In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

The cardio-renal syndrome

Heart Failure

There is an expanding use of the term cardiorenal syndrome (CRS) in the medical literature. The negative prognostic impact of impaired renal function in patients with heart failure is nowadays well recognized by cardiologists and many clinicians are also faced with the trouble of managing patients with acute heart failure and not responding to diuretic treatment, eventually with deteriorating renal function and clinical status.

For many years, the term CRS was mostly used to describe the latter. In spring 2010, the acute dialysis quality initiative (ADQI) consensus document was published in the European Heart Journal. Through collaboration between cardiologists, nephrologists and intensivists a definition of CRS was put forward. The new definition and classification emphasizes the bidirectional nature (cardio-renal and reno-cardiac) and multilevel (biological, physical and chemical) interaction between the heart and kidney. The new classification and clinical management of patients with the cardio-renal syndrome were discussed as a Focus session here at the ESC.

Dr Mikko Haapio (Helsinki, Finland), one of the co-authors of the original CRS classification presented a case clearly showing that primary renal disease in a very short time led to disturbance in cardiac structure and function, an example of the type 4 chronic cardiorenal syndrome. Even though CRS is most common in patients with acute and chronic heart failure, the novel CRS classification extends the definition far beyond heart failure. The impact of renal dysfunction on prognosis is very much present in cardiovascular disease in general. Conversely, patients with primary kidney disease have a much higher risk of dying of cardiovascular reasons than progressing to renal failure requiring dialysis. Therefore, special attention should be paid to symptoms of heart disease in these patients and cardiovascular disease should be actively looked for. Patients with renal insufficiency should not be denied invasive procedures or treatment because of the fear of kidney complications. The cardiovascular morbidity and mortality risk usually outweighs the increased procedural risk.

The importance of accurate assessment of kidney function was again emphasized. Preferably, glomerular filtration rate should be estimated from creatinine values using equations such as the MDRD equation (eGFR). Although useful when renal function is stable, neither the Cockcroft-Gault formula nor the MDRD equation are accurate in acute kidney injury (AKI) when rapid changes in renal function occur. So far, we have relied on the rather slow marker creatinine but novel markers, rapid and more specific of kidney injury (KIM, NGAL), are entering the scene. Their clinical utility remains to be determined.

In his presentation about managing a patient with chronic heart failure and renal dysfunction, Dr Kevin Damman (Groningen, Netherlands) admitted that there is very limited evidence to guide clinicians. The fact that ACE-inhibitors can affect renal function negatively is well known. Some patients have a clear rise in creatinine, but if it stays below 50%, ACE-inhibitors can be continued while monitoring kidney function. Here again, the long-term benefit of ACE-inhibition on cardiac end renal function is well documented, and in some patients initiation of ACE-inhibitors can actually improve kidney function.

Both impaired and progressively deteriorating renal function are associated with an increased risk of mortality in heart failure patients. Doses of ACE-inhibitors and diuretics need to be adjusted individually, but there is really not much data on what the optimal dose is for each patient. Since both the heart disease and medications can have unfavourable effects on kidney function, regular and repeated assessments of renal function are required. Hypovolemia and nephrotoxic drugs need to be avoided but Dr Damman strongly discouraged stopping the ACE-inhibitor therapy. Halving the dose may be necessary temporarily, and the diuretic dose can be decreased or increased as needed. The take home message was that these patients very much need individualised therapeutic strategies.

In the final presentation of the session, Prof. John McMurray (Glasgow, UK) used the example of a patient with acute heart failure, volume overload and elevated creatinine to discuss the issue of diuretic use for decongestion. The results of the DOSE trial, presented previously this year but not yet published, showed that similar degrees of decongestion were achieved with both furosemide boluses and continuous infusion without any difference in renal effects. The trial also assessed two different dosing strategies of intravenous diuretics: a higher-dose (2.5x the oral dose) and a lower dose (1x the oral dose). The high-dose group had increased diuresis and weight loss, translating into better symptom relief and there were no evident negative effects on renal function in this trial. An early initiation of ACE-inhibitor was discussed, and use of short-acting agents could be preferred in the initial phase in case adverse effects occur. How to overcome diuretic resistance is a difficult question, but sometimes combining loop diuretics and thiazides can be very effective. Watch out for the potassium level though!




The cardio-renal syndrome
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.