Cardiorenal syndrome— common, complex, deadly

Martha J Wrigley, Clinical Trials Manager, Senior Lead Research Nurse Surrey and Sussex CLRN, Ashford and St Peter’s Hospitals NHS Foundation Trust C ardiorenal syndrome is an umbrella term for the range of interactions between the heart and kidneys. Commonly it focuses on the potential for reducing renal function as a result of heart disease and the impact on the heart of reduced renal functional reserve. Importantly, these interactions include both consequences of the disease state and those arising from therapeutic cardio-renal interventions. Renal dysfunction has consistently been shown to be one of the strongest predictors of morbidity and all-cause mortality in a broad spectrum of patients with cardiovascular diseases including heart failure (HF) (Hillege et al, 2006). According to a recent meta-analysis including over 80000 chronic HF patients, mortality worsens incrementally across the range of renal function (Smith et al, 2006). Worsening renal function is also a common complication during the treatment of acute decompensated HF (ADHF). Around 20–40% of ADHF patients concurrently develop reducing renal function (Ronco et al, 2010). Studies have repeatedly linked the development of this reduction in renal function to greater short and long-term all-cause and cardiovascular mortality, prolonged hospitalizations, increased readmission rates, accelerated progression to CKD stages 4–5 and higher health-care costs (Damman et al, 2007). The complex pathophysiology of renal dysfunction in HF appears to be multi-factorial and is not well defined. Traditionally, renal dysfunction in HF was thought to be caused by reduced renal perfusion as a result of depleted intravascular volume and/or low cardiac output. However, a large trial of pulmonary catheter-guided treatment of patients with ADHF failed to confirm this (Nohria et al, 2008). Consequently, the pathophysiological concept has been broadened and an overall imbalance between the failing heart, the neurohumoral system and inflammatory responses has been associated with the occurrence of renal dysfunction. Haemodynamic factors, including the adequacy of renal perfusion and the degree of venous congestion as well as drug nephrotoxicity, all appear to contribute to the development of worsening renal function in this context. Furthering our understanding of these interactions and how both drug and dialysis treatment (McIntyre, 2010) affect the interactions between kidneys and heart is a crucial target for cooperative and combined renal and cardiology research. Cardiorenal syndrome— common, complex, deadly