Diabetes Mellitus and Osteoporosis After Organ Transplantation

Frequency, Clinical Features, and Treatment

Background: Organ transplantation is an effective treatment option, often the last remaining one, for terminal organ failure. 22–32% of transplant recipients, however, develop metabolic-endocrine complications that markedly impair transplant function and overall survival. We provide an evidence-based narrative review of the clinical features, diagnostic evaluation, and treatment of post-transplantation diabetes mellitus (PTDM) and osteoporosis.

Methods: This review is based on pertinent publications that were retrieved by a selective search in PubMed, MEDLINE, and the Cochrane Library (01/1995–09/2025), including systematic reviews, clinical studies, randomized controlled trials, register data analyses, observational studies, and guidelines.

Results: Post-transplantation diabetes affects 9–40% of organ recipients in the first year after transplantation, corresponding to a two- to threefold risk elevation compared to the general population. Its incidence and course are organ-specific and characterized by further risk factors, including a 3.3-fold elevation of the risk of cardiovascular events. Studies have shown that, alongside insulin and metformin, newer antidiabetic agents such as GLP-1 receptor agonists and SGLT2 inhibitors also improve glycemic control, reduce cardiovascular events, and, as far as can be determined, do not endanger the transplant.

Transplantation-associated osteoporosis affects 23–67% of transplant recipients, causing the most marked bone loss in the first 6–18 months after transplantation. Approximately 20% of the affected patients sustain fractures. Bisphosphonate, denosumab, and teriparatide have been found to be treatment options. Treatment should be initiated as early as possible.

Conclusion: Thorough screening and timely, specialist-coordinated interdisciplinary care in specialized transplantation centers are decisive for the recognition and risk-adapted, evidence-based treatment of PTDM and transplantation-associated osteoporosis.

Cite this as: Sarabhai T, Mathew A, Rashidi-Alavijeh J, Willuweit K, Gallinat A, Führer D: Diabetes mellitus and osteoporosis after organ transplantation: Frequency, clinical features, and treatment. Dtsch Arztebl Int 2026; 123: 281–8. DOI: 10.3238/arztebl.m2026.0019

Today, the clinical course after organ transplantation is greatly influenced by metabolic complications related to immunosuppressive treatment. Within the first year after transplantation, 32% (95% CI: [32; 33]) of affected patients developed arterial hypertension, 28% [17; 28] diabetes mellitus and 22% [19; 24] dyslipidemia (1). In addition, these patients are at increased risk of osteoporotic fractures (HR: 1.19 [1.01; 1.39]) (2). Thus, early detection and treatment of endocrine-metabolic complications are critical to preserve transplant function and ensure favorable outcomes in the long term.

Methods

This review is based on pertinent publications published from 1 January 1995 to 20 September 2025 that were retrieved by a selective search in the PubMed, MEDLINE and Cochrane Library databases. Systematic reviews, randomized controlled trials (RCTs), registry data analyses, and observational studies on organ transplantation, post-transplantation diabetes mellitus and bone complications were included in this review. Of the 264 publications identified, we included 35 studies reporting evidence relevant to therapeutic efficacy and safety. Both the search strategy and the criteria are described in the eSupplement (eMethods). Diagnosis and treatment are fundamentally based on the pertinent general guidelines. In the following, we will describe transplant-specific issues. Overall, the available therapeutic evidence related to the post-transplant course is commonly observational and heterogeneous. The body of evidence is more extensive for post-transplantation diabetes mellitus (PTDM) compared to osteoporosis where the majority of studies are small organ-specific surrogate studies and fracture/long-term data are scarce.

Post-transplantation diabetes mellitus

The prevalence of PTDM varies by organ and observation period after transplantation: Within the first year, 10–40% of kidney transplant recipients, 9–21% of liver transplant recipients and 20% of heart and lung transplant recipients developed PTDM (3). This stands in contrast to the age-standardized incidence of type 2 diabetes in the general population, which is about 0.8–1.5% per year (4). In 60–70% of affected organ transplant recipients, the hyperglycemic metabolic state persists; weight gain, inactivity and immunosuppressive therapies can further aggravate pre-existing metabolic disorders (5). Glucocorticoids, calcineurin inhibitors (CNIs) and mTOR inhibitors increase insulin resistance and have a lasting adverse effect on insulin secretion (6). In addition, well-established risk factors such as

