Cardiorenal Dysfunction Mechanisms and Management

Cardiorenal dysfunction encompasses a spectrum of conditions in which impairment of the heart and kidneys interact bidirectionally, amplifying organ injury and clinical risk. Central mechanisms include haemodynamic alterations, neurohormonal activation, inflammation and oxidative stress. Reduced cardiac output and elevated venous pressure diminish renal perfusion, triggering compensatory activation of the renin–angiotensin–aldosterone system and sympathetic nervous system. While these responses initially support blood pressure and volume, chronic activation promotes fibrosis, endothelial dysfunction and further cardiac remodelling. Concurrently, systemic inflammation and reactive oxygen species exacerbate cellular injury in both organs. Management strategies span modulation of neurohormonal axes, optimisation of fluid status and targeted therapies such as sodium–glucose cotransporter 2 inhibitors, which have demonstrated efficacy in preserving both cardiac and renal function. Biomarkers and advanced imaging facilitate early diagnosis and phenotype-directed treatment, while novel interventions, including precision ultrafiltration and device therapies, offer avenues to mitigate progressive dysfunction. A multidisciplinary approach is essential to address the complex interplay of haemodynamic, hormonal and inflammatory pathways and to improve outcomes globally.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Cardiorenal Dysfunction Mechanisms and Management publication trend

The graph below shows the total number of articles in cardiorenal dysfunction mechanisms and management across all publications each year (not limited to Nature Index journals).

Technical terms

Cardiorenal syndrome: A classification of disorders in which acute or chronic dysfunction in the heart or kidneys induces dysfunction in the other organ.

Neurohormonal activation: Engagement of hormonal systems such as the renin–angiotensin–aldosterone system and sympathetic nervous system in response to reduced perfusion or pressure.

Oxidative stress: An imbalance favouring reactive oxygen species over antioxidant defences, leading to cellular injury.

Glomerular filtration rate: A measure of kidney function reflecting the volume of blood filtered by glomeruli per unit time.

Sodium–glucose cotransporter 2 inhibitors (SGLT2i): A class of medications that reduce glucose and sodium reabsorption in the renal proximal tubule, with benefits extending to cardiac and renal protection.

Biomarkers: Biological molecules or imaging measures used to detect or predict organ injury, guide therapy and assess prognosis.

References

1. Identification of novel biomarkers, shared molecular signatures and immune cell infiltration in heart and kidney failure by transcriptomics. Frontiers in Immunology (2024).
2. The Need to Identify Novel Markers for Early Renal Injury in Cardiorenal Syndrome. Cells (2024).
3. Oxidative Stress: Dual Pathway Induction in Cardiorenal Syndrome Type 1 Pathogenesis. Oxidative Medicine and Cellular Longevity (2015).
4. The Physiopathology of Cardiorenal Syndrome: A Review of the Potential Contributions of Inflammation. Journal of Cardiovascular Development and Disease (2017).
5. Current and Potential Therapeutic Strategies for Hemodynamic Cardiorenal Syndrome. Cardiorenal Medicine (2015).
6. New Insight in Cardiorenal Syndrome: From Biomarkers to Therapy. International Journal of Molecular Sciences (2023).
7. Role and Mechanism of the Renin-Angiotensin-Aldosterone System in the Onset and Development of Cardiorenal Syndrome. Journal of the Renin-Angiotensin-Aldosterone System (2022).
8. Cardiorenal Syndrome: An Updated Classification Based on Clinical Hallmarks. Journal of Clinical Medicine (2022).