Management of bone health in adult solid organ transplant recipients: a multidisciplinary care pathway

Abstract

Bone fragility is a major cause of morbidity and reduced quality of life among adult solid organ transplant (SOT) recipients. Despite guideline recommendations, bone health screening and posttransplant treatment remain inconsistent, and optimal therapeutic strategies are not well standardized. We reviewed the relevant literature, along with professional society guidance, and integrated institutional clinical experience to develop a streamlined multidisciplinary care pathway and define key performance indicators for transplant and bone health specialist teams. All non-kidney SOT candidates should undergo spine and hip dual-energy X-ray absorptiometry (DXA) with vertebral fracture assessment at listing, whereas kidney transplant candidates should undergo DXA only when the results are expected to influence management. High-risk patients, defined by a fragility fracture or a T-score ≤−2.5, should be referred for specialist care. After transplantation, non-kidney SOT recipients should receive osteoporosis therapy within 2 to 4 months if they have not been treated in the prior year, with treatment guided by renal function and bone turnover status. Kidney transplant recipients should undergo DXA, with referral and treatment tailored to fracture risk, bone turnover, and renal function. Bone biopsy should be considered when the underlying bone disease is unclear. Early risk stratification, standardized assessment, and coordinated multidisciplinary management are essential for fracture prevention and improved outcomes in SOT recipients.

HIGHLIGHTS

Bone fragility is a major cause of morbidity and reduced quality of life in transplant recipients, yet screening and posttransplant fracture prevention remain inconsistent. A multidisciplinary bone health care pathway with key performance indicators may improve outcomes. At listing, perform dual-energy X-ray absorptiometry (DXA) and vertebral fracture assessment and optimize modifiable lifestyle and nutritional risk factors, including calcium and vitamin D status. Refer patients with fragility fractures or high-risk DXA findings for specialist evaluation before transplantation. After transplantation, refer all non-kidney recipients within 2–4 months; in kidney transplant recipients, perform DXA within 2–4 months and refer high-risk patients.

INTRODUCTION

Solid organ transplantation (SOT) is an established and effective treatment for end-stage organ failure, including diseases of the kidney, liver, heart, lung, pancreas, and intestine [1–3]. Over the past 30 years, transplantation rates have increased worldwide, driven by technological advances such as machine perfusion and surgical innovations, along with improved donor and recipient selection and postoperative management. These developments have contributed to improved posttransplant survival [1–3]. However, both short- and long-term complications, particularly osteoporosis and fragility fractures, remain significant concerns [1–7].

Transplant recipients experience higher rates of fracture-related morbidity and mortality than the general population. Contributing factors include the underlying disease, prolonged corticosteroid and immunosuppressive therapy, sarcopenia, nutritional deficiencies, and hypogonadism [1–7]. Fracture risk varies by organ type: lung and heart transplant recipients are at the highest risk, whereas first-year risk is lowest among kidney transplant recipients (KTRs) [6,7]. Most fractures occur within 6 to 12 months after transplantation and frequently involve the thoracic spine [8,9]. The strongest predictors of fracture include a history of pretransplant fracture, older age, menopausal status, and reduced bone mineral density (BMD) measured by dual-energy X-ray absorptiometry (DXA) [4,10,11]. Although the fracture risk assessment tool (FRAX) is used to estimate fracture risk in men and women aged >40 years [12], its accuracy in SOT candidates and recipients remains uncertain; however, observational data support its use in KTRs [13,14]. Additionally, the trabecular bone score derived from DXA has been used to refine fracture risk prediction in KTRs, although it has not yet been validated for recipients of other organ transplants [11,15].

Despite professional society recommendations for bone health screening around the time of transplantation [16–21], many eligible patients do not receive appropriate screening or treatment [3,8,22,23]. Moreover, consensus remains limited regarding which patients should receive posttransplant therapy and which treatment regimens are most appropriate [3,11,16–21]. Network meta-analysis incorporating all available randomized controlled trial data has been proposed as an approach to compare antiosteoporotic interventions based on their effects on fracture incidence and BMD in SOT recipients [22]. In addition, the development of a multidisciplinary bone health protocol may improve screening, prevention, and management of bone loss and reduce fracture risk [3,4,23].

