Figure 1.
Biochemical assessment of kidney function and mineral metabolism.
These previously published data (Allen et al., 2013) show abnormalities in kidney function and mineral metabolism resulting from hyperparathyroidism in the animals utilized in the current work. Data are presented as a percentage of non-affected normal animals with (*) representing statistical significance.
Figure 2.
Structural mechanical properties and estimated material properties.
These previously published data (Allen et al., 2013) show compromised whole bone mechanical properties from femoral 3-point bending and apparent material-level mechanical properties derived from standard beam bending equations in the animals utilized in the current work. Data are presented as a percentage of non-affected normal animals with (*) representing statistical significance.
Figure 3.
Microindentation reveals that CKD skeletal tissue is less able to resist damage.
Using reference point indentation (RPI), the indentation distance increase (IDI) was found to be significantly higher in CKD animals compared to normal. These data indicate that the mechanical integrity of the bone is less able to resist microscale damage formation and propagation. Data are presented as mean and standard deviation. *p<0.05 versus normal controls.
Table 1.
Mechanical properties from microindentation and nanoindentation.
Figure 4.
Nanoindenation reveals that CKD skeletal tissue has increased heterogeneity in the elastic modulus compared to normal bone.
There was no significant difference in the average elastic modulus (A), but the distribution of elastic modulus values was significantly broader (B), with a greater proportion of both high and low values in CKD relative to normal (p<0.0001).
Table 2.
Tissue composition and collagen morphology.