Clinical Endocrinology
Clinical Endocrinology
5 years ago

Serum chemerin levels are inversely associated with renal function in a general population

Rainer Rettig, Nele Friedrich, Karlhans Endlich, Matthias Nauck, Henry Völzke, Stephanie Zylla
Objective Chemerin has been found to be highly expressed in the kidneys of rodents and has been suggested to affect metabolic syndrome (MetS)-related phenotypes which are in turn related to kidney damage. Only few clinical studies have addressed the relation between circulating chemerin and renal function in humans, and no population-based analyses have yet been performed. The potential influence of MetS-related phenotypes on the assumed association has been largely neglected. We aimed to investigate the association of serum chemerin with renal function in a general population with special regard to possible interactions between chemerin and metabolic phenotypes. Design, patients and measurements Linear and logistic regression models were applied to analyse data from 4082 subjects of the German Study of Health in Pomerania. Main outcomes included estimated glomerular filtration rate (eGFR), serum creatinine and cystatin C and chronic kidney disease. Results Inverse associations of chemerin with eGFR were observed. The components of the MetS emerged as modulating factors in this relation and enhanced the association. Logistic regression models confirmed the relation between chemerin and eGFR and revealed that each increase in chemerin per 25 ng/mL was associated with an about threefold higher odds of chronic kidney disease [odds ratio 2.72 (95% confidence interval 2.26-3.29)]. Conclusions Our results demonstrate a strong inverse association between serum chemerin levels and renal function. This association might be explained by MetS-related phenotypes, which lead to renal damage and are associated with increased chemerin levels and/or an impaired renal elimination of chemerin by diseased kidneys.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1111/cen.13449

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