METHODS

We conducted a literature review of English-language articles relevant to bone health and SOT. We also performed an in-depth review of recommendations from professional societies [16–21] and integrated our institutional clinical experience to develop a streamlined care pathway for adult SOT recipients (aged ≥18 years). Our institution performs more than 1,000 organ transplants annually across its international sites. In addition, we developed key performance indicators (KPIs) for the transplant team and bone health specialist team, including endocrinology and rheumatology, to support optimal care delivery. The >90% KPI threshold represents an institutional quality benchmark derived from transplant governance frameworks to support high-reliability pathway implementation.

RESULTS

Pretransplant Evaluation: Transplant Team

Upon listing, the transplant team should perform a comprehensive evaluation of fracture risk factors and relevant laboratory parameters. For kidney transplantation, the timing of this evaluation may vary, as some programs defer assessment until after transplantation.

1. History

1) Glucocorticoid dose and duration

2) Use of glucocorticoid-sparing immunosuppressants (e.g., calcineurin inhibitors)

3) History of adult fragility fractures

4) Prior osteoporosis treatment

5) Bone pain or back pain

6) Smoking and alcohol use

7) Nutritional assessment, including dietitian consultation and supplement use

8) Menstrual history in female patients and symptoms of hypogonadism in male patients (e.g., decreased libido, erectile dysfunction)

9) Family history of osteoporosis and hip fracture

2. Recommended initial tests

1) In non-kidney SOT candidates, perform DXA of the spine and hip, together with vertebral fracture assessment (VFA) by DXA or thoracic and lumbar spine radiography, to identify prevalent vertebral fractures. For kidney transplant candidates, DXA of the spine, hip, and forearm should be performed only if the results are expected to influence treatment decisions [17].

2) Use the Z-score rather than the T-score in premenopausal women and men younger than 50 years; a Z-score ≤−2.0 indicates low BMD for age.

3) Review existing imaging studies, including radiographs and computed tomography scans, for evidence of vertebral fracture.

4) Use the FRAX score to estimate 10-year fracture risk. If applicable, adjust FRAX for glucocorticoid use as follows: for a glucocorticoid dose ≥7.5 mg/day, multiply the 10-year risk of major osteoporotic fracture (MOF) by 1.15 and the 10-year risk of hip fracture by 1.2 [12].

5) Measure the 25-hydroxyvitamin D [25(OH)D] level.

3. Suggested management plan

1) Refer patients to a bone health specialist if there is evidence of a fragility fracture, a DXA T-score ≤−2.5 at any site, or osteopenia with a high-risk FRAX score (≥20% for MOF or ≥3% for hip fracture). Referral should also be considered for patients with osteopenia and additional risk factors, such as chronic glucocorticoid use, or with a moderate FRAX score (≥10% for MOF or ≥1% for hip fracture) [4,16,18,24]. Premenopausal women and men younger than 50 years with evidence of a fragility fracture or a Z-score ≤−2.0 plus clinical risk factors or secondary causes should also be referred.

2) Address modifiable lifestyle factors

2-1) Encourage weight-bearing exercise.

2-2) Provide fall prevention assessment, balance evaluation, and therapy.

2-3) Promote smoking cessation and limit alcohol intake.

2-4) Optimize nutritional status, with attention to adequate protein intake.

2-5) Minimize medications that adversely affect bone health when feasible.

3) Optimize vitamin D status

3-1) If the patient’s 25(OH)D level is <30 ng/mL (75 nmol/L), administer 50,000 IU of vitamin D2 or D3 weekly for 12 weeks, followed by maintenance therapy with 1,000–2,000 IU daily.

3-2) If the 25(OH)D level is ≥30 ng/mL (75 nmol/L), administer maintenance vitamin D at 1,000–2,000 IU daily.

