Inflammation, oxidative stress, glomerular filtration rate, and albuminuria in elderly men: a cross-sectional study
1 Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, SE- 751 85, Uppsala, Sweden
2 Department of Public Health and Caring Sciences/Clinical Nutrition and Metabolism, Uppsala University, SE-751 85, Uppsala, Sweden
3 Department of Public Health and Caring Sciences/Oxidative stress and Inflammation, Uppsala University, SE-751 85, Uppsala, Sweden
4 Department of Medical Sciences, Acute and Internal Medicine, Uppsala University, SE-751 85, Uppsala, Sweden
5 Clinical chemistry, University hospital, SE-751 85, Uppsala, Sweden
6 Uppsala Clinical Research Centre, Uppsala University, SE-752 37, Uppsala, Sweden
7 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, SE-171 77, Stockholm, Sweden
8 Biochimie, Biologie Moléculaire et Nutrition, Faculté de Pharmacie, Université d'Auvergne, Clermont-Ferrand, 63001, Clermont-Ferrand cedex 1, France
9 School of Health and Social Studies, Dalarna University, SE-79188, Falun, Sweden
BMC Research Notes 2012, 5:537 doi:10.1186/1756-0500-5-537Published: 27 September 2012
The role of inflammation and oxidative stress in mild renal impairment in the elderly is not well studied. Accordingly, we aimed at investigating the associations between estimated glomerular filtration rate (eGFR), albumin/creatinine ratio (ACR), and markers of different inflammatory pathways and oxidative stress in a community based cohort of elderly men.
Cystatin C-based GFR, ACR, and biomarkers of cytokine-mediated inflammation (interleukin-6, high-sensitivity C-reactive protein[CRP], serum amyloid A[SAA]), cyclooxygenase-mediated inflammation (urinary prostaglandin F2α [PGF2α]), and oxidative stress (urinary F2 isoprostanes) were assessed in the Uppsala Longitudinal Study of Adult Men(n = 647, mean age 77 years).
In linear regression models adjusting for age, BMI, smoking, blood pressure, LDL-cholesterol, HDL-cholesterol, triglycerides, and treatment with statins, ACE-inhibitors, ASA, and anti-inflammatory agents, eGFR was inversely associated with CRP, interleukin-6, and SAA (β-coefficient −0.13 to −0.19, p < 0.001 for all), and positively associated with urinary F2-isoprostanes (β-coefficient 0.09, p = 0.02). In line with this, ACR was positively associated with CRP, interleukin-6, and SAA (β- coefficient 0.09-0.12, p < 0.02 for all), and negatively associated with urinary F2-isoprostanes (β-coefficient −0.12, p = 0.002). The associations were similar but with lower regression coefficients in a sub-sample with normal eGFR (>60 ml/min/1.73 m2, n = 514), with the exception that F2-isoprostane and SAA were no longer associated with eGFR.
Our data indicate that cytokine-mediated inflammation is involved in the early stages of impaired kidney function in the elderly, but that cyclooxygenase-mediated inflammation does not play a role at this stage. The unexpected association between higher eGFR/lower albuminuria and increased F2-isoprostanes in urine merits further studies.