Association between C-reactive protein levels and N-terminal pro-B-type natriuretic peptide in pre-dialysis patients

The prevalence of inflammation is high among patients with chronic renal failure but the reason of inflammation is unclear. We test the hypothesis that inflammation in chronic renal failure could be the consequence of an increased left-ventricular wall tension related to ventricular dysfunction, hypervolemia or both.

For assessing left-ventricular filling pressure, plasma level of N-terminal pro-B-type natriuretic peptide (N-BNP) was used, as B-type natriuretic peptide is secreted from the cardiac ventricles in response to increased wall tension. N-BNP levels and C-reactive protein (CRP) were measured on the same day in 75 pre-dialysis patients. A previous history of cardiomiopathy with systolic dysfunction was present in 27 (36%) of them.

The levels of N-BNP were not normally distributed (mean: 2,589 +/- 4,514 pg/ml; median: 789 pg/ml). The distribution of CRP levels was also not normal (mean: 15 +/- 27 mg/l; median: 5 mg/l). Both parameters correlated significantly (r: 0.41; p < 0.005). N-BNP was higher (p < 0.001) in patients with known ventricular dysfunction. Excluding these patients, the correlation between N-BNP and CRP was stronger (r: 0.88; p < 0.001). Univariate analysis in these patients without known cardiomyopathy showed that N-BNP levels also correlated with systolic and diastolic blood pressure (r: 0.54; p < 0.005) and inversely with creatinine clearance (r: -0.43; p < 0.01), serum albumin (r: 0.6; p < 0.001) and hemoglobin levels (r: 0.37; p < 0.05). CRP levels correlated significantly (p < 0.01) with the same parameters as N-BNP in univariate analysis. However, in multiple stepwise regression analysis in which CRP was the dependent variable, only the association with N-BNP remained significant (r: 0.87; p < 0.001).

Our results suggest a link between left-ventricular filling pressure and inflammation in patients with advanced renal insufficiency. The importance of strict volume control in these patients, in order to reduce left-ventricular pressure and therefore inflammation, should be considered.