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Updated: May 31, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Differential effect of chronic kidney disease on right-sided extravalvular damage in low-flow, low-gradient aortic
Eric J Kim1, Yash Prakash1, Hassan Beesley1
1Samuel Bronfman Department of Medicine at Mount Sinai Hospital, New York, New York.
Insights
Advanced kidney dysfunction and right-sided damage significantly increase mortality after transcatheter aortic valve replacement (TAVR) in low-flow, low-gradient aortic stenosis (LFLG AS), especially in paradoxical subtypes.
Area of Science:
- Cardiology
- Nephrology
- Cardiac Surgery
Background:
- Transcatheter aortic valve replacement (TAVR) is a key intervention for low-flow, low-gradient aortic stenosis (LFLG AS).
- Chronic kidney disease (CKD) and right-sided extravalvular damage (RSED) complicate risk assessment in TAVR patients.
- The interplay between CKD, RSED, and outcomes in LFLG AS subtypes is not fully understood.
Purpose of the Study:
- To investigate the association between CKD stages and RSED in patients with LFLG AS undergoing TAVR.
- To evaluate the combined impact of CKD and RSED on post-TAVR mortality across LFLG AS subtypes.
Main Methods:
- Retrospective analysis of 402 patients with LFLG AS who underwent TAVR (2019-2022).
- Stratification by CKD stage (including end-stage renal disease [ESRD]) and LFLG AS subtype (classical vs. paradoxical).
- RSED defined by pulmonary hypertension, tricuspid regurgitation, or RV systolic dysfunction; statistical models assessed associations and mortality.
Main Results:
- End-stage renal disease (ESRD) was independently linked to RSED and RV dysfunction.
- ESRD increased RV dysfunction in paradoxical LFLG AS but not classical.
- Both advanced CKD and RSED independently raised post-TAVR mortality; their combination significantly elevated mortality in paradoxical LFLG AS.
Conclusions:
- Advanced renal dysfunction is associated with RSED in LFLG AS patients.
- The combination of RSED and advanced CKD has a potentially multiplicative impact on mortality in paradoxical LFLG AS.
Objectives:
In the transcatheter aortic valve replacement (TAVR) era, the presence of low-flow, low-gradient aortic stenosis (LFLG AS) itself does not preclude intervention. However, chronic kidney disease (CKD) and right-sided extravalvular damage (RSED) complicate procedural risk assessment. Both their association with each other and their joint impact on post-TAVR mortality in LFLG AS and across its subtypes remain incompletely characterized.
Methods:
The authors performed a retrospective study of patients with LFLG AS who underwent TAVR between 2019 and 2022, stratified by CKD stage (from no CKD to end-stage renal disease [ESRD]) and LFLG AS subtype (classical vs paradoxical). RSED was defined by greater than or equal to moderate pulmonary hypertension, greater than or equal to moderate tricuspid regurgitation, or right ventricular (RV) systolic dysfunction. Poisson regression models assessed associations between CKD stage and RSED, while multivariable Cox regression models and Wald tests compared mortality across cohorts.
Results:
Among 402 patients (137 classical, 265 paradoxical), ESRD was independently associated with RSED and RV dysfunction, whereas earlier CKD stages were not. ESRD was associated with increased RV dysfunction in paradoxical LFLG AS but not in classical LFLG AS. Advanced CKD and RSED were each associated with increased post-TAVR mortality. In paradoxical LFLG AS, combined RSED and advanced CKD were associated with significantly higher mortality than either condition alone. This effect was not observed in classical LFLG AS patients.
Conclusions:
Advanced renal dysfunction is associated with RSED in LFLG AS. In paradoxical LFLG AS, their combination has a possibly multiplicative association with mortality.
Related Concept Videos
Aortic Regurgitation I: Introduction
Mitral Stenosis I: Introduction
Aortic Regurgitation II: Clinical Features and Diagnostic Tests
Mitral Regurgitation I: Introduction
Acute Kidney Injury II: Pathophysiology

