67% of CKD5D patients have low bone mass and present with high (HTO) or non-high (N-HTO) bone turnover. HTO has excessive resorption calling for anti-resorbers, while in N-HTO, anabolic therapy appears preferable. There are no data on this tailored approach. Adult CKD5D patients with dual energy X-ray absorptiometry (DXA) t-scores ≤ -1.0 were enrolled into this 12-month randomized controlled trial and stratified as HTO or N-HTO using values of parathyroid hormone (PTH), PTH-ratio, and TRAP5b. HTO patients were randomized into treatment with alendronate or controls, and N-HTO patients into teriparatide or controls. Clinical, lab, DXA, quantitative computed tomography bone mineral density (QCT BMD), and coronary artery calcifications (CAC) and aorta calcifications (AoC) MSQCT data were obtained at 0 and 12 months. Primary outcome was change (Δ) in BMD by QCT, secondary outcomes were changes in CAC (ΔCAC), in AoC (ΔAoC), and death. There were 80 HTO and 61 N-HTO patients. Median HTO baseline PTH was 664 and N-HTO 183. Bone loss improved in treated N-HTO (5.7 g/cm3 vs. -10.7) but not in HTO (0.2 g/cm3 vs. -3.5) patients. There were no differences in ΔAoC or ΔCAC between treatment groups in either arm. Across all patients in the study, ΔAoC was lower in Blacks than Whites. (3.6 vs. 8.8) The HTO ΔAoC was 5 Hounsfield Units higher than N-HTO. In N-HTO, there were 0 deaths, but 20% in HTO (p = 0.005). N-HTO patients (PTH range 138 - 337 pg/mL) had better survival and less ΔAoC than those with HTO. Teriparatide treatment significantly improved low bone mass in N-HTO patients. Blacks had less ΔAoC regardless of turnover or treatment.