Discrepancy of interleukin‐6 levels between end‐stage renal disease patients and patients with acute‐phase response with increased lipoprotein(a) concentrations

Abstract

Though the concentration of serum lipoprotein(a) [Lp(a)] is mostly determined by genetic factors, secondary factors such as acute‐phase response (APR) and end‐stage renal disease (ESRD) also contribute to its increase. Lp(a) is known to be one of the acute‐phase reactants and interleukin‐6 (IL‐6) is the key cytokine in the hepatic synthesis of acute‐phase proteins. The serum concentrations of Lp(a) and IL‐6 were measured in patients with APR and in patients with ESRD to investigate the relationship between Lp(a) and IL‐6. A total of 180 patients were selected for the study: 60 patients were normal controls, 60 were patients with renal disease who had been on hemodialysis for more than 6 months [C‐reactive protein (CRP)<4.0 mg/L], and 60 were APR patients who had a erythrocyte sedimentation rate (ESR) of over 50 mm/h. The three groups were age‐ and sex matched. The serum concentrations of Lp(a) and IL‐6 were measured by ELISA. The serum concentrations of Lp(a) [median (interquartile range)] in normal controls, ESRD patients, and APR patients were 0.222 (0.103–0.364) g/L, 0.511 (0.308–0.755) g/L, and 0.546 (0.234–0.747) g/L, respectively; those of IL‐6 were 1.0 (0.7–1.3) pg/mL, 2.1 (1.4–3.3) pg/mL, and 26.2 (15.2–35.6) pg/mL. The concentration of IL‐6, which increases Lp(a) synthesis, was much lower in ESRD patients than in APR patients (p<0.001). However, there were no significant differences in Lp(a) concentration between the two groups (p=0.88). In APR patients, the increase in Lp(a) synthesis seems to play a significant role in the increase in blood Lp(a), but there might be different mechanisms that regulate the increment of serum Lp(a) concentrations in ESRD patients other than synthesis of Lp(a).

• Acute‐phase response
• end‐stage renal disease
• interleukin‐6
• lipoprotein(a)