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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Oxidative stress drives chronic kidney disease (CKD) progression. F2-isoprostane as a stable product of free-radical lipid peroxidation, is the most specific and reliable indicator of in-vivo oxidative injury. F2-isoprostane is chemically stable and not confounded by dietary lipid intake or enzymatic formation. Yet individual CKD studies reported mixed results, with some showing significant elevations in F2-isoprostanes and others finding non-significant differences. To resolve this uncertainty, we conducted the first systematic review and meta-analysis on F2-isoprostanes, quantifying stage-dependent patterns across CKD and renal replacement modalities.
We conducted comprehensive searches on PubMed, Scopus, ScienceDirect and Cochrane from inception to October 2025. Eligible studies compared plasma and/or urine F2-isoprostanes between adults with CKD (non-dialysis or dialysis) and healthy controls using gas chromatography–mass spectrometry (GC-MS), or enzyme-linked immunosorbent assay (ELISA). Data were extracted using standardized form. Random-effects models pooled standardized mean differences (SMDs).
Our search identified 1,546 records. After screening and selection, 33 studies were included. There were 2,189 participants with CKD and 1,205 controls. Plasma F2-isoprostanes were significantly higher in CKD than controls (SMD = 1.93; 95% CI 1.39–2.48; P < 0.0001; I² = 97%). Sub-group analysis by assay method for ELISA and GC-MS reduced heterogeneity (I² = 0%). Pooled means by group indicated higher plasma concentrations in CKD than controls for both ELISA (CKD ⟨309.3 pg/mL, 95% CI 259.25-359.35⟩; controls ⟨121.27, 95% CI 103.51-139.02 ⟩) and GC-MS (CKD ⟨43.1 pg/mL, 95% CI 40.51-45.68 ⟩; controls ⟨2.97, 95% CI 2.61-3.37⟩).
Stage 3 pooled mean plasma concentration was 313 pg/mL (95% CI 100–526), and the pooled mean increased to 638 (95% CI 394–882) in Stage 4. For Stage 5, the pooled mean was 441 pg/mL (95% CI 301–582) by ELISA and 13.2 pg/mL (95% CI 11.1–15.3) by GC-MS.
Treatment-modality subgrouping by pre-dialysis, mixed (pre-dialysis and dialysis), dialysis, and transplantation only reduced the heterogeneity to I² = 79.6%. Pooled means plasma concentration were 392.2 (95% CI 303.7–480.6) in pre-dialysis, 397.6 (95% CI 312.3–482.8) in hemodialysis (HD), and 430.02 pg/mL in peritoneal dialysis (PD) (95% CI -8.5-868.5) analyzed by ELISA. Pooled means plasma concentration were 207.6 (95% CI 120.9–293.5) in pre-dialysis, 21.64 (95% CI 19.31-23.96) in HD analyzed by GC-MS, and 128.963 pg/mL (95% CI 63.27-192.5) in transplantation analyzed by ELISA and GC-MS
Urinary analysis showed higher F2-isoprostanes in CKD than controls (SMD -0.52; 95% CI -2.89-1,85; I² = 96%; P = 0.67). Pooled means within the urine were 0.598 ng/mg creatinine; 95% CI 0.16-1.02 in CKD compared with 0.402; 95% CI 0.27-0.53 in controls.
Plasma F2-isoprostanes are significantly elevated in CKD, with a rise from Stage 3 to 4 and attenuation at Stage 5 while remaining above healthy levels. On ELISA, pre-dialysis and HD showed comparable plasma levels, with PD appearing higher. On GC-MS, pre-dialysis exceeded plasma level of those with HD and post-transplantation. Urinary F2-isoprostanes were higher in CKD but not statistically significant.
