Abstract

Aim: To assess oxidative-inflammatory biomarker prediction of incident CKD after 1-year follow-up in a population with overweight/obesity and metabolic syndrome. Methods: Prospective nested case-control study comprising 117 CKD incident cases and 117 matched controls free of CKD after 1-year follow-up conducted in 55-75-year-old participants. Controls were time-matched 1:1 to cases by intervention group, age (<= 65 vs. >65 years), and sex. Serum creatinine (SCr), cystatin C (CyC), and urine albumin-to-creatinine ratio (UACR) were measured at baseline, and CKD Epidemiology Collaboration equations for Caucasians were used to assess SCr, CyC, and CyC-SCr-based estimated Glomerular Filtration Rate (eGFR). Baseline levels of malondialdehyde (MDA), carbonyls, tumour necrosis factor alpha (TNF alpha), interleukin (IL)-1 beta, IL-1ra, IL-6, monocyte chemoattractant protein 1 (MCP-1), and leptin were determined from fasting serum samples. An inflammatory-oxidative stress score based on these biomarkers was calculated. Incident CKD was defined by eGFR-SCr <60 mL/min/1.73 m(2), and/or UACR >= 30 mg/g in the absence of CKD at baseline. Results: UACR positively correlated with pro-inflammatory markers (IL-1 beta; TNF alpha) and oxidative damage marker (MDA); eGFR-cyC showed negative correlations with IL-1 beta and IL-1ra, and eGFR-SCr with leptin. The odds ratios (OR; 95% CI) for incident CKD in the highest vs. the lowest tertile of IL-1ra IL-6 and TNF alpha were (2.22; 1.22-4.04), (7.03; 2.88-17.14), and (3.79; 1.79-8.02), respectively. The inflammatory-oxidative stress score was associated with incident CKD (OR per 1-SD increment: 2.06; 1.49-2.83). Conclusions: Inflammatory/oxidative stress is associated with CKD incidence in individuals with high cardiovascular risk, underscoring the importance in identify early inflammation to prevent this disease.