The cardiorenal syndrome: making the connection

Abstract

The heart and the kidneys share responsibility for maintaining hemodynamic stability and end-organ perfusion. Connections between these organs ensure that subtle physiologic changes in one system are tempered by compensation in the other through a variety of pathways and mediators. In the setting of underlying heart disease or chronic kidney disease, the capacity of each organ to respond to perturbation caused by the other may become compromised. This has recently led to the characterization of the cardiorenal syndrome (CRS). This review will primarily focus on CRS type 1 where acute decompensated heart failure (ADHF) results in activation of hemodynamic and neurohormonal factors leading to an acute drop in the glomerular filtration rate and the development of acute kidney injury. We will examine the scope and impact of this problem, the pathophysiology associated with this relationship, including underperfuson and venous congestion, diagnostic tools for earlier detection, and therapeutic interventions to prevent and treat this complication.

Figure 1

Pathophysiology of the relation between venous congestion and reduced glomerular filtration rate (GFR). Reprinted with modification from Damman et al. [28].

Figure 2

Hypothetical vicious circle of decreased glomerular function, endothelial injury, and tubular damage in heart failure. GFR: glomerular filtration rate. NGAL: neutrophil gelatinase associated lipocalin. NAG: N-acetyl-beta-D-glucosaminidase. KIM-1: kidney injury molecule 1. Adapted and reprinted with permission from Norman and Fine [59] and Damman et al. [60].

Figure 3

Urinary biomarker profiles in subjects who develop AKI after cardiopulmonary bypass (CPB) surgery. Abbreviations: AKI: acute kidney injury, defined as a 50% increase in serum creatinine from baseline; NGAL: neutrophil gelatinase associated lipocalin; IL-18: interleukin 18; KIM-1: kidney injury molecule 1; L-FABP: liver-type fatty acid binding protein; Cys: cystatin c; creat: creatinine. Adapted and modified with permission from Devarajan [65].