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Cardiorenal and renocardiac syndromes: the need for a comprehensive classification and consensus

Nature Clinical Practice Nephrology volume 4, pages 310–311 (2008)Cite this article

The term 'cardiorenal' has been used in the medical literature for several decades, principally to describe the hemodynamic and neurohormonal connections between the heart and the kidneys. In recent years, the term 'cardiorenal syndrome' (CRS) has enjoyed widespread use, yet a precise definition is lacking. Some investigators have suggested that this term should be used to describe patients with coexisting severe cardiac and renal dysfunction,1 and other experts have recommended the use of a specified serum creatinine level as one of the criteria for CRS.2 Many others have posited that the term be used to describe the state in which advanced congestive heart failure (CHF) becomes complicated by acute impairment of kidney function.3 In August 2004, the US National Heart, Lung, and Blood Institute convened a working group to examine the state of knowledge regarding heart–kidney interactions and to develop recommendations for future investigation.3 This group focused its attention on the situation in which renal responses are thought largely to be the result of primary changes in cardiac function. The following definition of CRS arose from these discussions: 'a state in which therapy to relieve CHF symptoms is limited by further worsening renal function'. However, we believe that this and other definitions are too narrow in scope and ignore the bidirectional nature of a relationship we have described as a complex symbiosis.4

The view of cardiorenal interactions as simply analogous to those between a pump and a filter has been challenged as our understanding of the complex relationship between these organs grows. Both organs contribute to regulation of blood pressure, vascular tone, diuresis, natriuresis, circulating volume homeostasis, peripheral perfusion and tissue oxygenation. Dysfunction of one of these organs can lead to considerable and lasting damage to the other, leading to a spiral of dysfunction in both. Possible mechanisms of this spiraling dysfunction include altered balance between nitric oxide and reactive oxygen species, systemic inflammation and apoptosis, activation of both the sympathetic nervous system and the renin–angiotensin–aldosterone system (RAAS), and the paracrine and systemic actions of various substances such as endothelin, prostaglandins, vasopressin and natriuretic peptides.1,2 We4 and others5 have suggested that the definition of CRS should be expanded and refined, to better reflect the bidirectional nature of heart–kidney interactions. A new, more comprehensive definition and classification will focus much needed interdisciplinary attention upon cardiorenal interactions and will foster recognition of the complex and serious nature of the clinical disorders that arise from this symbiosis.

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Authors and Affiliations

  1. C Ronco is Head of the Department of Nephrology, Dialysis and Transplantation at St Bortolo Hospital, Vicenza, Italy,

    Claudio Ronco

  2. AA House is Medical Director of Hemodialysis and Chief of Nephrology at University Hospital and Associate Chief of Nephrology at the University of Western Ontario, London, ON, Canada.,

    Andrew A House

  3. M Haapio is a Consulting Nephrologist in the Division of Nephrology at Helsinki University Central Hospital, Helsinki, Finland,

    Mikko Haapio

Authors
  1. Claudio Ronco
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  2. Andrew A House
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  3. Mikko Haapio
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Corresponding author

Correspondence to Mikko Haapio.

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The authors declare no competing financial interests.

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Supplementary Table 1

'Cardiorenal syndrome classification' (PPT 33 kb)

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Ronco, C., House, A. & Haapio, M. Cardiorenal and renocardiac syndromes: the need for a comprehensive classification and consensus. Nat Rev Nephrol 4, 310–311 (2008). https://doi.org/10.1038/ncpneph0803

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