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Updated: Jun 21, 2026
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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
Published on: May 22, 2013
Renal dysfunction is associated with shorter telomere length in heart failure
Liza S M Wong1, Pim van der Harst, Rudolf A de Boer
1Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, The Netherlands.
Summary
Shorter leukocyte telomere length, a marker of biological aging, is linked to reduced kidney function in chronic heart failure (CHF) patients. This suggests aging impacts kidney resilience in heart failure.
Area of Science:
- Cardiology
- Nephrology
- Gerontology
Background:
- Renal dysfunction is common in chronic heart failure (CHF) and increases mortality.
- Biological aging may impair kidney function in the context of CHF.
- Leukocyte telomere length serves as a marker for biological age.
Purpose of the Study:
- To investigate the association between leukocyte telomere length and renal function in CHF patients.
- To explore if biological age influences kidney function in heart failure.
Main Methods:
- Real-time quantitative polymerase chain reaction (PCR) was used to measure telomere length in 866 CHF patients.
- Renal function was estimated using the simplified Modification of Diet in Renal Disease (MDRD) equation.
- Statistical analyses adjusted for age, gender, CHF onset age, and disease severity.
Main Results:
- A significant association was found between telomere length and renal function (correlation coefficient 0.123, P < 0.001).
- This relationship remained significant after adjusting for demographic factors and CHF onset age (standardized-beta 0.091, P = 0.007).
- Further adjustments for CHF severity and baseline differences did not alter the findings.
Conclusions:
- Shorter leukocyte telomere length is associated with reduced renal function in patients with heart failure.
- Intrinsic biological aging appears to affect the kidney's ability to adapt to systemic changes in CHF.
- These findings highlight the role of aging in the pathophysiology of cardiorenal syndrome.
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