Evidence map›Paper›PMID 38610646›Full record

ReviewJournal of clinical medicine2024

Fibrosis in Chronic Kidney Disease: Pathophysiology and Therapeutic Targets.

Allison B Reiss, Berlin Jacob, Aarij Zubair, Ankita Srivastava, Maryann Johnson, Joshua De Leon

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
23.7field-weighted citation impact, top 1% 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

56 citing papers in PubMed, 70 citations in OpenAlex.

  1. T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  2. Kidney Elastography in Adult Nephrology: A Narrative Review.Diagnostics (Basel, Switzerland) · 2026
    Review
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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 1 institution in 1 country.

Allison B ReissDepartment of Medicine and Biomedical Research Institute, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.ORCID 0000-0002-4478-2441
Berlin JacobDepartment of Medicine and Biomedical Research Institute, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.
Aarij ZubairDepartment of Medicine and Biomedical Research Institute, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.ORCID 0000-0003-3629-6184
Ankita SrivastavaDepartment of Medicine and Biomedical Research Institute, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.
Maryann JohnsonDepartment of Medicine and Biomedical Research Institute, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.ORCID 0009-0007-8368-2199
Joshua De LeonDepartment of Medicine and Biomedical Research Institute, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.
Biomedical Research Institute · US

Funding

CSRD VA 1
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a slowly progressive condition characterized by decreased kidney function, tubular injury, oxidative stress, and inflammation. CKD is a leading global health burden that is asymptomatic in early stages but can ultimately cause kidney failure. Its etiology is complex and involves dysregulated signaling pathways that lead to fibrosis. Transforming growth factor (TGF)-β is a central mediator in promoting transdifferentiation of polarized renal tubular epithelial cells into mesenchymal cells, resulting in irreversible kidney injury. While current therapies are limited, the search for more effective diagnostic and treatment modalities is intensive. Although biopsy with histology is the most accurate method of diagnosis and staging, imaging techniques such as diffusion-weighted magnetic resonance imaging and shear wave elastography ultrasound are less invasive ways to stage fibrosis. Current therapies such as renin-angiotensin blockers, mineralocorticoid receptor antagonists, and sodium/glucose cotransporter 2 inhibitors aim to delay progression. Newer antifibrotic agents that suppress the downstream inflammatory mediators involved in the fibrotic process are in clinical trials, and potential therapeutic targets that interfere with TGF-β signaling are being explored. Small interfering RNAs and stem cell-based therapeutics are also being evaluated. Further research and clinical studies are necessary in order to avoid dialysis and kidney transplantation.

Indexed as

chronic kidney diseaseinflammationnuclear factor kappa Brenal fibrosisSGLT2 inhibitors

Identifiers

PMID38610646
PMCPMC11012936
OpenAlexW4393163787

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.