The rationale for this thesis was to study the effects of chronic renal insufficiency (CRI) on bone structure. CRI has been associated with skeletal lesions and this related bone disorder has been termed renal osteodystrophy or more extensively as chronic kidney disease-bone and mineral disorder (CKD-BMD). The definition and evaluation of renal osteodystrophy has predominantly focused on changes in the trabecular bone and circulating systemic biochemical markers of bone turnover. Accordingly, one objective of this study was to assess the changes in the cortical bone with peripheral quantitative tomography, and particularly, in the bone structural strength with mechanical testing. In this study, experimental CRI was shown to be associated with decreased volumetric cortical bone mineral density and that along with the progression of CRI bone strength may eventually deteriorate. Other main objective of this study was to assess the efficacy of four different pharmacological treatments (calcium carbonate, sevelamer, paricalcitol, pamidronate) on bone in CRI. These were chosen to represent clinical treatment options for the consequences of impaired renal function. It is hypothesized that the general treatment of renal condition is beneficial also to the bones, but there is also some concern about the possible adverse skeletal side effects. In this study, calcium carbonate, sevelamer, and paricalcitol treatments were observed to alleviate the CRI-induced detrimental changes in bone. Calcium salts and sevelamer are phosphate binding agents are clinically used to alleviate hyperphosphatemia in CRI. Sevelamer treatment was associated with positive effects on bone, and although calcium carbonate treatment simultaneously suppressed parathyroid hormone secretion, no detrimental effects on bone strength were observed. Similarly, the amelioration of secondary hyperparathyroidism with vitamin D analogue paricalcitol was beneficial also on bone. In addition, it was shown that pamidronate treatment was associated with increased bone mineral content in CRI. Altogether these findings suggest that experimental CRI exerts detrimental effects on bone, but however, these above mentioned treatments were shown to be effective in preventing these changes.