Redox Stress Biomarkers and Their Association With Renal Dysfunction in Chronic Kidney Disease

Chronic 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.

A 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.

Patients 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).

The 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.