Author + information
- Julio Núñez, MD∗ (, )
- Eduardo Núñez, MD,
- Gema Miñana, MD,
- Antoni Bayés-Genis, MD and
- Juan Sanchis, MD
- ↵∗Servicio de Cardiología, Hospital Clínico Universitario, Universitat de Valencia, Avenida Blasco Ibáñez 17, 46010 Valencia, Spain
We read with interest the article published by Salah et al. (1) in which they compared the prognostic meaning of plasma N-terminal pro–B-type natriuretic peptide (NT-proBNP) and creatinine changes in acute decompensated heart failure (ADHF). First, we would like to commend the authors for providing new valuable information aiming to unravel the clinical meaning of worsening renal failure (WRF) in ADHF. In this work, the authors found in a multicenter cohort of 1,232 patients admitted for ADHF that NT-proBNP changes during admission (a decrease higher than 30%), but not WRF, independently related to 180-day all-cause mortality and the composite of all-cause mortality and/or readmission for a cardiovascular reason (1).
These results are in agreement with recent reports in which WRF in ADHF patients lacked significant prognostic effect in a large spectrum of patients (2). WRF in ADHF is a final common pathway where several mechanisms and risk factors converge. This complex and multifactorial pathophysiology may explain why patients with WRF show mixed clinical response and outcomes (2). On one hand, WRF may be the mirror of low cardiac output and renal hypoperfusion, which lead to worse clinical outcomes (2); on the other hand, recent findings support that aggressive decongestion-mediated WRF may be also mirroring hemoconcentration, a condition associated to decongestion and clinical improvement (3).
In light of the current available knowledge, and to better understand the prognostic effect of renal kinetics in ADHF patients, we identify 3 scenarios that must be considered:
1. Clinical course and fluid overload status: A comprehensive approach, considering symptoms’ evolution, vital signs, fluid overload surrogates, volume of diuresis, and, maybe, natriuretic changes is mandatory. Thus, WRF may be a proxy of hemoconcentration rather than true glomerular filtration impairment in congestive patients subjected to an aggressive depletive treatment and showing clinical improvement, adequate diuresis, and/or significant decrease of natriuretic peptides. In contrast, clinical awareness should be adopted in cases of coexistence of WRF with clinical deterioration, persistent hypotension, oliguria, and either no significant decrease or even increase of natriuretic peptides. Thus, and relative to the Salah et al. (1) data, we speculate a potential differential prognostic effect of WRF across NT-proBNP changes.
2. Baseline renal function and magnitude of changes: Recently, we reported that the clinical impact of ADHF renal function kinetics is largely determined by the presence of renal failure on admission and the magnitude of changes (4). Most creatinine changes are mild and lack significant prognostic effect in patients with normal renal function. It is very likely that in this subgroup of patients, WRF is just a surrogate of hemoconcentration as a result of decongestive treatment. Conversely, in patients with renal failure on admission, any increase in creatinine, even mild, was independently associated with a higher risk of 1-year mortality (4). In this scenario, and particularly in those with unequivocal fluid overload, an appropriate decongestive response would result in an improvement of renal function rather than WRF. Therefore, in this subset of patients, WRF might truly represent glomerular filtration rate, as a reflection, among others, of more severe illness, inappropriate aggressive decongestion, or even nonresponse to decongestive therapy.
3. WRF time of onset and duration: In contrast to persistent WRF, which is usually associated with hemodynamic derangements and higher risk of adverse outcomes, transient WRF as a result of aggressive decongestive therapy may not be associated with poor outcomes (5).
Finally, we would like to highlight that current WRF definitions have been validated mostly in non–heart failure scenarios (2). In absence of well-validated and widely accepted cutoff in ADHF, we believe evaluating the continuum of renal changes may provide more valuable information.
Acknowledging that several pieces are still missing to complete this difficult puzzle, current knowledge suggests that despite WRF in ADHF shares a similar phenotype, it has very different underlying pathophysiological derangements and clinical meaning.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
- Salah K.,
- Kok W.E.,
- Eurlings L.W.,
- et al.
- Testani J.M.,
- Chen J.,
- McCauley B.D.,
- et al.
- Núñez J.,
- Garcia S.,
- Núñez E.,
- et al.