• Age
• Obesity
• Ethnicity
• Familial predispositions

as well as chronic inflammation and viral infections (e.g., by the cytomegalovirus) contribute to the development and persistence of PTDM (5). Sex-specific differences also play a role: A prospective multi-cohort analysis including 417 kidney transplant recipients found that 152 patients (36.5%) developed PTDM; the incidence was 39.1% in men compared to 31.5% in women (p = 0.37) and thus showed a trend toward higher PTDM rates among men (7). While a pattern of insulin resistance and metabolic syndrome is more common in men, marked β-cell dysfunction is more prevalent in women (8). PTDM is a clinically relevant complication and associated with:

• a 14% reduction in graft survival
• a 3.3-fold higher risk of cardiovascular events
• and a 1.8-fold increase in all-cause mortality (9, 10, 11).

Screening

According to the international consensus, a structured diabetes screening should be performed multiple times in all patients post-organ transplantation: at 10–13 weeks, at six months and at one year (12). Screening is not recommended during the early postoperative period (<3 months) or in cases with concurrent graft rejection or infection (12). The oral glucose tolerance test (OGTT) is considered the gold standard in diagnosing PTDM. Relying solely on fasting glucose levels is inadequate, as postprandial hyperglycemia following the morning dose of immunosuppressants may not always be detected.

Diagnostic criteria

PTDM is diagnosed according to the criteria specified in the guidelines of the American Diabetes Association (ADA) (13). The diagnosis of PTDM is established when the OGTT 2-hour value is ≥ 200 mg/dL or the fasting glucose level is ≥ 126 mg/dL, or when a random glucose level is ≥ 200 mg/dL in patients with typical symptoms of hyperglycemia, such as polyuria or polydipsia (12). An HbA1c level of ≥ 6.5% is considered diagnostic for PTDM no earlier than 6–12 months after organ transplantation and should only be used in patients with stable kidney function and without anemia (12).

Management of post-transplantation diabetes mellitus

Pharmacological treatment strategies and special clinical features

Treatment should be initiated once a definite diagnosis has been established; it should be combined with structured lifestyle interventions (Box 1) (17). The pharmacological treatment of PTDM follows the ADA guideline recommendations (17). However, treatment should be adapted to the individual patient in cases where there are particular combinations of risk factors and comorbidities, taking into account the known side effect profiles of the various substances (Box 2) (12).

Box 1

Lifestyle interventions for post-transplantation diabetes mellitus

Box 2

Core recommendations for screening and treatment of post-transplantation diabetes mellitus

Management of steroid-induced or marked hyperglycemia

Insulin—whether short-acting or long-acting—is the treatment of choice in the immediate postoperative period, especially in patients with steroid-induced hyperglycemia and patients with inadequate response to non-insulin-based treatments (12). A randomized trial including 50 kidney transplant recipients found that early initiation of basal insulin therapy after transplantation reduced the risk of hyperglycemic episodes (≥ 200 mg/dL) by 73% and was associated with improved preservation of β-cell function at twelve months (18). Given that glucose profiles can change rapidly during steroid tapering and when changes are made to immunosuppressive therapy, insulin therapy should be adjusted accordingly.

Management of patients with low cardiometabolic risk profile

In clinical practice, metformin is primarily used in transplant recipients whose kidney function is stable (eGFR ≥ 30 mL/min). In observational studies, the use of metformin was associated with a reduced risk of transplant-related mortality, albeit without any proven benefit in relation to cardiovascular events (19). In patients who are at increased risk of cardiorenal complications, preference should be given to newer antidiabetic drugs, and metformin should be considered as an additional treatment option or when other therapies are contraindicated.

Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as sitagliptin and linagliptin, are well tolerated and provide good glycemic control (Table 1) (20).Their use may be considered in particular in the early postoperative period, e.g., in cases of impaired renal function or as part of a combination therapy (12, 20). However, unlike newer antidiabetic drugs, no additional cardiorenal benefits have been demonstrated (12, 20).

