Page 142 - Biomarkers for risk stratification and guidance in heart failure

Prognostic impact of change in NT-proBNP versus change in eGFR.
in combination with an increase in NT-proBNP might be caused by dilution caused by fluid accumulation in worsening HF with the need of intensifying HF medication. Given the positive results of those natriuretic peptide-guided trials intensifying evidence based HF medication, this should focus on increasing diuretic therapy only in those patients with clinically evident congestion. Although these hypotheses and recommendations are plausible and supported not only by our results but also by the studies discussed above,14,26,29 they should be confirmed and tested prospectively by future clinical research.
Limitations
There are some limitations to our study. The data used for this analysis was
derived from a multicenter trial assessing the effect of NT-proBNP-guided therapy
in chronic heart failure. Therefore, in half of the study-population, NT-proBNP concentration was known to the treating physician at the outpatient clinic, and in
all of the patients included for this subanalysis, renal function at discharge and at 1
month follow-up visit was available. Knowledge of NT-proBNP and renal function
may have influenced therapeutic decisions. However, in multivariate analysis
correcting for randomization group, results regarding the effects of changes in NT-
proBNP and eGFR were not significantly altered. In order to be included into the
PRIMA study NT-proBNP concentration during admission needed to decrease at
least 10% with a minimum of 850 pg/ml. Therefore, we cannot exclude that results 6 in patients with a smaller decrease or an increase in NT-proBNP concentration
during hospital admission could have been different. Furthermore, as the current study is a post-hoc analysis the hypothesis derived from our data needs to be tested in a prospective, preferably larger study.
Conclusion
In HF patients early after hospital discharge, change in NT-proBNP may give insight in the potential cause of worsening renal function because it specifically addresses the cardiac part of the cardiorenal syndrome. Our data suggest that this cardiac part is significantly more important than the renal part and may help to better target therapy in this patient group prone to cardiovascular events. However, future studies on the correlation of specific treatment strategies in different cardiorenal groups is needed to propose an individual treatment algorithm based on the combination of changes in natriuretic peptides and renal function.
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