Author + information
- Karien van der Putten, MD,
- Lennart G. Bongartz, MD,
- Branko Braam, MD, PhD and
- Carlo A.J.M. Gaillard, MD, PhD* ()
- ↵*Department of Internal Medicine, Meander Medical Centre, P.O. Box 1502, 3800 BM Amersfoort, the Netherlands
The recent publication by Ronco et al. (1) provides a thorough description of the pathophysiology of the cardiorenal syndrome (CRS) and comes with a proposal for a new classification.
The innovative classification is based on the putative causative pathophysiological mechanism that underlies failure of the heart and kidneys. The classification focuses on 2 aspects of the process: duration (acute onset vs. chronic disease), and the sequence of events (kidney failure first vs. heart failure first). For clinical purposes, the distinction between acute and chronic CRS proposed by the authors seems very useful: they propose a clinical syndrome where acute heart failure (HF) leads to acute kidney injury (AKI) (type 1) and vice versa (AKI leading to acute HF; type 3). This seems relevant, because both conditions have a different pathogenesis and require a different clinical approach. However, the distinction between CRS type 2 (chronic HF leading to progressive chronic kidney disease [CKD]) and CRS type 4 (CKD leading to chronic HF and increased risk of cardiovascular events) is based on the assumption that, also in advanced and chronic disease, 2 different pathophysiological mechanisms can be distinguished.
In the paper by Bongartz et al. (2), we postulate a model of (chronic) cardiorenal interactions, with a quite different philosophy. In that model, we have searched for the common denominators in heart and renal failure (i.e., for similar pathophysiological interactions in “heart-kidney” and “kidney-heart” failure). We have been able to identify 4 cardiorenal connectors: inflammation, nitric oxide/reactive oxygen species balance, the sympathetic nervous system, and the renin-angiotensin system. In our view these connectors are, in addition to the well-known hemodynamic interactions between heart and kidney, responsible for the strongly progressive nature of the disease process, because they evoke positive feedback mechanisms. Therefore, the sequence in which the 2 conditions arise is not important.
Furthermore, we question the feasibility of the distinction between CRS type 2 and 4 in terms of diagnosis. In addition, both groups are similar in terms of management, because they both should receive optimal interventions to block the interaction between the cardiorenal connectors, in addition to the specific measures that apply to chronic HF and CKD.
- American College of Cardiology Foundation