Kidney Week 2025 Annual Meeting-Effects of Diabetes and Diabetes Therapies on the Skeleton

Video Transcription

Video Summary

The session reviewed how diabetes and chronic kidney disease (CKD) affect bone health and fracture risk, and how common therapies (diabetes drugs, osteoporosis medications, bariatric surgery) influence the skeleton.<br /><br />Fractures are now recognized as a major complication of diabetes, with hip fracture risk markedly increased in type 1 diabetes and modestly increased in type 2 diabetes—despite bone mineral density (BMD) being only slightly reduced in type 1 and often normal or high in type 2. This “BMD–fracture risk disconnect” means DEXA and FRAX tend to underestimate risk; suggested workarounds include adjusting interpretation (treating a higher T-score as higher risk) and using trabecular bone score (TBS). Key predictors of fractures include longer diabetes duration, poor glycemic control, and microvascular disease. Mechanisms include degraded microarchitecture (notably in type 1), low bone turnover with suppressed bone formation (linked to increased sclerostin and reduced WNT signaling), accumulation of advanced glycation end products that make collagen more brittle, and impaired osteoblast energy metabolism.<br /><br />CKD independently increases fracture risk and post-fracture mortality, especially in dialysis patients. Newer framing emphasizes “CKD-associated osteoporosis” alongside CKD-associated cardiovascular disease. When diabetes and CKD coexist, skeletal fragility may be compounded, though data—especially for mild-to-moderate CKD—remain limited.<br /><br />Regarding therapies: thiazolidinediones worsen bone; metformin is neutral/slightly beneficial; insulin and sulfonylureas increase fall risk via hypoglycemia; GLP-1 agents appear bone-neutral and nephroprotective. SGLT2 inhibitors are strongly kidney-protective; overall fracture risk in CKD appears similar to controls, including emerging dialysis data. Osteoporosis drugs generally work in diabetes; in advanced CKD, treatment should consider turnover status and safety risks (e.g., denosumab hypocalcemia).<br /><br />Finally, bariatric surgery improves obesity and diabetes outcomes but can harm bone. Gastric bypass causes high-turnover bone loss and increased fractures (notably hip); banding is largely neutral; sleeve effects are intermediate with mixed fracture data. Calcium/vitamin D and exercise help but may be insufficient; parenteral antiresorptives (e.g., denosumab) show promise in preventing bone loss post-surgery.

Asset Subtitle

Moderator(s): Annabel Biruete, Thomas Nickolas

Presentation(s):

Diabetic Bone Disease - Mishaela Rubin
Effects of Diabetes and CKD on Bones - Anne Schafer
Effects of SGLT2 Inhibitors on Mineral Metabolism in Patients with CKD - Rodrigo Oliveira
Managing MBD in Patients with Bariatric Surgery - Elaine Yu

Meta Tag

Date 11/7/2025

Pathway 1 Bones, Stones, and Mineral Metabolism

Pathway 2 CKD Non-Dialysis

Session ID 507252

Keywords

diabetes-related fractures

chronic kidney disease bone health

BMD fracture risk disconnect

DEXA underestimation

FRAX limitations in diabetes

trabecular bone score (TBS)

type 1 diabetes hip fracture risk

type 2 diabetes fracture risk

low bone turnover and sclerostin

advanced glycation end products (AGEs) collagen

CKD-associated osteoporosis

dialysis fracture risk and mortality

SGLT2 inhibitors kidney protection fracture risk

denosumab hypocalcemia advanced CKD

bariatric surgery bone loss gastric bypass fractures