Evidence map›Paper›PMID 29312499›Full record

ArticleAmerican journal of translational research2017

LCZ696 (Sacubitril/valsartan) ameliorates oxidative stress, inflammation, fibrosis and improves renal function beyond angiotensin receptor blockade in CKD.

Wanghui Jing, Nosratola D Vaziri, Ane Nunes, Yasunori Suematsu, Ted Farzaneh, Mahyar Khazaeli, Hamid Moradi

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
6.6field-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

62 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
  2. Review
  3. Observational
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

2 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

7 authors at 2 institutions in 2 countries.

Wanghui JingDivision of Nephrology and Hypertension, University of CaliforniaIrvine, CA, USA.
Nosratola D VaziriDivision of Nephrology and Hypertension, University of CaliforniaIrvine, CA, USA.
Ane NunesDivision of Nephrology and Hypertension, University of CaliforniaIrvine, CA, USA.
Yasunori SuematsuDivision of Nephrology and Hypertension, University of CaliforniaIrvine, CA, USA.
Ted FarzanehDepartment of Pathology and Laboratory Medicine, University of CaliforniaIrvine, USA.
Mahyar KhazaeliDivision of Nephrology and Hypertension, University of CaliforniaIrvine, CA, USA.
Hamid MoradiDivision of Nephrology and Hypertension, University of CaliforniaIrvine, CA, USA.
Hypertension Institute · USUniversity of California System · US

Funding

HDL function and mortality in end stage renal diseaseIK2CX001043 · VA · VETERANS HEALTH ADMINISTRATION · PI MORADI, HAMID · 2015 to 2020
–
CSRD VA IK2 CX001043
6 · The paper itself

Abstract

Progressive deterioration of kidney function in chronic kidney disease (CKD) is mediated by hypertension, oxidative stress, inflammation, and fibrosis. Renin-angiotensin blockade is commonly used to retard CKD progression. In addition, vasoactive peptides have been shown to reduce blood pressure and exert antioxidant, anti-inflammatory and anti-fibrotic effects. We hypothesized that administration of LCZ696 (sacubitril/valsartan) is more effective than valsartan alone in slowing progression of CKD. Male Sprague Dawley rats underwent sham surgery or 5/6 nephrectomy and after two weeks the CKD animals were randomized to no treatment, valsartan (30 mg/kg), or LCZ696 (60 mg/kg) daily by gavage. Serum, urine and kidney tissue analyses were performed after 8 weeks. The untreated CKD rats exhibited hypertension, proteinuria, tubular and glomerular damage, upregulation of pro-inflammatory, pro-oxidant and pro-fibrotic pathways; reduction in nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its key target products. LCZ696 administration improved renal function and histology and attenuated most of the molecular markers of oxidative stress, inflammation and fibrosis. Furthermore, LCZ696 was more effective than valsartan therapy alone in delaying the progression of kidney disease. Future clinical trials are needed to determine the safety and efficacy of this agent in treatment of patients with CKD.

Indexed as

Chronic kidney diseasefibrosisinflammationLCZ696natriuretic peptidesoxidative stress

Identifiers

PMID29312499
PMCPMC5752897
OpenAlexW2793811377

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.