***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: UNLABELLED Osteoporosis is a frequent complication after renal transplantation . Some workers have shown that bisphosphonates may be effective to prevent and treat corticosteroid-induced osteoporosis in these patients . In this study we report our experience with administration of the biphosphonate alendronate to treat renal transplanted patients with established osteoporosis . MATERIAL S AND METHODS Twelve to 24 months after transplantation ( 9 women , 5 men ) 14 renal transplant patient were treated with alendronate and 12 patients ( 7 women , 5 men ) were untreated . All patients displayed an iPTH < 240 pg/mL and a bone mineral density ( BMD ) t-score < -2.5 . All patients received cyclosporine and prednisone therapy .  Biochemical measurements , BMD , and X-rays of the lumbar spine were measured during study . Patients in the treatment group received alendronate 10 mg/d ( po ) and vitamin D plus calcium ( 800 UI cholecalciferol and 2.5 g of CaCO(3 ) ) per day while those in the control group only received vitamin D plus calcium , at the same dose . RESULTS There was no difference in mean age , weight , time after transplantation , or immunosuppression between the treatment and control groups . There were no significant differences in the biochemical parameters during the study period . Over the 1-year study period , patients receiving alendronate displayed a greater increase in BMD . Lumbar spine BMD increased 4.3 + /- 6.1 % in the treatment group versus 0.55 + /- 5.30 % in controls . Femoral neck BMD increased 10.3 + /- 11.9 % and 2.2 + /- 5.7 % , respectively , in the treatment and control groups . Patients receiving alendronate frequently experienced intestinal disconfort . CONCLUSIONS The bisphosphonate alendronate is effective to treat renal transplant patients suffering from established osteporosis BACKGROUND Kidney transplantation is associated with an increased risk of bone fracture and rapid loss of bone mineral density after kidney transplantation . STUDY DESIGN R and omized controlled trial . SETTING & PARTICIPANTS Patients were r and omly assigned to treatment ( n = 46 ) or control ( no treatment ; n = 47 ) groups . Patients were stratified according to parathyroid hormone level and sex . Those with parathyroid hormone level less than 150 pg/mL were excluded . INTERVENTION The treatment and control groups received pamidronate , 1 mg/kg , perioperatively and then at 1 , 4 , 8 , and 12 months or no treatment , respectively . All received calcium ( 500 mg ) and vitamin D ( 400 units ) daily . Immunosuppression was cyclosporine and prednisolone , with no difference in dosing between the 2 groups . OUTCOMES & MEASUREMENTS Bone mineral density was evaluated by means of dual-energy x-ray absorptiometry of the lumbar spine and hip at baseline and 3 , 6 , 12 , and 24 months , with the primary end point at 1 year of percentage of change in bone mineral density from baseline . Clinical fractures were recorded and also evaluated by means of spinal radiographs at baseline and 1 and 2 years . RESULTS Pamidronate protected bone mineral density at the lumbar spine ; bone mineral density increased by 2.1 % in the treatment group and decreased by 5.7 % in the control group at 12 months ( P = 0.001 ) . Protection was also seen in Ward 's area of the hip ( P = 0.002 ) and the total hip ( P = 0.004 ) . There was no difference in femoral neck bone mineral density loss between the 2 groups . Fracture rates in the treatment and control groups were 3.3 % and 6.4 % per annum , respectively . LIMITATIONS This study was not powered to detect differences in fracture rates . CONCLUSION Pamidronate protects against posttransplantation bone loss at the lumbar spine and Ward 's area of the hip Severe osteoporosis frequently is observed after organ transplantation . In kidney transplantation , it adds to pre-existing renal bone disease and strategies to prevent osteoporosis are not established . Eighty kidney recipients were included in a r and omized controlled prospect i ve intervention trial . Treated patients ( n = 40 ) received an injection of ib and ronate , a bisphosphonate , immediately before and at 3 , 6 , and 9 mo after transplantation . The primary outcome measured was the change in bone mineral density . Secondary measures included graft outcome , spinal deformities , fracture rate , body height , and hormonal and metabolic data . Loss of spongy and cortical bone after transplantation was prevented by ib and ronate .  Changes of bone mineral density ( ib and ronate versus controls ) were as follows : lumbar spine , -0.9 + /- 6.1 % versus -6.5 + /- 5.4 % ( P < 0.0001 ) ; femoral neck , + 0.5 + /- 5.2 % versus -7.7 + /- 6.5 % ( P < 0.0001 ) ; and midfemoral shaft , + 2.7 + /- 12.2 % versus -4.0 + /- 10.9 % ( P = 0.024 ) . Fewer spinal deformities developed with ib and ronate ( 7 patients with 7 deformities versus 12 patients with 23 deformities ; P = 0.047 ) . Loss of body height was 0.5 + /- 1.0 cm versus 1.1 + /- 1.0 cm in control subjects ( P = 0.040 ) . Two bone fractures occurred in each group . There were fewer acute rejection episodes with ib and ronate ( 11 versus 22 ; P = 0.009 ) . Graft function after 1 yr was comparable . Bone loss , spinal deformation , and loss of body height during the first year after kidney transplantation are prevented by injection of ib and ronate at intervals of 3 mo . The smaller number of rejection episodes of the ib and ronate-treated group should be confirmed and its mechanism should be explored in additional studies Flaws in the design , conduct , analysis , and reporting of r and omised trials can cause the effect of an intervention to be underestimated or overestimated . The Cochrane Collaboration ’s tool for assessing risk of bias aims to make the process clearer and more The clinical profile of ib and ronate as add‐on to calcitriol and calcium was studied in this double‐blind , placebo‐controlled trial of 129 renal transplant recipients