ArticleKidney3602026
Chronic Psychologic Stress in Mice Induces Kidney Inflammation.
Article in Kidney360, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Article
- Immune cells during compensatory renal hypertrophy after unilateral nephrectomy.Research square · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
key pointsChronic stress elevates neutrophil gelatinase-associated lipocalin and cystatin C. Chronic stress increases T helper 17 and regulatory T-cell populations in the kidney. Chronic stress could increase susceptibility to kidney diseases.
backgroundChronic stress (CS) due to prolonged exposure to negative life events increases the risk of psychiatric illnesses and significantly affects physiologic processes. CS has also been linked to sustained systemic inflammation, resulting in dysregulated immune responses and organ function. We hypothesized that CS would lead to kidney inflammation and tested this in mice.
methodsMale C57BL/6J mice were subjected to CS by pair-housing them with CD-1 retired breeder mice. Kidney immune cells were isolated and evaluated by spectral flow cytometry. Cytokines were measured using a multiplex assay in kidney tissue and serum. Serum creatinine, cystatin C, and neutrophil gelatinase-associated lipocalin levels were measured.
resultsMice subjected to CS exhibited greater weight gain than the control group and had reduced fur quality. CS led to a decrease in the percentage of kidney CD4 + T cells (54.26%±0.89% versus 59.88%±1.25%, P < 0.001) and an increase in T helper 17 (2.3%±0.3% versus 0.83%±0.15%, P < 0.001) and regulatory T cells (3.42%±0.45% versus 1.53%±0.21%, P < 0.001). There was an increase in the kidney macrophage percentage in CS mice (88.33%±1.16% versus 84.26%±0.73%, P < 0.01). TNF- α levels were higher in the kidney of stressed mice (8.53±1.18 versus 3.15±1.29 pg/ml, P < 0.01). CS led to elevated levels of serum cystatin C (515.9±16.88 versus 456.6±14.79 ng/ml, P < 0.05) serum neutrophil gelatinase-associated lipocalin (833.1±282.4 versus 90.58±5.57 ng/ml, P < 0.0001).
conclusionsCS in mice led to kidney inflammation and immunologic changes. These could predispose to acute and CKDs in which inflammation plays a pathogenic role.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.