Evidence map›Paper›PMID 26936874›Full record

ArticleAmerican journal of physiology. Renal physiology2016

Spontaneous one-kidney rats are more susceptible to develop hypertension by DOCA-NaCl and subsequent kidney injury compared with uninephrectomized rats.

Xuexiang Wang, Ashley C Johnson, Jennifer M Sasser, Jan M Williams, Leah C Solberg Woods, Michael R Garrett

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.6field-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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Canonical Wnt signaling in the kidney in different hypertension models.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    Article
  5. Article
  6. Article
  7. Loss ofHypertension (Dallas, Tex. : 1979) · 2020
    Article
  8. Article
  9. Article
  10. Renal Inflammation in DOCA-Salt Hypertension.Hypertension (Dallas, Tex. : 1979) · 2019
    Article
  11. Article
  12. 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

6 authors at 2 institutions in 1 country.

Xuexiang WangDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;
Ashley C JohnsonDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;
Jennifer M SasserDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;
Jan M WilliamsDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;
Leah C Solberg WoodsDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
Michael R GarrettDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; Department of Medicine (Nephrology), University of Mississippi Medical Center, Jackson, Mississippi; and mrgarrett@umc.edu.
University of Mississippi Medical Center · USMedical College of Wisconsin · US

Funding

Training and Mentoring Core P20GM103476 · NIGMS · UNIVERSITY OF SOUTHERN MISSISSIPPI · PI Yufeng Zheng · 2012 to 2026
$60.2M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
Center for Psychiatric NeuroscienceP30GM103328 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI STOCKMEIER, CRAIG ALLEN · 2013 to 2017
$5.5M
Genetics of Renal End Organ Damage in HypertensionR01HL094446 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI GARRETT, MICHAEL R · 2009 to 2013
$1.8M
Mechanisms of Renoprotection by Relaxin in HypertensionK01DK095018 · NIDDK · UNIVERSITY OF MISSISSIPPI MED CTR · PI SASSER, JENNIFER M · 2012 to 2016
$634k
NHLBI NIH HHS R01 HL094446NIDDK NIH HHS K01 DK095018NIGMS NIH HHS P20 GM103476NIGMS NIH HHS P20 GM104357NIGMS NIH HHS P30 GM103328
6 · The paper itself

Abstract

There is little clinical data of how hypertension may influence individuals with nephron deficiency in the context of being born with a single kidney. We recently developed a new rat model (the heterogeneous stock-derived model of unilateral renal agenesis rat) that is born with a single kidney and exhibits progressive kidney injury and decline in kidney function with age. We hypothesized that DOCA-salt would induce a greater increase in blood pressure and therefore accelerate the progression of kidney injury in rats born with a solitary kidney compared with rats that have undergone unilateral nephrectomy. Time course evaluation of blood pressure, kidney injury, and renal hemodynamics was performed in the following six groups of animals from weeks 13 to 18: 1) DOCA-treated rats with a solitary kidney (DOCA+S group), 2) placebo-treated rats with a solitary kidney, 3) DOCA-treated control rats with two kidneys (DOCA+C group), 4) placebo-treated control rats with two kidneys, 5) DOCA-treated rats with two kidneys that underwent uninephrectomy (DOCA+UNX8 group), and 6) placebo-treated rats with two kidneys that underwent uninephrectomy. DOCA+S rats demonstrated a significant rise (P < 0.05) in blood pressure (192 ± 4 mmHg), proteinuria (205 ± 31 mg/24 h), and a decline in glomerular filtration rate (600 ± 42 μl·min(-1)·g kidney weight(-1)) relative to the DOCA+UNX8 (173 ± 3 mmHg, 76 ± 26 mg/24 h, and 963 ± 36 μl·min(-1)·g kidney weight(-1)) and DOCA+C (154 ± 2 mmHg, 7 ± 1 mg/24 h, and 1,484 ± 121 μl·min(-1)·g kidney weight(-1)) groups. Placebo-treated groups showed no significant change among the three groups. An assessment of renal injury markers via real-time PCR/Western blot analysis and histological analysis was concordant with the measured physiological parameters. In summary, congenital solitary kidney rats are highly susceptible to the induction of hypertension compared with uninephrectomized rats, suggesting that low nephron endowment is an important driver of elevated blood pressure, hastening nephron injury through the transmission of elevated systemic blood pressure and thereby accelerating decline in kidney function.

Indexed as

AnimalsCongenital AbnormalitiesDesoxycorticosterone AcetateDisease ProgressionFemaleHypertensionKidneyKidney DiseasesMaleMyocardiumNephrectomyRatsRenal InsufficiencySodiumDesoxycorticosterone AcetateSodiumchronic kidney diseasedeoxycorticosterone acetatefibrosishigh blood pressureunilateral renal agenesis

Identifiers

PMID26936874
PMCPMC5002061
OpenAlexW2290798722

What OpenQuestion holds

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Registered trials

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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.