Table 1

Studies on oral antidiabetic drugs and incretin-based therapies after solid organ transplantation and post-transplantation diabetes mellitus

Management of patients with moderate to increased cardiorenal risk

Sodium–glucose linked transporter 2 (SGLT2) inhibitors, such as empagliflozin and dapagliflozin, are associated with lower all-cause mortality as well as with a reduction in cardiovascular events and severe renal complications (Table 1) (21). An RCT evaluating empagliflozin in kidney transplant recipients demonstrated effective reduction in glucose levels, the extent of which decreased with decreasing eGFR, while the cardiorenal protective effects appeared to be sustained (22). There is currently no evidence to suggest an increased risk of very frequent urinary tract infections (22). In light of the rare risk of euglycemic ketoacidosis (1–2 cases per 1000 patient-years), the use of an SGLT2 inhibitor should be paused during periods of fasting and in the presence of acute conditions, such as transplant failure or transplant inflammation (12, 17).

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) (e.g., semaglutide) are associated with effective glycemic control and weight reduction in kidney transplant recipients (Table 1) (23). In addition, a lower all-cause mortality as well as reduced rates of cardiovascular events and severe renal end points (dialysis, eGFR < 15 mL/min/1.73 m²) was observed compared to patients not receiving GLP-1RAs (23). For combination therapy with basal insulin, a reduction in insulin dose and injection frequency was demonstrated (24). Irrespective of body weight, the use of GLP-1 receptor agonists may be useful in patients with a corresponding cardiometabolic risk profile (23). The authors are of the opinion that a slow, gradual increase in dose, combined with counseling on nutrition and treatment breaks during acute illnesses, improves treatment adherence. At present, there is a lack of reliable data on the use of newer dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptor agonists (e.g., tirzepatide) after organ transplantation.

Management in case of a limited recommendation for certain substance classes

In light of potential side effects, such as fluid retention and weight gain, as well as in cases of reduced kidney function and elevated fracture risk, thiazolidinediones, especially pioglitazone, should be used with caution and only after weighing the risks and benefits on a case-by-case basis (Table 1) (20).

Given their high risk of hypoglycemia and potential arrhythmogenic effects after organ transplantation, sulfonylureas, such as glibenclamide and glimepiride, and glinides, such as repaglinide, should be viewed with caution and are now considered largely obsolete (12).

Conclusion

PTDM is a common complication after organ transplantation that is relevant to prognosis; it requires early diagnostic evaluation and structured metabolic care. Modern antidiabetic drugs appear to be safe and effective treatment options; however, their use requires careful selection and close monitoring. Interdisciplinary care in transplantation centers is still key to achieving stable glycemic control and preventing cardiometabolic complications.

Transplantation-related bone disease

Organ transplant recipients are at a significantly higher risk of osteoporosis (HR 1.46 [1.29; 1.65]) and pathological fractures (HR 1.19 [1.01; 1.39]) compared to the general population in which the prevalence of osteoporosis is 5.6% (2, 27). High rates of osteopenia or osteoporosis are already observed prior to transplantation, especially in patients with end-stage lung disease (67%) (28). The next highest rates are found among candidates for liver (31%), kidney (24%) and heart (23%) transplantations (28). Apart from glucocorticoids and calcineurin inhibitors, mineral metabolism disorders associated with chronic kidney disease (CKD), hypogonadism and PTDM significantly contribute to bone disease before and after transplantation (2, 28). The most severe bone density loss occurs during the first 6 to 18 months after organ transplantation; depending on the transplanted organ, the loss is 4–10% at the lumbar spine and 5–11% at the femoral neck (29). According to population-based administrative data, there is a 5.14-fold [3.13; 8.43] increase in the risk of osteoporosis after transplantation and a 5.76-fold [3.80; 8.74] increase in the risk of fracture (30). This is most commonly seen after lung transplantation, followed by heart, liver and kidney transplantations (30). Compared to men, women have a 3.3 times higher risk of osteoporosis and a 2.1 times higher risk of fractures after transplantation (2). Regardless of sex, age and cumulative glucocorticoid dose, the increased risks of osteoporosis and fractures persists in the long term, even after more than ten years (30).

