PURPOSE OF REVIEW: The purpose of this study is to review current perspectives 
regarding the pathogenesis of cardiorenal syndrome (CRS) in chronic kidney 
disease (CKD), and current treatment guidelines for this condition.
RECENT FINDINGS: The pathophysiological mechanisms underlying the development of 
CRS in CKD include neurohumoral, haemodynamic and CKD-related mechanisms. Recent 
evidence suggests that sympathetic nerve activity plays a role in CRS, but the 
SYMPLICITY HTN-3 trial failed to show a reduction of blood pressure after 
catheter-based renal denervation in patients with resistant hypertension. Kidney 
injury in patients with heart failure was previously considered to result from 
arterial underfilling due to low cardiac output, but the role of renal venous 
hypertension in this process has also recently been investigated. It would be 
useful to develop a reliable treatment option for CRS due to haemodynamic 
mechanism other than volume control using diuretics. Fibroblast growth factor 23 
(FGF23) is a phosphaturic hormone that has recently been identified as a 
CKD-related factor affecting CRS. FGF23 treatment has both advantages and 
disadvantages in terms of CRS progression.
SUMMARY: Multiple disorders underlie the development of CRS. Current treatment 
options include renin-angiotensin system blockade and volume control, but remain 
limited. A multidisciplinary approach is required to prevent CRS, including 
renal sympathetic denervation, treatment of renal venous hypertension and FGF23 
treatment.