Author + information
- James L. Januzzi, MD, FACC⁎ (, )
- Donald M. Lloyd-Jones, MD, ScM, FACC and
- Saif Anwaruddin, MD
- ↵⁎Massachusetts General Hospital, Cardiology/Internal Medicine, Yawkey 5984, 55 Fruit Street, Boston, Massachusetts 02114
Lamb and colleagues attempt to compare the results of our study to their previously published (1) data, derived from a small cohort of nondyspneic subjects (the vast majority of whom did not have heart failure [HF]). These comparisons are uninformative, and the more appropriate approach would be to examine our data in the context of the currently available data examining the utility of B-type natriuretic peptide (BNP) in the breathless patient (with and without HF) (2).
In our study, the area under the receiver operating characteristic curve (AUC) for amino-terminal pro-B-type natriuretic peptide (NT-proBNP) for diagnosis of acute HF in those with moderate or worse chronic kidney disease (CKD) was 0.88, comparable to the data from such patients in the Breathing Not Properly Multinational Study renal analysis (AUC between 0.81 and 0.86) (2). It is of great interest to us that specificity for BNP in those with CKD was not reported (2); however, with such similar AUC, there is little chance that the specificity of BNP in those with CKD is any different than demonstrated for NT-proBNP in our study. We point out that the specificity of NT-proBNP >1200 pg/ml for acute HF in patients with CKD was 72%, comparing favorably to the overall specificity of 76% reported among allsubjects in the Breathing Not Properly Multinational Study of BNP (3). As well, NT-proBNP <300 pg/ml had 100% negative predictive value in patients with CKD in our study, and concentrations of NT-proBNP were also strongly prognostic in those with CKD.
Thus, although correlations between renal function and BNP or NT-proBNP may differ, at optimal cut-points it would be rather hard to argue that a clinically meaningful difference between BNP and NT-proBNP exists in those with CKD, and the assertion by Lamb and colleagues that NT-proBNP has “unacceptable performance” in the patient with CKD is not accurate.
Lamb and colleagues quite incorrectly suggest that we asserted NT-proBNP testing to be “unaffected” by renal function. We emphasized the effects of renal function on NT-proBNP, but concluded “even in the presence of impaired renal function, NT-proBNP measurement is a valuable tool for the diagnostic and prognostic evaluation of dyspneic patients,” a conclusion supported by our data.
Whereas observationalstudies demonstrate that CKD leads to elevations in both BNP and NT-proBNP (with modest differences with respect to the magnitude of elevation of each), it is dangerous to necessarily ascribe such phenomena entirely to differential dependence on renal clearance. Indeed, early mechanisticstudies of renal function and natriuretic peptides suggest the kidneys clear both markers equally(and at only 20%) (4).
The interaction between natriuretic peptides and CKD is a complex one; we concede the potential for difficulties in interpretation of NT-proBNP concentrations in those with impaired kidney function, but we strenuously emphasize that this is a circumstance that also hinders use of BNP (5). In summary, the available data do not support a clinically meaningful difference between NT-proBNP and BNP in those with CKD, and the data contradict the tacit suggestion by Lamb and colleagues that BNP is superior to NT-proBNP in those with impaired renal function.
- American College of Cardiology Foundation