4) Provide calcium supplementation

4-1) If dietary calcium intake is insufficient, provide 600 mg of elemental calcium daily. If dietary calcium intake exceeds 1.5 g/day, supplementation is generally unnecessary.

Pretransplant Evaluation: Patients Referred to Bone Health Specialists

1. Identify and treat underlying causes of secondary osteoporosis.

2. Suggested laboratory tests

1) Renal profile (creatinine, estimated glomerular filtration rate [eGFR])

2) Bone profile (corrected or ionized calcium, phosphorus, alkaline phosphatase)

3) Parathyroid hormone (PTH)

4) 25(OH)D

5) Thyroid-stimulating hormone and free thyroxine, if indicated

6) Fasting bone turnover markers (BTMs), such as serum C-terminal telopeptide (CTX) and bone-specific alkaline phosphatase (BSAP). CTX is renally cleared so in kidney transplant patients and/or chronic kidney disease consider measuring TRAP5b (tartrate-resistant acid phosphatase 5b) instead of CTX.

7) Testosterone and luteinizing hormone in male patients, or estradiol and follicle-stimulating hormone in female patients, if clinically indicated (e.g., menstrual irregularities in premenopausal women or decreased libido or erectile dysfunction in men)

8) 24-Hour urine calcium

9) Screening for celiac disease

10) Serum and urine protein electrophoresis

Additional Considerations

1. Definition of severe osteoporosis: BMD in the osteoporotic range on DXA in the presence of one or more fragility fractures; low BMD with a recent fragility fracture (within 12 months) or multiple fragility fractures; a DXA T-score ≤−3.5; or a glucocorticoid-adjusted FRAX 10-year probability of ≥4.5% for hip fracture or ≥30% for MOF [12]. FRAX high-risk categories are defined as ≥3% to <4.5% for hip fracture or ≥20% to <30% for MOF; moderate risk as >1% to <3% for hip fracture or 10%–19% for MOF; and low risk as ≤1% for hip fracture and <10% for MOF [16].

2. FRAX has not been validated in patients younger than 40 years and may underestimate risk in SOT candidates.

3. Low BTMs are defined as CTX and BSAP concentrations in the lower one-third of the assay-specific reference range for premenopausal women, or as values trending downward over time. If the results are indeterminate, bone biopsy may be helpful.

4. Monitoring: perform DXA annually after transplantation for 1–3 years, until findings are stable.

5. Premenopausal women: use bisphosphonates with caution.

6. Hypogonadism: consider hormone replacement therapy in premenopausal women and hypogonadal men.

7. Vitamin D repletion: ensure that the 25(OH)D level is ≥30 ng/mL (75 nmol/L), particularly before administering intravenous bisphosphonates or denosumab, to reduce the risk of hypocalcemia, especially in patients with renal insufficiency.

Pharmacological Therapy Before Non-Kidney Solid Organ Transplantation

Indications for osteoporosis treatment in patients undergoing evaluation for non-kidney SOT largely mirror those established for the general population. Men older than 50 years and postmenopausal women with pretransplant osteoporosis, defined by a prior fragility fracture, a T-score ≤−2.5, or osteopenia with a high-risk FRAX score, should receive pharmacological treatment [2,3,11,18–21]. Treatment may also be considered for individuals with osteopenia and an intermediate-risk FRAX score, particularly those receiving chronic glucocorticoid therapy (≥5 mg/day prednisone or equivalent) [16,24].

First-line agents include intravenous zoledronic acid for patients with an eGFR ≥35 mL/min/1.73 m² and stable renal function, or denosumab for those with an eGFR <35 mL/min/1.73 m². Anabolic agents, such as teriparatide and abaloparatide, can be considered in cases of intolerance to antiresorptive therapy, contraindications or in severe osteoporosis [25]. If these therapies are contraindicated or poorly tolerated, calcitriol may be helpful, particularly in patients with chronic liver disease; however, its use requires close monitoring for hypercalcemia and hypercalciuria [2,26].

