| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2857140 | The American Journal of Cardiology | 2010 | 7 Pages |
The nonosmotic release of arginine vasopressin, concurrent with the activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, is thought to represent the maladaptive response that is central to the pathophysiology of heart failure (HF). The degree of neurohormonal activation correlates with the severity of the disease and can predict the outcomes. However, quantification of components of neurohormonal axis (e.g., serum arginine vasopressin level) is mainly reserved for research purposes rather than routine practice. The results of several recent HF trials have shed light on the differential role of blood urea nitrogen (BUN) and creatinine in predicting the outcomes in this setting. These studies suggest that BUN could indeed represent a surrogate marker for “renal response” to neurohormonal activation in this setting, above and beyond its role in the estimation of renal function. In this report, the relevant physiologic mechanisms underlying urea and water transport in the kidney are first reviewed. Then, the activation of the neurohormonal axis and the impact of its components on renal urea transport, independent of changes in renal function, are explained. Finally, the unique role of BUN as a biomarker of neurohormonal activation in the setting of HF is discussed, and the potential clinical implication of this novel concept is emphasized. In conclusion, this review explains the pathophysiologic basis for the emerging role of BUN as a biomarker in HF.
