Residual Kidney Function and Prevention of Cardiovascular Risk – Have We Said It All?
Chronic kidney disease (CKD) has a strong association with increased cardiovascular (CV) risk, and residual kidney function (RKF) has recently been recognized as a key determinant of this burden. Through the removal of fluids and uremic toxins, modulation of systemic inflammation, and improved metabolic stability, RKF is linked to better cardiovascular outcomes. Despite advances in pharmacological therapies, dialysis innovation, and lifestyle interventions, patients with CKD still generally experience increased CVD mortality. This highlights the necessity of evaluating the multifactorial function of RKF in CV risk reduction. It highlights processes and pathophysiological mechanisms linking RKF and CV health, especially with its role in systemic inflammation, oxidative stress, and regulation of volume. Data from several large clinical trials suggest the benefit of RKF preservation, including lower arterial stiffness, better BP control, and lower left ventricular hypertrophy (LVH) and CV mortality. Presently, pharmacological approaches are recommended to prevent the progression of RKF (e.g.,sodium-glucose co-transporter-2 (SGLT2) inhibitors and renin-angiotensin-aldosterone system (RAAS) blockers), along with lifestyle changes as well as advances in dialysis technology (e.g., incremental and peritoneal dialysis). Novel strategies like regenerative therapies and muscle biomarkers bring hope for personalized care. This paper provides a roadmap for enhancing our understanding of and approach to CKD care by drawing attention to the role of RKF in preventing CV risk and knowledge gaps in the field. In essence, inventive strategies are needed to realize RKF’s capacity to enhance cardiovascular outcomes.“
Authors
- Zorica Dimitrijević (ORCID: https://orcid.org/0000-0002-4944-1822)
Publication Details
- Published
- 2025-01-01
- DOI
- https://doi.org/10.46793/karnef25.095d
- Primary Topic
- Blood Pressure and Hypertension Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00