Premenopausal women and men younger than 50 years with evidence of a fragility fracture or a Z-score ≤−2.0 plus clinical risk factors, such as chronic glucocorticoid use, are also at high fracture risk and should receive treatment. DXA cannot distinguish osteomalacia from osteoporosis; thus, caution is warranted, particularly in this age group, to identify and treat osteomalacia. This condition is characterized by elevated serum alkaline phosphatase, low 25(OH)D, low phosphate, low or low-normal calcium, and elevated PTH levels. In younger adults, low BMD may also reflect low peak bone mass rather than osteoporosis and can be differentiated by the absence of clinically significant fragility fractures. Medical management in premenopausal women should be individualized because bisphosphonates remain incorporated in the bone matrix for prolonged periods and may pose a theoretical risk to fetal health if pregnancy occurs after treatment. When not contraindicated, hormone replacement therapy may be initiated in hypogonadal premenopausal women, and testosterone therapy may be used in hypogonadal men, together with calcium and plain vitamin D supplementation; additional pharmacological therapy may still be required in those at high fracture risk. Fig. 1 shows the proposed flowchart for pharmacological therapy before non-kidney SOT.

Fig. 1.

Clinical flowchart for pharmacological therapy before non-kidney solid organ transplant. DXA, dual-energy X-ray absorptiometry; FRAX, fracture risk assessment tool; MOF, major osteoporotic fracture; eGFR, estimated glomerular filtration rate; BMD, bone mineral density.

Pharmacological Therapy After Non-Kidney Solid Organ Transplantation

Although the characteristics of bone disease may differ according to the failing organ, recipients of non-kidney SOT are at increased fracture risk during the early posttransplant period [11]. Evidence supporting pharmacological treatment in this population remains limited; therefore, treatment selection should be guided by individual patient factors [2,3,21,27–36]. One possible approach is to target patients at moderate to high fracture risk, consistent with the American College of Rheumatology guidelines for the prevention and treatment of glucocorticoid-induced osteoporosis [11,16]. Our approach, however, is to offer preventive medical therapy to all patients because rapid bone loss and frequent fractures occur soon after transplantation, particularly within the first year, even in patients with normal BMD [9]. In addition, most patients receive glucocorticoids (≥5 mg/day prednisone or equivalent) for at least 3 to 6 months after transplantation. This strategy reflects expert consensus intended to mitigate the period of greatest skeletal vulnerability after transplantation rather than a universal recommendation based on fracture-outcome trial data in patients with normal baseline BMD. For adults with SOT and an eGFR ≥35 mL/min/1.73 m² who continue chronic glucocorticoid treatment, the American College of Rheumatology conditionally recommends bisphosphonates, denosumab, teriparatide or abaloparatide, or raloxifene over no treatment, based on individual patient factors, but conditionally recommends against romosozumab due to potential harms in this population [16]. Table 1 summarizes protocols used in some studies after liver, heart, and lung transplantation. Fig. 2 shows the proposed flowchart for pharmacological therapy after non-kidney SOT.

Table 1.

Organ-specific recommendations after non-kidney solid organ transplant

Transplant type	Medication/regimen	Alternatives/adjuncts	Key evidence/notes	References
Liver	Zoledronic acid 5 mg IV single infusion, or oral alendronate 70 mg weekly	Denosumab 60 mg SC every 6 months (if renal dysfunction/intolerance); calcium 1,000 mg/day + vitamin D 800 IU/day	Both alendronate and zoledronic acid prevent hip bone loss; zoledronic acid increases spine BMD; denosumab is safe and effective. Teriparatide has been used in post-OLT severe osteoporosis unresponsive to standard therapy.	[27–30]
Heart	Zoledronic acid 5 mg IV single infusion, or oral alendronate 70 mg weekly	Denosumab 60 mg SC every 6 months (if renal dysfunction/intolerance); calcium 1,000 mg/day + vitamin D 800 IU/day	Zoledronic acid is superior to alendronate for spine BMD; both agents stabilize hip BMD. Teriparatide was used in a heart transplant patient with chronic kidney disease and low bone turnover.	[31–34]
Lung	Zoledronic acid 5 mg IV single infusion (or every 6–12 months)	Denosumab 60 mg SC every 6 months (if renal dysfunction/intolerance), or PTH analogs (teriparatide 20 μg SC daily, abaloparatide 80 μg SC daily); calcium 1,000 mg/day + vitamin D 800 IU/day	All agents increase lumbar spine BMD; only PTH analogs improve hip BMD; infection risk is similar across agents. Fracture data are limited, but PTH analogs may be preferred for severe osteoporosis.	[21,35,36]

