Abstract: TH-PO990
Early Evidence of Tendon Dysfunction in a Rat Model of CKD
Session Information
- Physical Activity and Lifestyle in Kidney Diseases
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Health Maintenance, Nutrition, and Metabolism
- 1500 Health Maintenance, Nutrition, and Metabolism
Authors
- Hayden, Christopher, University of California Davis, Davis, California, United States
- Gilmore, Natalie K., University of California Davis, Davis, California, United States
- Roshanravan, Baback, University of California Davis School of Medicine, Sacramento, California, United States
- Baar, Keith, University of California Davis, Davis, California, United States
Background
Spontaneous tendon ruptures are debilitating injuries that are disproportionately high in individuals with chronic kidney disease (CKD). Despite this, almost no data exists regarding CKD-related tendon pathology. Thus, we used a rat model of CKD to determine whether tendon mechanics are altered by CKD.
Methods
Sprague-Dawley rats (n=32, 50% female, age=8wk) were equally divided into a control group (CON) and a group fed chow with 0.25% adenine to induce CKD. After 8wk, blood markers for CKD were evaluated, and Achilles and tibialis anterior (TA) tendons were collected. Tendons were then tested in tension to failure using a single-column tensile tester with a 100N load cell. Maximum tensile load (MTL), failure stress, Young’s modulus, and cross-sectional area (CSA) were determined. The strongest of each tendon for every animal was used in analysis. The effect of CKD was evaluated for each tendon by two-way ANOVA (main and interaction effects: CKD and sex).
Results
CKD was confirmed through elevated creatinine (1.99 vs 0.61mg/dL, CKD vs CON, P=0.001), blood urea nitrogen (93.4 vs 21.4mg/dL, P<0.001), kidney mass (2.7 vs 1.25g, P<0.001), and lower hematocrit levels (34 vs 47%, P<0.001). Final body weight did not differ for the females (282 vs 284g, P=0.9), but the CKD males were lighter than controls (438 vs 585g, P<0.001). The failure stress of TA tendons was significantly lower in CKD vs CON (18.8 vs 24.8 mPa, P=0.039). There were no statistically significant differences in MTL, modulus, or CSA (p>0.097) or for any parameter for the Achilles (P=0.73). Sex did not modify the effects of CKD (P=0.86).
Conclusion
We demonstrate that, early in the development of CKD in rats, TA tendons failed at a lower stress. These results along with the finding that there were no differences in CSA between groups suggest that CKD diminishes tendon material properties. To our knowledge, this is the first direct evidence of changes in tendon mechanics caused by kidney disease, providing a model for further evaluating mechanisms and interventions.
Funding
- NIDDK Support