Heart-Kidney Cross-Talk

Abstract Heart-kidney cross-talk is illustrated best in cardiorenal syndrome (CRS) type, which is characterized by the development of acute kidney injury (AKI) and dysfunction in the patient with acute heart failure (AHF). Multiple pathophysiologic mechanisms operating simultaneously and sequentially to result in the clinical syndrome characterized by a rise in serum creatinine, oliguria, diuretic resistance, and in many cases, worsening symptoms of congestion. The milieu of chronic kidney disease has associated factors including obesity, cachexia, hypertension, diabetes, proteinuria, uremic solute retention, anemia, and repeated subclinical AKI events work to escalate individual risk of CRS in the setting of AHF. Many of these conditions have been linked to progressive cardiac and renal fibrosis. In the hospitalized patient, hemodynamic changes leading to venous renal congestion, neurohormonal activation, hypothalamic-pituitary stress reaction, inflammation and immune cell signaling, systemic endotoxemic exposure from the gut, superimposed infection, and iatrogenesis contribute to CRS type 1. The final common pathway of bidirectional organ injury appears to be cellular, tissue, and systemic oxidative stress, which worsens cellular and tissue function. This chapter explores in the detail the pathophysiologic pathways that describe heart-kidney cross-talk in the setting of AHF.