Prevention and diagnosis of post-transplantation osteoporosis

Despite the high incidence of fractures and the, at times, rapid bone loss after organ transplantation, there are currently no screening and treatment recommendations available in Germany that extend beyond the guideline of the German Osteology Society (DVO, Dachverband Osteologie) for postmenopausal women and men over the age of 50 years (31). Bone density measurements with dual-energy X-ray absorptiometry (DXA) at the lumbar spine and the proximal femur, bilaterally, as well as assessment of the bone microarchitecture using the Trabecular Bone Score (TBS) is indicated in patients with known risk factors or likely osteoporosis-related fractures (31). Risk factors include general parameters, a history of fractures, internal medical/endocrinological conditions, and certain medications. Basic laboratory tests (serum sodium, serum calcium, serum phosphate, blood count, eGFR, TSH, alkaline phosphatase (AP), γ-GT, protein electrophoresis) are performed to identify additional risk factors (31). DXA should ideally be carried out before transplantation in a risk-adapted manner. After organ transplantation, a repeat DXA scan is recommended after three to six months as well as follow-up scans based on risk assessment (28, 30). In cases of contradictory findings or unsatisfactory response to treatment, further diagnostic testing includes parathyroid hormone, 25-OH vitamin D and markers of bone remodeling (31). In selected cases, a diagnostic bone biopsy may be indicated, to be performed preferably in collaboration with a specialized transplantation center (31).

Basic therapy in patients at elevated risk of fracture

In line with the DVO guideline, a basic therapy is recommended for all patients at an increased risk of fracture (31), such as patients with:

• Osteopenia
• Osteoporosis
• Status post osteoporotic fractures, and
• Adults aged 65 and older.

The basic therapy comprises 1000 mg calcium daily, preferably from food. In addition to the administration of calcium, supplementation of a daily dose of 800–2000 IU vitamin D is indicated as is a bone health-promoting lifestyle with regular physical activity—particularly exercises that build strength and improve coordination—as well as a high-protein diet from age 65 years onwards (1 g/kg body weight) (31).

Initiation of antiresorptive or osteoanabolic therapy

With reference to the 2023 DVO guideline, the decision to prescribe a specific osteoporosis treatment can be guided by the “3-year fracture risk for vertebral or proximal femoral fractures“. Taking into account defined risk factors and DXA values (total femur/femoral neck bone densities), the classification is based on the following four cut-off values:

• < 3% (no specific indication for treatment)
• 3–5 % (specific therapy on a case-by-case basis)
• > 5 % (specific therapy recommended; consider osteoanabolic therapy in high-risk patients)
• > 10% (indication for osteoanabolic therapy) (31).

Antiresorptive treatment options in patients with moderate and high fracture risk

Antiresorptive treatments are used primarily in patients with moderate fracture risk (3–5%) or with increased risk (> 5%) in cases where osteoanabolic therapy is contraindicated (Box 3). Prior to the start of an antiresorptive treatment or romosozumab treatment, patients should be informed about the risk of drug-induced osteonecrosis of the jaw, and a dentist should be consulted to perform a comprehensive dental assessment (31). The absolute risk associated with intravenous administration of highly potent bisphosphonates or denosumab is up to 0.1–0.3%, depending on the duration of therapy and the patient’s risk profile (32).

Box 3

Osteoporosis treatment of patients on glucocorticoids and immunosuppression

The most comprehensive evidence base is available for bisphosphonates (orally daily/IV annually), especially on their use after kidney transplantation. A Cochrane meta-analysis found for this drug class a potential reduction in fractures of about 38% (RR 0.62; [0.38; 1.01]; low quality of evidence) as well as a moderate reduction in acute graft rejection events (RR 0.70; [0.55; 0.89]; low quality of evidence) (33) (Table 2). Alendronate (10 mg orally once daily), risedronate (5 mg orally once daily; only for women) and zoledronate have been approved for use in patients with glucocorticoid- induced osteoporosis (GIOP); their antiresorptive effects also increase in this order. In the current literature, their use is described for patients with an eGFR of ≥ 35 mL/min/1.73 m² (34).

Table 2

Selective review of the clinical evidence on bisphosphonates, denosumab and teriparatide in organ transplant recipients

Denosumab (subcutaneously every 6 months) is an appropriate treatment option for postmenopausal women, men at high risk of fracture and for GIOP. In randomized trials, the use of denosumab in kidney transplant recipients was associated with a greater increase in bone density compared to bisphosphonates (Table 2) (35, 36). Thanks to its targeted inhibition of osteoclast activity, it effectively counteracts glucocorticoid- and CNI-induced bone loss. Denosumab is also suitable for use in patients with severe renal impairment (eGFR <30 mL/min). There is, however, no reliable data available on its use in patients undergoing long-term glucocorticoid therapy.

