Supplementary Material for: Not All Inflammatory Markers Are Linked to Kidney Function: Results from a Population-Based Study
2012-03-06T00:00:00Z (GMT) by
<i>Background:</i> Several studies have reported increased levels of inflammatory biomarkers in chronic kidney disease (CKD), but data from the general population are sparse. In this study, we assessed levels of the inflammatory markers C-reactive protein (hsCRP), tumor necrosis factor α (TNF-α), interleukin (IL)-1β and IL-6 across all ranges of renal function. <i>Methods:</i> We conducted a cross-sectional study in a random sample of 6,184 Caucasian subjects aged 35–75 years in Lausanne, Switzerland. Serum levels of hsCRP, TNF-α, IL-6, and IL-1β were measured in 6,067 participants (98.1%); serum creatinine-based estimated glomerular filtration rate (eGFR<sub>creat</sub>, CKD-EPI formula) was used to assess renal function, and albumin/creatinine ratio on spot morning urine to assess microalbuminuria (MAU). <i>Results:</i> Higher serum levels of IL-6, TNF-α and hsCRP and lower levels of IL-1β were associated with a lower renal function, CKD (eGFR<sub>creat</sub> <60 ml/min/1.73 m<sup>2</sup>; n = 283), and MAU (n = 583). In multivariate linear regression analysis adjusted for age, sex, hypertension, smoking, diabetes, body mass index, lipids, antihypertensive and hypolipemic therapy, only log-transformed TNF-α remained independently associated with lower renal function (β –0.54 ±0.19). In multivariate logistic regression analysis, higher TNF-α levels were associated with CKD (OR 1.17; 95% CI 1.01–1.35), whereas higher levels of IL-6 (OR 1.09; 95% CI 1.02–1.16) and hsCRP (OR 1.21; 95% CI 1.10–1.32) were associated with MAU. <i>Conclusion:</i> We did not confirm a significant association between renal function and IL-6, IL-1β and hsCRP in the general population. However, our results demonstrate a significant association between TNF-α and renal function, suggesting a potential link between inflammation and the development of CKD. These data also confirm the association between MAU and inflammation.