Related Experiment Video
Updated: Apr 18, 2026
A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
Published on: November 7, 2017
Cardiorenal syndrome in chronic kidney disease
Kazuhiko Tsuruya1, Masahiro Eriguchi
1aDepartment of Integrated Therapy for Chronic Kidney Disease bDepartment of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Insights
Cardiorenal syndrome (CRS) in chronic kidney disease (CKD) involves complex mechanisms. Current treatments are limited, necessitating a multidisciplinary approach for effective prevention and management.
Area of Science:
- Nephrology
- Cardiology
- Internal Medicine
Background:
- Cardiorenal syndrome (CRS) is a complex condition involving interactions between the heart and kidneys.
- Chronic kidney disease (CKD) significantly contributes to the pathogenesis of CRS.
- Understanding the interplay between cardiac and renal dysfunction is crucial for patient outcomes.
Purpose of the Study:
- To review current understanding of cardiorenal syndrome (CRS) pathogenesis in chronic kidney disease (CKD).
- To examine existing treatment guidelines for CRS in the context of CKD.
- To explore novel therapeutic targets and approaches for managing CRS.
Main Methods:
- Literature review of current perspectives on CRS pathogenesis.
- Analysis of recent findings on pathophysiological mechanisms.
- Evaluation of current treatment strategies and guidelines.
Main Results:
- CRS pathogenesis involves neurohumoral, hemodynamic, and CKD-related factors.
- Sympathetic nerve activity and renal venous hypertension are implicated in CRS.
- Fibroblast growth factor 23 (FGF23) emerges as a key CKD-related factor influencing CRS.
Conclusions:
- Current treatments for CRS, including RAS blockade and volume control, are limited.
- A multidisciplinary approach is essential for CRS prevention.
- Emerging strategies include renal sympathetic denervation, managing renal venous hypertension, and FGF23-targeted therapies.
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.
Related Concept Videos
01:18Chronic Kidney Disease IV: Nursing Management
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:28Chronic Kidney Disease III: Interprofessional Care
01:24Chronic Kidney Disease II: Clinical Manifestations
01:25Chronic Kidney Disease I: Introduction
01:22Heart Failure Drugs: Diuretics