with early stable renal function ( ≤ 28 days posttransplantation , GFR ≥ 30 mL/min ) . Patients were r and omized to receive i.v . ib and ronate 3 mg or i.v . placebo every 3 months for 12 months on top of oral calcitriol 0.25 mcg/day and calcium 500 mg b.i.d . At baseline , 10 weeks and 12 months bone mineral density ( BMD ) and biochemical markers of bone turnover were measured . The primary endpoint , relative change in BMD for the lumbar spine from baseline to 12 months was not different , + 1.5 % for ib and ronate versus + 0.5 % for placebo ( p = 0.28 ) . Ib and ronate demonstrated a significant improvement of BMD in total femur , + 1.3 % versus −0.5 % ( p = 0.01 ) and in the ultradistal radius , + 0.6 % versus −1.9 % ( p = 0.039 ) . Bone formation markers were reduced by ib and ronate , whereas the bone resorption marker , NTX , was reduced in both groups . Calcium and calcitriol supplementation alone showed an excellent efficacy and safety profile , virtually maintaining BMD without any loss over 12 months after renal transplantation , whereas adding ib and ronate significantly improved BMD in total femur and ultradistal radius , and also suppressed biomarkers of bone turnover . Ib and ronate was also well tolerated The aim of this study was to investigate the effects of alendronate , calcitriol , and calcium in bone loss  after kidney transplantation . We enrolled 40 patients ( 27 men and 13 women , aged 44.2 + /- 11.6 years ) who had received renal allograft at least 6 months before ( time since transplant , 61.2 + /- 44.6 months ) . At baseline , parathyroid hormone ( PTH ) was elevated in 53 % of the patients and the Z scores for bone alkaline phosphatase ( b-ALP ) and urinary type I collagen cross-linked N-telopeptide ( u-NTX ) were higher than expected ( p < 0.001 ) . T scores for the lumbar spine ( -2.4 + /- 1.0 ) , total femur ( -2.0 + /- 0.7 ) , and femoral neck ( -2.2 + /- 0.6 ) were reduced ( p < 0.001 ) . After the first observation , patients were advised to adhere to a diet containing 980 mg of calcium daily and their clinical , biochemical , and densitometric parameters were reassessed 1 year later . During this period , bone density decreased at the spine ( -2.6 + /- 5.7%;p < 0.01 ) , total femur ( -1.4 + /- 4.2 % ; p < 0.05 ) , and femoral neck ( -2.0 + /- 3.0 % ; p < 0.001 ) . Then , the patients were r and omized into two groups : ( 1 ) group A-10 mg/day of alendronate , 0.50 microg/day of calcitriol , and 500 mg/day of calcium carbonate ; and ( 2 ) group B-0.50 microg/day of calcitriol and 500 mg/day of calcium carbonate . A further metabolic and densitometric reevaluation was performed after the 12-month treatment period . At the r and omization time , group A and group B patients did not differ as to the main demographic and clinical variables . After treatment , bone turnover markers showed a nonsignificant fall in group B patients , while both b-ALP and u-NTX decreased significantly in alendronate-treated patients . Bone density of the spine ( + 5.0 + /- 4.4 % ) , femoral neck ( + 4.5 + /- 4.9 % ) , and total femur ( + 3.9 + /- 2.8 % ) increased significantly only in the alendronate-treated patients . However , no trend toward further bone loss was noticed in calcitriol and calcium only treated subjects . No drug-related major adverse effect was recorded in the two groups . We conclude that renal transplanted patients continue to loose bone even in the long-term after the graft . Alendronate normalizes bone turnover and increases bone density . The association of calcitriol to this therapy seems to be advantageous for better controlling the complex abnormalities of skeletal metabolism encountered in these subjects Kidney transplant recipients develop secondary osteoporosis induced by immunosuppressive medication , with a high risk of fracture , and abdominal aortic calcification ( AC ) is a known predictor of cardiovascular mortality . In this study of 12 stable kidney recipients , we estimated the preventive effect of bisphosphonate treatment on bone loss and progression of AC . We r and omly divided the subjects into a treatment group with alendronate ( group A : 5 subjects ) and a control group ( group C : 7 subjects ) . Group A patients received 35 mg/week of alendronate over 24 months , while group C patients were not administered with any bisphosphonates . Two major endpoints were established : ( 1 ) the time-dependent change in bone mineral density ( BMD ) estimated with DEXA and ( 2 ) progression of abdominal AC , calculated twice as an index ( ACI ) using computed tomography data . Over the 2-year study period , group A patients showed significantly increased BMD of 1.86 ± 0.85 % ( P = 0.015 versus baseline ) , and almost complete inhibition of ACI progression ( 38.2 ± 24.2 % to 39.6 ± 24.3 % ) , but group C patients showed a decrease in BMD decline with bone loss and progression of ACI ( 32.8 ± 25.0 % to 37.8 ± 29.2 % , P = 0.061 ) . In conclusion , alendronate therapy was an effective treatment in kidney transplant recipients for secondary osteoporosis and vascular calcification as ectopic calcification . This clinical trial is registered with number JMA-IIA00155 of JMACCT CTR Bisphosphonates may prevent or treat the bone loss promoted by the immunosuppressive regimens used in renal transplantation .  Risedronate is a commonly used third-generation amino-bisphosphonate , but little is known about its effects on the bone health of renal transplant recipients . We r and omly assigned 42 new living-donor kidney recipients to either 35 mg of risedronate weekly or placebo for 12 months . We obtained bone biopsies at the time of renal transplant and after 12 months of protocol treatment . Treatment 
    Output:
    
No significant differences were found in vertebral fractures , nonvertebral fractures , adverse events , and gastrointestinal adverse events .
Bisphosphonates appear to have a beneficial effect on BMD at the lumbar spine and do not significantly decrease fracture events in recipients .