In a recent study of patients with non–dialysis-dependent chronic renal failure and no clinical history of heart failure, circulating B-type natriuretic peptide (BNP) levels were independently correlated with echocardiographic evidence of left ventricular overload but not with serum creatinine. These findings suggested that subclinical cardiac dysfunction, and not renal insufficiency itself, raised BNP levels.
Now, researchers have measured levels of both BNP and its precursor, N-terminal pro-BNP (NT-proBNP), in 213 patients with chronic kidney disease (mean serum creatinine level, 3.3 mg/dL) and a mean ejection fraction of 68%; only 6% of patients had histories of heart failure. Mean BNP level was 14 pmol/L, and mean NT-proBNP level was 89 pmol/L. In multivariate analyses, both left ventricular mass index and the extent of renal dysfunction were associated independently with levels of both BNP and NT-proBNP. Declining renal function affected NT-proBNP more than BNP levels.
In this study, unlike the previously cited study, both reduced glomerular filtration and subclinical cardiac dysfunction affected plasma natriuretic peptide levels in patients with chronic renal insufficiency. Perhaps different patient populations in the two studies account for the different findings. In any case, the effect of renal failure on mean BNP level was modest: Levels ranged from 9 pmol/L among patients whose serum creatinine levels were around 2.0 mg/dL, to 22 pmol/L among patients whose serum creatinine levels were around 6.0 mg/dL. These results suggest that markedly elevated BNP levels should not be attributed simply to reduced renal function.
Reference:
Vickery S et al. B-type natriuretic peptide (BNP) and amino-terminal proBNP in patients with CKD: Relationship to renal function and left ventricular hypertrophy. Am J Kidney Dis 2005 Oct; 46:610-20.