The cardiorenal syndrome: a review

Abstract

Cardiorenal syndrome (CRS) is the umbrella term used to describe clinical conditions in which cardiac and renal dysfunctions coexist. Much has been written on this subject, but underlying pathophysiological mechanisms continue to be unravelled and implications for management continue to be debated. A classification system-incorporating five subtypes-has recently been proposed though it has yet to permeate into day-to-day clinical practice. CRS has garnered much attention from both the cardiological and nephrological communities since the condition is associated with significant morbidity and mortality. Renal dysfunction is highly prevalent amongst patients with heart failure and has been shown to be as powerful and independent a marker of adverse prognosis as ejection fraction. Similarly, patients with renal failure are considerably more likely to suffer cardiovascular disease than matched subjects from the general population. This paper begins by reviewing the epidemiology and classification of CRS before going on to consider the different pathological mechanisms underlying cardiorenal dysfunction. We then focus on management strategies and conclude by discussing future directions in the diagnosis and management of patients suffering with CRS.

Figure 1

Illustration of the pathophysiological pathways activated by angiotensin II. Both preload and afterload are ultimately increased, leading to worsening cardiac and renal function (IL-6  =  Interleukin 6; TNF-α  =  Tumour necrosis factor alpha; TGF-β  =  Transforming growth Factor beta; ROS  =  Reactive oxygen species).