ArticleCureus2026
Redox Stress Biomarkers and Their Association With Renal Dysfunction in Chronic Kidney Disease.
Article in Cureus, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic kidney disease (CKD) is characterised by progressive loss of renal function and is closely associated with enhanced oxidative and nitrosative stress. Excess production of reactive oxygen and nitrogen species contributes to cellular injury, inflammation, and accelerated disease progression. This study aimed to evaluate oxidative and nitrosative stress markers in CKD patients and compare them with healthy controls.
methodsA hospital-based case-control study was conducted, including 80 diagnosed CKD patients and 80 age- and sex-matched healthy individuals. Blood samples were analysed for markers of oxidative stress, such as malondialdehyde (MDA), superoxide dismutase (SOD), and catalase, along with nitrosative stress marker nitric oxide (NO). Standard biochemical methods were used for estimation. Statistical analysis was performed using appropriate parametric and non-parametric tests, with p < 0.05 considered significant.
resultsPatients with CKD demonstrated significantly greater oxidative and nitrosative stress than healthy controls, as reflected by higher malondialdehyde levels (5.8 ± 1.2 vs. 2.9 ± 0.8 nmol/mL, p < 0.001) and nitric oxide levels (62.4 ± 10.5 vs. 34.7 ± 7.9 µmol/L, p < 0.001). Antioxidant enzyme activity was significantly reduced in the CKD group, with superoxide dismutase measuring 1.9 ± 0.6 U/mL compared with 3.8 ± 0.9 U/mL in controls, and catalase measuring 28.5 ± 6.7 kU/L compared with 46.2 ± 8.1 kU/L, respectively (p < 0.001 for both). Estimated glomerular filtration rate was negatively correlated with malondialdehyde levels among CKD patients, suggesting that oxidative stress increased as renal function declined (r = -0.62, p < 0.001).
conclusionThe findings indicate a pronounced imbalance between oxidant production and antioxidant defence in CKD. Elevated oxidative and nitrosative stress may play a key role in disease progression and complications. Monitoring these biomarkers could aid in early intervention and therapeutic strategies targeting oxidative damage.
Indexed as
Identifiers
What Socratic 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 Socratic graph.