Evidence map›Paper›PMID 28680564›Full record

ReviewPulmonary circulation2017

Kidney dysfunction in patients with pulmonary arterial hypertension.

N P Nickel, J M O'Leary, E L Brittain, J P Fessel, R T Zamanian, J D West, E D Austin

Open access · bronzeAbstract readReview
In one paragraph

Review in Pulmonary circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
4.1field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Right Heart Function in Cardiorenal Syndrome.Current heart failure reports · 2022
    Pooled it
  3. Pooled it
  4. Trial
  5. Observational
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Observational
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 1 country.

N P NickelDepartment of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
J M O'LearyDivision of Cardiovascular Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
E L BrittainDivision of Cardiovascular Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
J P FesselDivision of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
R T ZamanianDivision of Pulmonary and Critical Care Medicine, Stanford University School of Medicine, Stanford, CA, USA.
J D WestDivision of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
E D AustinDepartment of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN, USA.
Vanderbilt University · USStanford Medicine · US

Funding

Metabolic Reprogramming in Pulmonary Arterial HypertensionK08HL121174 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI FESSEL, JOSHUA PATRICK · 2014 to 2018
$723k
NHLBI NIH HHS K08 HL121174
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PH) and chronic kidney disease (CKD) both profoundly impact patient outcomes, whether as primary disease states or as co-morbid conditions. PH is a common co-morbidity in CKD and vice versa. A growing body of literature describes the epidemiology of PH secondary to chronic kidney disease and end-stage renal disease (ESRD) (WHO group 5 PH). But, there are only limited data on the epidemiology of kidney disease in group 1 PH (pulmonary arterial hypertension [PAH]). The purpose of this review is to summarize the current data on epidemiology and discuss potential disease mechanisms and management implications of kidney dysfunction in PAH. Kidney dysfunction, determined by serum creatinine or estimated glomerular filtration rate, is a frequent co-morbidity in PAH and impaired kidney function is a strong and independent predictor of mortality. Potential mechanisms of PAH affecting the kidneys are increased venous congestion, decreased cardiac output, and neurohormonal activation. On a molecular level, increased TGF-β signaling and increased levels of circulating cytokines could have the potential to worsen kidney function. Nephrotoxicity does not seem to be a common side effect of PAH-targeted therapy. Treatment implications for kidney disease in PAH include glycemic control, lifestyle modification, and potentially Renin-Angiotensin-Aldosterone System (RAAS) blockade.

Indexed as

disease mechanismsepidemiologykidney diseasepulmonary arterial hypertension

Identifiers

PMID28680564
PMCPMC5448543
OpenAlexW2541872774

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.