IV, intravenous; SC, subcutaneous; BMD, bone mineral density; OLT, orthotopic liver transplantation; PTH, parathyroid hormone.

Fig. 2.

Clinical flowchart for pharmacological therapy after non-kidney solid organ transplant. DXA, dual-energy X-ray absorptiometry; eGFR, estimated glomerular filtration rate; IV, intravenous; BTM, bone turnover marker; BMD, bone mineral density; FRAX, fracture risk assessment tool.

All patients should undergo baseline DXA if it has not already been performed, and they should receive treatment within 2 to 4 months after transplantation if they have not received osteoporosis therapy in the previous year. Bisphosphonates, preferably intravenous zoledronic acid, are the first-line treatment when eGFR is ≥35 mL/min/1.73 m². Oral bisphosphonates are alternatives, but they are contraindicated in patients with esophageal stricture or varices, Barrett esophagus, achalasia, prior gastric bypass surgery, or an inability to follow administration instructions. Denosumab should be used when eGFR is <35 mL/min/1.73 m² or in cases of bisphosphonate intolerance. Infection risk and hypocalcemia should be monitored, although recent studies in lung transplant recipients suggest that denosumab is safe [36].

Given the well-described risk of rapid bone loss and rebound vertebral fractures after denosumab discontinuation, consolidation therapy with a bisphosphonate is recommended when eGFR is ≥35 mL/min/1.73 m²; if eGFR is <35 mL/min/1.73 m², denosumab should be continued. This typically involves administration of an intravenous bisphosphonate, such as zoledronic acid 5 mg, 6 to 7 months after the last denosumab dose. Some patients may require a second infusion of zoledronic acid (5 mg) 6 months after the first infusion when bone resorption remains inadequately suppressed, as reflected by persistently elevated serum CTX levels, typically ≥280–300 pg/mL. An oral bisphosphonate may also be used if intravenous therapy is not suitable and should be continued for at least 1 to 2 years. Teriparatide or abaloparatide may also be considered in severe osteoporosis, particularly when BTMs are low [21,30,34,36]. Sequential antiresorptive therapy is essential after stopping teriparatide or abaloparatide in order to maintain BMD gains. Calcitriol may attenuate bone loss after SOT, but it is less effective for fracture prevention and may be associated with hypercalciuria [31,37]. For recipients of dual solid organ transplants that include a kidney, clinicians should follow the kidney transplant pathway described in the next section.

Pharmacological Therapy After Kidney Transplant

DXA and BTMs should be measured 2 to 4 months after transplantation. Bone evaluation by DXA should include the forearm or high-resolution peripheral quantitative computed tomography, because peripheral BMD may decline without substantial axial changes [38,39]. Although bone biopsy remains the gold standard for characterizing bone disease phenotypes and distinguishing bone turnover states, its limited accessibility has led to widespread use of BTMs in clinical practice. Several studies have shown that these markers correlate with the histological pattern of bone disease identified on iliac crest biopsy in KTRs [40,41]. Treatment should be initiated when there is evidence of a fragility fracture, a DXA T-score ≤−2.5, or osteopenia with a high-risk FRAX score. The optimal timing of pharmacological therapy to prevent bone loss and fractures after kidney transplantation remains unclear [17,42], but treatment is generally started after optimal management, when feasible, of chronic kidney disease-mineral and bone disorder, including persistent hyperparathyroidism. This timing helps ensure that bone remodeling has stabilized before osteoporosis medications are initiated.

