Key result
Urinary NT-proBNP excretion was substantially lower in patients with chronic heart failure compared with healthy controls (median, 0.13 vs 2.3 mL/min; P<0.001).
Why the study?
Is urinary NT-proBNP excretion altered in patients with chronic heart failure compared to healthy controls?
Case-Control (n=114)
Is urinary NT-proBNP excretion altered in patients with chronic heart failure compared to healthy controls?
Elevated plasma NT-proBNP levels in heart failure patients may be partially explained by a marked decrease in urinary excretion associated with reduced renal plasma flow, rather than solely by increased myocardial stress.
Answers are grounded in this paper and cite their sources.
Reduced urinary NT-proBNP excretion may contribute to elevated plasma levels in HF; hypothesis-generating and requires prospective validation before clinical use.
BACKGROUND: Urinary excretion is currently regarded as the main mechanism of elimination of N-terminal prohormone brain natriuretic peptide (NT-proBNP). The clinical implications and the value of measurement of urinary NT-proBNP in patients with heart failure are largely unknown. METHODS AND RESULTS: We studied 94 patients (age, 58+/-11 years; 79% men) with chronic heart failure (CHF) and 20 age- and sex-matched healthy control subjects. Glomerular filtration rate and effective renal plasma flow were measured as clearance of (125)I-iothalamate and (131)I-hippuran, respectively. NT-proBNP levels were determined in both plasma and 24-hour urine collections. Mean left ventricular ejection fraction of CHF patients was 0.28+/-0.09. Plasma NT-proBNP levels were higher in CHF patients compared with control subjects (median, 547 versus 41 pg/mL; P<0.001). Urinary NT-proBNP excretion, however, was substantially lower in CHF patients (median, 0.13 versus 2.3 mL/min; P<0.001). Urinary NT-proBNP excretion was independent of estimated glomerular filtration rate. In both CHF patients and control subjects, there was a strong and inverse relation between plasma NT-proBNP concentrations and urinary NT-proBNP excretion (r=-0.72 and r=-0.65 respectively; both P<0.001). Decreased renal plasma flow in CHF was significantly associated with a lower excretion of NT-proBNP (P=0.026). CONCLUSIONS: Urinary NT-proBNP excretion is lower in patients with CHF compared with control subjects and is inversely related to plasma NT-proBNP. Urinary NT-proBNP is associated with renal plasma flow but not with estimated glomerular filtration rate. Elevated levels of plasma NT-proBNP in patients with CHF might be explained not only by myocardial stress but also by a marked decrease in urinary excretion.
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Linssen et al. (2009) conducted a case-control in Chronic heart failure (n=114). Chronic heart failure vs. Healthy control subjects was evaluated on Urinary NT-proBNP excretion (mL/min) (p=<0.001). Urinary NT-proBNP excretion was substantially lower in patients with chronic heart failure compared with healthy controls (median, 0.13 vs 2.3 mL/min; P<0.001).
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