Evidence map›Paper›PMID 42558570›Full record

ReviewFrontiers in nephrology2026

Inflammation, infection, and immune dysregulation in chronic kidney disease: translational and epidemiological perspectives.

Aminu Shittu

Abstract readReview
In one paragraph

Review in Frontiers in nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Aminu ShittuDepartment of Veterinary Public Health and Preventive Medicine, Faculty of Veterinary Medicine, Usmanu Danfodiyo University, Sokoto, Nigeria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) represents a growing global health challenge associated with substantial morbidity, mortality, and healthcare burden. Although metabolic and haemodynamic factors, particularly diabetes mellitus and hypertension, remain major contributors, increasing evidence demonstrates that persistent inflammation and immune dysregulation are central mechanisms influencing CKD initiation, progression, and complications. The renal immune microenvironment consists of complex interactions among resident kidney cells, infiltrating immune cells, inflammatory mediators, and molecular signalling networks that regulate tissue repair, fibrosis, and disease outcomes. Persistent activation of innate and adaptive immune responses promotes cytokine release, oxidative stress, endothelial dysfunction, and maladaptive tissue remodelling, contributing to progressive loss of kidney function. Infectious diseases and altered host-microbiome interactions may further amplify systemic inflammation and immune imbalance, particularly in vulnerable populations. Advances in immunology and molecular medicine have identified inflammatory biomarkers and immune-related pathways with potential applications in early detection, risk stratification, and targeted interventions. This Mini Review synthesizes current evidence linking inflammation, infection, and immune dysregulation with CKD progression, highlighting translational opportunities and epidemiological perspectives. Integrating mechanistic insights with population-level evidence may accelerate precision approaches for improving CKD prevention, monitoring, and therapeutic outcomes.

Indexed as

biomarkerschronic kidney diseaseimmune dysregulationinfectioninflammationprecision medicinerenal immune microenvironmenttranslational nephrology

Identifiers

PMID42558570
PMCPMC13437631

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.