Cardiorenal syndrome in chronic kidney disease.

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.