ArticleJournal of medical biochemistry2026
Biochemical alterations in inflammation, oxidative stress, and urinary biomarkers associated with renal damage in systemic lupus erythematosus.
Article in Journal of medical biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Renal damage is a major complication of systemic lupus erythematosus (SLE) and is closely linked to biochemical disturbances involving inflammation, oxidative stress, and renal tubular injury. However, the biochemical signatures that differentiate SLE patients with and without renal involvement remain insufficiently characterized. To evaluate the biochemical profiles of inflammatory cytokines, oxidative stress markers, and urinary renal-injury biomarkers in SLE patients with and without renal damage, and to explore their associations with microbial alterations. Methods: Sixty-four SLE patients were classified into a renal damage group (n = 36; positive urine protein) and an SLE-only group (n = 28; negative urine protein). Serum cytokines (TGF-R, IL-4, IL-17, IL-1P) and oxidative stress indicators (SOD, T-AOC, MDA) were quantified using ELISA. Urinary microprotein, microglobulin, and N-acetyl-P-D-glucosaminidase (NAG) were used as biochemical markers of renal injury. Oral and intestinal microbial profiles were analyzed by sequencing, and correlations between biochemical markers and microbial alterations were assessed. Results: SLE patients with renal damage showed significantly elevated urinary microprotein, microglobulin, and NAG (all p < 0.001). Inflammatory cytokines were markedly increased in the renal damage group (TGF-P, IL-4, IL-17, IL-1P; all p < 0.05), whereas oxidative stress capacity was significantly reduced (SOD, T-AOC, MDA; all p < 0.05). Several microbial taxa correlated positively or negatively with key biochemical markers, suggesting potential metabolic-immune interactions contributing to renal injury. Conclusions: Renal damage in SLE is characterized by distinct biochemical abnormalities involving intensified inflammation, impaired antioxidant defenses, and elevated urinary renal-injury biomarkers. These biochemical changes, together with specific microbial shifts, may contribute to the progression of SLE-related renal impairment and hold diagnostic value for early biochemical screening.
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.