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(Hypertension. 2004;43:e14.)
© 2004 American Heart Association, Inc.
Letters to the Editor |
Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands
Department of Nephrology, University Medical Center Utrecht, Utrecht, The Netherlands
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
With much interest we have read the article by Sarnak et al1 on the risk of kidney disease for the development of cardiovascular disease. Considering the rising prevalence of chronic kidney disease and heart failure, we propose to perceive the reciprocal relationship of heart and kidney failure as a separate disease entity. This severe cardiorenal syndrome (SCRS) can be defined as the accelerated and extensive cardiovascular disease exclusively related to the coexistence of renal failure and heart disease.
In agreement with Sarnak et al, we feel that many questions remain unanswered. However, we would like to underscore the lack of insight in how renal and heart failure-related risk factors interact to lead to the SCRS. This inspired us to attempt to develop a model of heart/kidney interaction. The legacy of the late professor Guyton is a solid model to explain heart/kidney interaction by cardiac output, regulation of the extracellular fluid volume, blood pressure, and renal sodium handling. Central in the model of Guyton is the reninangiotensin system (RAS), with its corresponding extensions (aldosterone, endothelin), and its antagonists (natriuretic peptides). While the model seems appropriate to explain extracellular fluid volume, blood pressure, and cardiac output in combined heart and renal failure, can it also explain the accelerated atherosclerosis, cardiac hypertrophy, and remodeling and progression of renal disease?
To answer these questions, we propose an extension to the Guytonian model for volume and blood pressure control, the cardiorenal connection (CRC) (Figure). At the corners of this model
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