C-Reactive Protein and Interleukin-6 Levels Are Related to Renal Function in Predialytic Chronic Renal Failure

Abstract

Background: Several studies have provided convincing evidence that in apparently healthy subjects elevated serum levels of plasma C-reactive protein (CRP) are associated with an increased risk of experiencing myocardial infarction and sudden cardiac death. It has been claimed that, in dialytic patients, the hepatic synthesis of this ‘acute phase response’ plasma protein is primarily induced by the macrophage-derived interleukin 6 (IL-6). Little information is available, however, regarding CRP and IL-6 plasma levels in pre-dialytic renal failure. Methods: Plasma CRP by a modification of the laser nephelometry technique, IL-6 and serum albumin were determined in 103 chronic pre-dialytic patients (mean age 50 ± 6.3 years; creatinine clearance (Cr.cl.) 36.3 ± 23.1 ml/min). Results: CRP was >5 mg/l (normal upper range) in 42% of the global population. CRP and IL-6 were significantly related (r = 0.35, p < 0.0004). CRP and IL-6 were related to renal function (CRP vs. Cr.cl., r = –0.56, p < 0.0001; IL-6 vs. Cr.cl., r = –0.55, p < 0.0001, Spearman correlation coefficient). When patients were divided in tertiles according to renal function, CRP median value resulted 7.9 mg/l (interquartile interval: 5–12) in the first tertile (Cr.cl. <18.5 ml/min), 4.0 mg/l (3–6) in the second tertile (Cr.cl. 18.5–45 ml/min) and 3.2 mg/l (2.7–4.0) in the last tertile (Cr.cl. >45 ml/min) (p < 0.0001). A negative correlation between CRP and S-albumin was also found (r = –0.52, p < 0.0001, Spearman correlation coefficient). Conclusions: IL-6 and CRP were increased and were inversely related to creatinine clearance in our population of 103 chronic predialytic patients. The possibility of a decreased renal clearance of CRP and/or cytokines as a cause of an activated acute-phase response is discussed. A negative correlation between CRP and S-albumin was found confirming the link between chronic inflammation and malnutrition in chronic renal patients.

Biomarkers in Chronic Kidney Disease - The Linkage Between Inflammation, Ventricular Dysfunction and Overhydration

“…However, a similar prevalence of inflammation has been described in patients with advanced renal failure not yet on dialysis (Ortega et al, 2002;Panichi et al, 2002;Stenvinkel et al, 1999). An inverse correlation between CRP levels and clearance of creatinine has been observed (Panichi et al, 2002); thus, CRP levels increase as renal function declines. This finding suggests the possibility of a decreased renal clearance of CRP as a cause of an activated acute-phase response in patients with chronic kidney disease.…”

“…Activation of monocytes with the subsequent enhanced release of inflammatory cytokines can be caused by membrane-induced complement activation, by direct cell-membrane interaction and by dialysis fluids containing endotoxins (Carracedo et al, 2006;Honkanen et al, 1991;Kerr et al, 2007;Schouten et al 2000). However, a similar prevalence of inflammation has been described in patients with advanced renal failure not yet on dialysis (Ortega et al, 2002;Panichi et al, 2002;Stenvinkel et al, 1999). An inverse correlation between CRP levels and clearance of creatinine has been observed (Panichi et al, 2002); thus, CRP levels increase as renal function declines.…”

Limitations of Cox Proportional Hazards Analysis in Mortality Prediction of Patients with Acute Coronary Syndrome

“…In the multivariable model, the following were considered risk of death factors that fulfilled the proportional hazard assumption: smoking and elevated concentrations of homocysteine and NTproBNP. The influence of these factors on long-term prediction in patients with ACS has been confirmed in numerous works (Akerblom et al, 2013;Bellomo et al, 2003;Bjorklund, 2005;Danaei et al, 2006;De Sutter, 2005;Fácila et al, 2005;Jernberg, 2004;Lawler et al, 2013;Panichi et al, 2002;Rutkowski et al, 2005;Sitkiewicz, 2007;Walker et al, 2006).…”

The Serum Irisin Level in Non-Diabetic Patients with Chronic Kidney Disease

“…In CKD patients progression of renal failure causes metabolic dysfunction, including metabolic acidosis, insulin resistance, and inflammation, which can lead to increased energy expenditure (4,19). In addition to metabolic dysfunction, uremic toxins and recurrent infections in CKD provide a foundation for chronic inflammation.…”

“…According to studies performed in numerous countries, metabolic imbalance and abnormal energy expenditure varies (18%-80%) in CKD patients according to the stage of disease (2). In most such studies metabolic imbalance has been hypothesized to be the result of chronic inflammation (3,4), oxidative stress (5), and insulin resistance (6), Among these three factors, chronic inflammation plays a primary role in energy expenditure.…”