Osteoanabolic treatment options for patients at high and very high risk of fracture

These therapies are indicated primarily in patients with high (>5%) or very high (>10%) fracture risk, and where there is evidence of an immediate increase in short-term in fracture risk. Examples of such imminence factors include:

• Recent fragility fracture
• Multiple fractures
• High-dose glucocorticoids
• A significant risk of falls (31).

Teriparatide (a recombinant parathyroid hormone analog, administered subcutaneously daily for 24 months; not to be repeated over a patient‘s lifetime) is currently approved for postmenopausal women and men at very high risk of fracture and for GIOP. It promotes bone formation by stimulating osteoblast activity in a targeted manner. Contraindications include:

• Hyperparathyroidism
• Hypercalcemia
• Elevated alkaline phosphatase
• Chronic kidney disease
• After radiotherapy
• Malignant bone diseases (primary and metastatic).

In an RCT with kidney transplant recipients, the use of teriparatide was associated with a less severe loss of bone density at the femoral neck compared to alendronate (Table 2) (37).

Abaloparatide (a member of the class of parathyroid hormone receptor agonists, administered subcutaneously daily for 18 months; not to be repeated over a patient‘s lifetime), has recently been approved for the treatment of postmenopausal osteoporosis (38). At present, no reliable data on organ transplant recipients is available.

Romosozumab (a monoclonal anti-sclerostin antibody, administered subcutaneously once a month for 12 months per cycle) has currently been approved only for postmenopausal women. Contraindications include an increased cardiovascular risk (status post myocardial infarction/stroke). Although there are no restrictions on the use of this substance in patients with reduced kidney function, it has rarely been used in this patient group (eGFR < 30 mL/min) thus far. A first retrospective observational study with twelve female kidney transplant recipients found that romosozumab treatment was associated with an increase in bone density of 8–15% at the femoral neck and spine (39). Until now, no reliable study data after organ transplantation has become available.

Follow-up care and long-term strategy

In patients receiving ongoing immunosuppressive and glucocorticoid therapy (at least ≥ 2.5 mg of prednisolone equivalent per day for ≥ 3 months), fracture risk assessments should be performed annually (31). Patients receiving osteoporosis-specific therapy should have regular follow-up DXA scans, usually at least once during the first five years (31). Treatment duration depends on the individual patient‘s risk of fracture and on the duration of exposure to immunosuppressants and glucocorticoids; after the end of treatment, a follow-up DXA scan may be performed within 12 months (31). After denosumab treatment, an antiresorptive sequential therapy is required due to post-treatment bone loss; osteoanabolic therapy should be followed by antiresorptive maintenance therapy (31).

Conclusion

Post-transplantation bone disease is a common and clinically relevant complication associated with increased osteoporosis and fracture incidence; it is already present before transplantation and is aggravated in the first 6–18 months by rapid loss of bone density. Management requires a structured diagnostic process, consistent basic therapy and risk-adapted antiresorptive or osteoanabolic treatment. Given the heterogeneous evidence base, interdisciplinary care in specialized transplantation and endocrinology centers is crucial.

In summary

While the body of evidence regarding post-transplantation diabetes mellitus is relatively substantial, osteoporosis management after transplantation is largely based on small studies with surrogate endpoints, while reliable fracture data are missing. Consequently, there is a need for structured screenings (OGTT, DXA) and early, risk-adapted treatment, along with further research in interdisciplinary transplantation centers.

Funding
This study received no specific funding from public, commercial or not-for-profit sectors. The work from TS is supported by the German Research Foundation (DFG, Deutsche Forschungsgemeinschaft) as part of the DFG-supported Clinician Scientist Program UMEA, FU 356/12–2.

Conflict of interest statement

AM received consulting fees and lecture fees from Ascendis Pharma, DVO e.V., Ipsen, Novartis, and NovoNordisk.

DF received consulting fees and lecture fees from Lilly, Amgen, Sanofi, Roche, Bayer, Eisai, Ipsen, IBSA, Merck, Novartis, Medupdate, and StreamedUp!.

The remaining authors declare that they have no conflict of interests.

Manuscript received on 23 June 2025; revised version accepted on 5 February 2026

Translated from the original German by Ralf Thoene, M.D.

Corresponding author
Dr. med. Theresia Sarabhai

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