Emerging device therapies targeting renal hemodynamics offer a potential new approach for managing acute cardiorenal syndrome beyond traditional diuretic therapy.
While the existence of cardiorenal perturbations has been known for nearly 2 centuries, only in the past 2 decades has significant progress been made in classifying these alterations and characterizing the pathobiology and hemodynamic signature of cardiorenal syndrome (CRS). Empiric intravenous diuretic therapy with fluid and sodium restriction and selective use of vasoactive agents have remained cornerstones of managing acute heart failure with or without acute CRS; however, recent clinical data has exposed the shortcomings of this approach. The traditional view of CRS has long focused on low cardiac output with resultant renal arterial hypoperfusion as the central hemodynamic derangement but this too, has been challenged by new preclinical and clinical observations. Renal venous congestion/hypertension has since been identified as an important hemodynamic contributor to the development of CRS, resulting in diminished renal perfusion pressure, defined as the difference between arterial driving pressure and renal venous pressure. Novel circulatory renal assist devices for the treatment of acute (type I) CRS are in development and may be divided into 2 broad categories: "pushers" which aim to improve renal arterial perfusion (renal preload) and "pullers" which are designed to reduce renal venous congestion (renal afterload). Numerous devices have shown promise in early-stage clinical studies but none have been approved yet for commercial use in the United States. The value of CRS device therapies will ultimately rest on safety as well as the ability of these devices to effect predictable, meaningful, and durable improvements in renal function along with clinical and hemodynamic markers of congestion.
Nathan et al. (Wed,) studied this question.