Evidence map›Paper›PMID 26510885›Full record

ReviewJournal of the American Society of Nephrology : JASN2016

Potassium and Its Discontents: New Insight, New Treatments.

David H Ellison, Andrew S Terker, Gerardo Gamba

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 76 citations in OpenAlex.

  1. Quantitative analysis of skeletal muscle contributions to ECF KAmerican journal of physiology. Cell physiology · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. The evolving concepts of KS-WNK1 effect on NCC activity.American journal of physiology. Renal physiology · 2025
    Review
  7. mTORc2 in Distal Convoluted Tubule and Renal K + Excretion during High Dietary K + Intake.Journal of the American Society of Nephrology : JASN · 2024
    Article
  8. KS-WNK1 is required for the renal response to extreme changes in potassium intake.American journal of physiology. Renal physiology · 2024
    Article
  9. Thirty years of the NaCl cotransporter: from cloning to physiology and structure.American journal of physiology. Renal physiology · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Inwardly rectifying KAmerican journal of physiology. Cell physiology · 2022
    Review
  14. Review
  15. Hyperkalemia in patients undergoing hemodialysis: Its pathophysiology and management.Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy · 2022
    Review
  16. The effect of high-dietary KFrontiers in physiology · 2022
    Article
  17. Review
  18. Article
  19. Review
  20. Article
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 2 countries.

David H EllisonDivision of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon; Renal Section, Veterans Affairs Portland Health Care System, Portland, Oregon; and ellisond@ohsu.edu.
Andrew S TerkerDivision of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon;
Gerardo GambaMolecular Physiology Unit, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán and Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Tlalpan, Mexico City, Mexico.
Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MXOregon Health & Science University · US

Funding

WNK Kinase Regulation of Thiazide-sensitive NaCl TransportR01DK051496 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI David Hoadley Ellison, CHAO-LING YANG · 1998 to 2026
$8.4M
Role of Kir4.1 in Regulating NCC and ROMK in DCTR01DK054983 · NIDDK · NEW YORK MEDICAL COLLEGE · PI ELLISON, DAVID H, WANG, WENHUI · 2001 to 2020
$7.4M
Nephrology Training GrantT32DK067864 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI ELLISON, DAVID H · 2006 to 2015
$1.2M
Renal Effects of AldosteroneI01BX002228 · VA · PORTLAND VA MEDICAL CENTER · PI ELLISON, DAVID H · 2014 to 2021
–
BLRD VA I01 BX002228NIDDK NIH HHS 2R01DK051496-15A1NIDDK NIH HHS 5T32DK067864-08NIDDK NIH HHS 5T32DK067864-10NIDDK NIH HHS R01 DK051496NIDDK NIH HHS R01 DK054983NIDDK NIH HHS T32 DK067864
6 · The paper itself

Abstract

Hyperkalemia is common in patients with impaired kidney function or who take drugs that inhibit the renin-angiotensin-aldosterone axis. During the past decade, substantial advances in understanding how the body controls potassium excretion have been made, which may lead to improved standard of care for these patients. Renal potassium disposition is primarily handled by a short segment of the nephron, comprising part of the distal convoluted tubule and the connecting tubule, and regulation results from the interplay between aldosterone and plasma potassium. When dietary potassium intake and plasma potassium are low, the electroneutral sodium chloride cotransporter is activated, leading to salt retention. This effect limits sodium delivery to potassium secretory segments, limiting potassium losses. In contrast, when dietary potassium intake is high, aldosterone is stimulated. Simultaneously, potassium inhibits the sodium chloride cotransporter. Because more sodium is then delivered to potassium secretory segments, primed by aldosterone, kaliuresis results. When these processes are disrupted, hyperkalemia results. Recently, new agents capable of removing potassium from the body and treating hyperkalemia have been tested in clinical trials. This development suggests that more effective and safer approaches to the prevention and treatment of hyperkalemia may be on the horizon.

Indexed as

HumansHyperkalemiaKidneyPotassiumPotassiumion channelion transportK channels

Identifiers

PMID26510885
PMCPMC4814195
OpenAlexW2213328738

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.