The hemodynamic and nonhemodynamic crosstalk in cardiorenal syndrome type 1

Abstract

The organ crosstalk can be defined as the complex biological communication and feedback between distant organs mediated via cellular, molecular, neural, endocrine and paracrine factors. In the normal state, this crosstalk helps to maintain homeostasis and optimal functioning of the human body. However, during disease states this very crosstalk can carry over the influence of the diseased organ to initiate and perpetuate structural and functional dysfunction in the other organs. Heart performance and kidney function are intimately interconnected, and the communication between these organs occurs through a variety of bidirectional pathways. The cardiorenal syndrome (CRS) is defined as a complex pathophysiological disorder of the heart and the kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. In particular, CRS type 1 is characterized by a rapid worsening of the cardiac function leading to acute kidney injury. This clinical condition requires a more complex management given its more complicated hospital course and higher mortality. A lot of research has emerged in the last years trying to explain the pathophysiology of CRS type 1 which remains in part poorly understood. This review primarily focuses on the hemodynamic and nonhemodynamic mechanisms involved in this syndrome.

Keywords: Acute kidney injury; Cardiorenal syndrome; Heart and renal dysfunction; Hemodynamic mechanisms; Organ crosstalk.

Fig. 1

CRS type 1 is characterized by an acute worsening of heart function leading to AKI and/or dysfunction. Acute cardiac events that may contribute to AKI include acute decompensated heart failure, acute coronary syndrome, cardiogenic shock and cardiac surgery-associated low cardiac output syndrome.

Fig. 2

Cellular types involved in CRS type 1.