Evidence map›Paper›PMID 39485496›Full record

ReviewPediatric nephrology (Berlin, Germany)2025

A new era in the treatment of kidney diseases: NLRP3 inflammasome and cytokine-targeted therapies.

Emre Leventoğlu, Sevcan A Bakkaloğlu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

2 authors.

Emre LeventoğluDepartment of Pediatric Nephrology, Konya City Hospital, Konya, Turkey. dremrelevent@gmail.com.ORCID http://orcid.org/0000-0002-0504-7911
Sevcan A BakkaloğluFaculty of Medicine, Department of Pediatric Nephrology, Gazi University, Ankara, Turkey.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kidneys are crucial for filtering blood, managing overall body water, electrolyte, and acid-base balance, and regulating blood pressure. They remove metabolic waste products, toxins, and drugs. In addition, they limit inflammation by clearing cytokines and reduce immune cell activation by removing bacterial components. Dendritic cells (DCs) in the kidney maintain peripheral tolerance. About 85% of filtered water is reabsorbed by the proximal tubule, exposing distal nephron cells to high concentrations of low molecular weight antigens. These antigens are captured by DCs, helping to inactivate potentially autoreactive T cells and maintain tolerance to circulating antigens. In kidney failure, immune function is severely compromised due to the retention of toxins and cytokines, which activate immune cells and increase systemic inflammation. The kidneys are also vulnerable to immune-mediated diseases. Loss of immune homeostasis, characterized by over- or under-activity of the immune response, can adversely affect kidney function. With advances in immunology and cellular biology, biologic therapies targeting various pathways involved in the pathophysiology of kidney diseases are being developed. In this review, the immunologic aspects of kidney diseases and focus on cytokine-based therapies that may hold promise for the treatment of kidney diseases in the future will be presented.

Indexed as

Carrier ProteinsCytokinesInflammasomesKidney DiseasesAnimalsHumansKidneyNLR Family, Pyrin Domain-Containing 3 ProteinCarrier ProteinsCytokinesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanCytokine-targeted therapiesKidney diseasesNLRP3 inflammasome

Identifiers

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.