.Pediatric nephrology (Berlin, Germany) · 2015
    Review
  9. Review
  10. New functional aspects of the extracellular calcium-sensing receptor.Current opinion in nephrology and hypertension · 2014
    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

3 authors at 2 institutions in 1 country.

Hakan R TokaDepartment of Nephrology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. htoka@partners.org
Jacob M Koshy
Ali Hariri
Harvard University · USTakeda (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advances in genetic mapping and sequencing techniques have led to substantial progress in the study of rare monogenic (Mendelian) forms of abnormal blood pressure. Many disease-defining pathways for hypertension have been identified in the past two decades. Perturbations in renal salt handling appear to be a common mechanism underlying these rare syndromes of hypertension. Excess activation at various points in the mineralocorticoid signaling pathway and malfunctioning of the autonomic (specifically sympathetic) nervous system have both been implicated in inducing hypertension, while complementary studies examining low blood pressure phenotypes have identified novel pathways exclusively linked to renal salt wasting in either the thick ascending limb or the distal nephron. The genetic defects and the physiological and cellular pathways affected in these various disorders are reviewed here. Importantly, studies have suggested that genetic variation affecting these same genes and pathways may play an important role in explaining the variation of blood pressure levels in the general population. The investigation of rare syndromes of human blood pressure variation has important implications for improving the diagnosis and treatment of hypertension.

Indexed as

AnimalsBlood PressureGenetic Predisposition to DiseaseHumansHypertensionHypotensionKidneyPhenotypePrognosisRenal Tubular Transport, Inborn Errors

Identifiers

PMID22763847
OpenAlexW1983129595

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.