Browsing by Subject "renal osteodystrophy"

Now showing 1 - 4 of 4
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    Fractures in Patients with CKD: Time for Action
    (American Society of Nephrology, 2016-11-07) Moe, Sharon M.; Nickolas, Thomas L.; Medicine, School of Medicine
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    Time course of rapid bone loss and cortical porosity formation observed by longitudinal μCT in a rat model of CKD
    (Elsevier, 2019-08) McNerny, Erin M. B.; Buening, Dorothy T.; Aref, Mohammad W.; Chen, Neal X.; Moe, Sharon M.; Allen, Matthew R.; Anatomy and Cell Biology, IU School of Medicine
    Background Rodent studies of bone in chronic kidney disease have primarily relied on end-point examinations of bone microarchitecture. This study used longitudinal in vivo microcomputed tomography (in vivo μCT) to characterize the onset and progression of bone loss, specifically cortical porosity, in the Cy/+ rat of model of CKD. Methods Male CKD rats and normal littermates were studied. In vivo μCT scans of the right distal tibia repeated at 25, 30, and 35 weeks were analyzed for longitudinal changes in cortical and trabecular bone morphometry. In vitro μCT scans of the tibia and femur identified spatial patterns of bone loss across distal, midshaft and proximal sites. Results CKD animals had reduced BV/TV and cortical BV at all time points but developed cortical porosity and thinning between 30 and 35 weeks. Cortical pore formation was localized near the endosteal surface. The severity of bone loss was variable across bone sites, but the distal tibia was representative of both cortical and trabecular changes. Conclusions The distal tibia was found to be a sensitive suitable site for longitudinal imaging of both cortical and trabecular bone changes in the CKD rat. CKD trabecular bone loss progressed through ~30 weeks followed by a sudden acceleration in cortical bone catabolism. These changes varied in timing and severity across individuals, and cortical bone loss and porosity progressed rapidly once initiated. The inclusion of longitudinal μCT in future studies will be important for both reducing the number of required animals and to track individual responses to treatment.
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    Voluntary Wheel Running Has Beneficial Effects in a Rat Model of CKD-Mineral Bone Disorder (CKD-MBD)
    (American Society of Nephrology, 2019-10-01) Avin, Keith G.; Allen, Matthew R.; Chen, Neal X.; Srinivasan, Shruthi; O’Neill, Kalisha D.; Troutman, Ashley D.; Mast, Garrison; Swallow, Elizabeth A.; Brown, Mary Beth; Wallace, Joseph M.; Zimmers, Teresa A.; Warden, Stuart J.; Moe, Sharon M.; Physical Therapy, School of Health and Human Sciences
    Background Reduced bone and muscle health in individuals with CKD contributes to their higher rates of morbidity and mortality. Methods We tested the hypothesis that voluntary wheel running would improve musculoskeletal health in a CKD rat model. Rats with spontaneous progressive cystic kidney disease (Cy/+ IU) and normal littermates (NL) were given access to a voluntary running wheel or standard cage conditions for 10 weeks starting at 25 weeks of age when the rats with kidney disease had reached stage 2–3 of CKD. We then measured the effects of wheel running on serum biochemistry, tissue weight, voluntary grip strength, maximal aerobic capacity (VO2max), body composition and bone micro-CT and mechanics. Results Wheel running improved serum biochemistry with decreased creatinine, phosphorous, and parathyroid hormone in the rats with CKD. It improved muscle strength, increased time-to-fatigue (for VO2max), reduced cortical porosity and improved bone microarchitecture. The CKD rats with voluntary wheel access also had reduced kidney cystic weight and reduced left ventricular mass index. Conclusions Voluntary wheel running resulted in multiple beneficial systemic effects in rats with CKD and improved their physical function. Studies examining exercise interventions in patients with CKD are warranted.
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    What Animal Models Have Taught Us About the Safety and Efficacy of Bisphosphonates in Chronic Kidney Disease
    (Springer, 2017) Allen, Matthew R.; Aref, Mohammad W.; Anatomy and Cell Biology, School of Medicine
    Purpose of Review Bisphosphonates (BPs) have long been the gold-standard anti-remodeling treatment for numerous metabolic bone diseases. Since these drugs are excreted unmetabolized through the kidney, they are not recommended for individuals with compromised kidney function due to concerns of kidney and bone toxicity. The goal of this paper is to summarize the preclinical BP work in models of kidney disease with particular focus on the bone, kidney, and vasculature. Recent Findings Summative data exists showing positive effects on bone and vascular calcifications with minimal evidence for bone or kidney toxicity in animal models. Summary Preclinical data suggest it may be worthwhile to take a step back and reconsider the use of bisphosphonates to lessen skeletal/vascular complications associated with compromised kidney function.