The choice of therapy depends on posttransplant bone turnover. Low BTMs favor anabolic therapy, such as teriparatide or abaloparatide [40], whereas no safety data are currently available for romosozumab in this setting. If BTMs are normal or high, treatment options include bisphosphonates when eGFR is ≥35 mL/min/1.73 m² [43] or denosumab when eGFR is <35 mL/min/1.73 m² [29,44]. If the underlying bone disease remains unclear, antiresorptive therapy should be avoided due to the risk of precipitating adynamic bone disease, and bone biopsy should be considered to guide treatment [17]. The proposed use of BTMs to guide selection of anabolic versus antiresorptive therapy in KTRs should be viewed as an evidence-informed, pragmatic strategy rather than a universally standardized approach. Interpretation of BTMs requires careful clinical contextualization, because assay-specific reference ranges, biological variability, and posttransplant metabolic factors may influence results. Accordingly, BTMs should complement, rather than replace, comprehensive clinical and densitometric assessment.

For KTRs who are not at high fracture risk but who are receiving ≥5 mg/day prednisone (or equivalent) or have persistent hyperparathyroidism, an active vitamin D analog may be considered [17,37]. Fig. 3 shows the proposed flowchart for pharmacological therapy after kidney transplantation.

Fig. 3.

Clinical flowchart for pharmacological therapy after kidney transplant. DXA, dual-energy X-ray absorptiometry; VFA, vertebral fracture assessment; BTM, bone turnover marker; FRAX, fracture risk assessment tool; eGFR, estimated glomerular filtration rate; BMD, bone mineral density.

Key Performance Indicators

1. Transplant team

1) Pretransplant bone health assessment (>90% of candidates)

1-1) At listing, screen all non-kidney SOT candidates for osteoporosis with axial DXA. For kidney transplant candidates, DXA of the spine, hip, and forearm should be performed before transplantation only if the results are expected to affect treatment decisions.

1-2) Perform VFA by DXA or thoracolumbar spine radiography to identify prevalent vertebral fractures.

1-3) Optimize vitamin D status to achieve a 25(OH)D level ≥30 ng/mL (75 nmol/L).

1-4) Refer patients to a bone health specialist if there is evidence of a fragility fracture, a DXA T-score ≤−2.5 at any site, or osteopenia with a high-risk FRAX score (≥20% for MOF or ≥3% for hip fracture). Additionally, consider referral for patients with osteopenia and additional risk factors, such as chronic glucocorticoid use, or with a moderate FRAX score (≥10% for MOF or ≥1% for hip fracture). Premenopausal women and men younger than 50 years with evidence of a fragility fracture or a Z-score ≤−2.0 plus clinical risk factors or secondary causes should also be referred.

2) Posttransplant (>90% of recipients)

2-1) Refer all non-kidney SOT recipients to a bone health specialist within 2–4 months after transplantation.

2-2) In KTRs, DXA and BTMs should be measured 2–4 months after transplantation, and patients should be referred to a bone health specialist if they are at high fracture risk, preferably after correction of hyperparathyroidism, hypophosphatemia, and vitamin D deficiency.

2. Bone health specialist team

1) Pretransplant (>90% of candidates)

1-1) Men older than 50 years and postmenopausal women with pretransplant osteoporosis, defined by a prior fragility fracture, a T-score ≤−2.5, or osteopenia with a high-risk FRAX score, should receive pharmacological treatment. Treatment should also be considered for individuals with osteopenia and an intermediate-risk FRAX score, particularly those receiving chronic glucocorticoid therapy (≥5 mg/day prednisone or equivalent).

1-2) Premenopausal women and men younger than 50 years with evidence of a fragility fracture or a Z-score ≤−2.0 plus clinical risk factors, such as chronic glucocorticoid use, are also at high fracture risk and should receive treatment.

2) Posttransplant (>90% of recipients)

2-1) Initiate treatment in all non-kidney SOT recipients within 2–4 months after transplantation if they have not received osteoporosis treatment in the previous year. Use intravenous zoledronic acid when eGFR is ≥35 mL/min/1.73 m², denosumab when eGFR is <35 mL/min/1.73 m², or an anabolic agent in the setting of severe osteoporosis or low BTMs. Repeat DXA after 1 year.

2-2) In KTRs at high fracture risk with low BTMs, initiate anabolic therapy. If BTMs are high, initiate bisphosphonate therapy, preferably intravenous zoledronate when eGFR is ≥35 mL/min/1.73 m² and denosumab when eGFR is <35 mL/min/1.73 m². If the underlying bone disease remains uncertain, antiresorptive therapy should be avoided due to the risk of precipitating adynamic bone disease, and bone biopsy should be considered to guide treatment.

2-3) Monitoring: perform DXA annually initially and vertebral imaging in the presence of height loss >1.5 inches (>3.8 cm) or back pain; perform femoral imaging if thigh pain occurs in patients receiving antiresorptive therapy; and monitor vitamin D, calcium, and phosphorus levels and BTMs.

DISCUSSION

Fractures are associated with substantial complications and reduced quality of life in transplant recipients. However, bone health screening and posttransplant fracture prevention have been inconsistently implemented. A multidisciplinary bone health care pathway, together with clearly defined KPIs, may improve outcomes. High adherence to these KPIs is expected to support timely risk identification, treatment initiation, and coordinated follow-up. Although fracture-specific outcome data linked directly to KPI adherence remain limited, the consistent implementation of structured care pathways is recognized as an important determinant of improved long-term outcomes in complex transplant populations. KPI adherence should be monitored through routine audits of documented pathway measures, with regular multidisciplinary review. At the time of transplant listing, DXA and VFA should be performed to identify osteoporosis and prevalent vertebral fractures. Modifiable lifestyle risk factors should be addressed, nutritional status should be optimized, and adequate calcium and vitamin D intake should be ensured. Patients with fragility fractures or those at high risk based on DXA findings should be referred to bone health specialists before transplantation. In addition, all non-kidney SOT recipients should be evaluated by a bone health specialist within 2 to 4 months after transplantation. A history of fragility fracture before transplantation is a strong predictor of subsequent fractures and warrants prompt, intensive intervention.

Bisphosphonates are the preferred option for both treatment and prevention, with intravenous zoledronic acid favored when renal function permits. Vitamin D should be repleted before initiation of intravenous bisphosphonates or denosumab to reduce the risk of severe hypocalcemia. BTMs may help guide treatment selection and are particularly useful in KTRs, in whom differentiation among bone disease phenotypes is especially important; if the diagnosis remains uncertain, bone biopsy may be required. Anabolic agents should be considered in patients with severe osteoporosis or multiple fractures, particularly when BTMs are low. Lifestyle modification, fall prevention, and balance training remain useful adjuncts to pharmacological treatment. Ongoing monitoring with laboratory testing, repeat DXA, and surveillance for incident fractures is necessary to assess treatment response and enable timely adjustment of management.

Effective care depends on collaboration among transplant teams, bone health specialists, nutritionists, and physical therapists. All recommendations should be individualized and coordinated across specialties to support patient-centered care. Effective multidisciplinary communication is central to the proposed care pathway. Within this model, structured referral triggers, shared clinical algorithms, and clearly defined decision points support timely bidirectional communication between the transplant team and bone health specialists, particularly during periods of risk reassessment and treatment modification. This coordinated approach is intended to support consistent implementation of bone health strategies while maintaining continuity of care across the transplant continuum.

CONCLUSION

Osteoporosis and fractures are major complications after SOT. Early assessment, risk modification, multidisciplinary care, and ongoing follow-up are essential for fracture prevention. Implementation of a clear care pathway, together with defined KPIs for the relevant teams, may improve outcomes.