Parathyroidectomy timing for persistent hyperparathyroidism in kidney transplant candidates and recipients: from secondary to tertiary disease: a literature review

Introduction

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a major complication of end-stage renal disease (ESRD), affecting bone metabolism, vascular calcification, and survival (1).

Secondary hyperparathyroidism (SHPT) represents an adaptive and physiologically appropriate response to CKD, driven by phosphate retention, reduced calcitriol synthesis, and hypocalcemia, leading to progressive parathyroid hyperplasia and elevated parathormone (PTH) levels (1-4).

Tertiary hyperparathyroidism (THPT) refers to the autonomous and persistent overproduction of PTH that may develop after prolonged SHPT, when hyperplastic glands become functionally independent and hypersecrete PTH even after the initial stimulus is removed, such as following successful kidney transplantation (KT) (2).

Accordingly, persistent hyperparathyroidism (HPT) after KT may reflect established THPT and is reported in 15–50% of recipients despite restoration of renal function (5,6). Parathyroidectomy (PTX) remains the most effective treatment for refractory SHPT and THPT (7). The timing of surgery has significant clinical implications, concerning in particular:

• Risk of HPT persistence after transplant;
• Bone and cardiovascular complications;
• Graft function;
• Risk of hungry bone syndrome (HBS);
• Cost-effectiveness of medical vs. surgical treatment.

This review evaluates current evidence on optimal timing of PTX in renal transplant candidates. We present this article in accordance with the Narrative Review reporting checklist (available at https://gs.amegroups.com/article/view/10.21037/gs-2025-1-556/rc).

Methods

This literature review was performed searching across three scholarly bibliographic databases: PubMed/MEDLINE, Scopus and Web of Science.

Three independent researchers (A.S., G.M. and G.O.) conducted the article search, filtering the results with the MeSH terms hyperparathyroidism, renal transplant, parathyroidectomy timing, cinacalcet, hungry bone syndrome, secondary hyperparathyroidism, tertiary hyperparathyroidism, CKD-MBD, graft survival, cost-effectiveness.

A time filter from January 2017 onwards was applied. This cut-off was chosen because the Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD update published in 2017 (1) established modern diagnostic and therapeutic standards for SHPT and THPT.

Studies prior to this date reflect heterogeneous management paradigms (including outdated surgical indications, lack of calcimimetic availability, and non-standardized transplant protocols), which would limit comparability and clinical applicability. Although some of them were cited for contextual completeness, they were not used to inform the analytic synthesis or conclusions of this review, as their management paradigms are not reflective of contemporary practice.

Therefore, this review focuses on contemporary evidence consistent with current clinical practice and guideline-based management. Articles such as trials (randomized/non-randomized), comparative studies, cohort studies, systematic/narrative reviews, and cost-analyses were included.

Pediatric studies, case reports and non-comparative series were excluded from the analysis. Insufficient outcomes were not taken into consideration.

Only articles in English language were taken into consideration for this review.

Although this article is a narrative review and not a systematic review, a structured search strategy was used to enhance transparency.

This screening process identified 15 studies for inclusion, as shown in Figure 1.

Figure 1 Flow diagram. PTX, parathyroidectomy; SHPT, secondary hyperparathyroidism; THPT, tertiary hyperparathyroidism.

As illustrated in this flow diagram, key sources include one randomized controlled trial (RCT), eight retrospective studies, one systematic review, two reviews and three cost-effectiveness analyses.

The PubMed strategy included: (“hyperparathyroidism, tertiary” OR tertiary hyperparathyroidism OR persistent hyperparathyroidism) AND (parathyroidectomy OR surgery) AND (kidney transplant OR renal transplant) AND (timing OR pre-transplant OR post-transplant) AND (cinacalcet OR calcimimetic OR etelcalcetide) AND (tertiary hyperparathyroidism) AND (transplant).

To ensure comprehensive coverage, we manually examined the reference lists of all included studies and recent review articles in order to identify further eligible publications not captured by the electronic search. Manual reference checking was performed as recommended by PRISMA to minimize the risk of missing eligible studies due to database indexing limitations.

The eligible population was adults with CKD-related SHPT awaiting KT or KT recipients with THPT.

The following operations/scenarios were compared: PTX before KT, PTX after KT; PTX vs. cinacalcet (or other calcimimetics); any technique: subtotal PTX (SPTX), total PTX (TPTX) with auto-transplantation (TPT + AT) was evaluated.

The predefined outcomes were:

• Primary: biochemical cure (normocalcemia for THPT; resolution of severe SHPT), persistence/recurrence;
• Secondary: HBS, bone mineral disease (BMD) change, vascular/valvular calcifications, quality of life (QoL), graft function/survival, adverse events, re-operation, and cost-effectiveness.

The disagreements in data interpretation were resolved by consensus.

The following data were extracted: design, setting, number of patients, transplant status, timing (pre- vs. post-KT), technique, comparators, follow-up, outcomes, and effect measures (e.g., risk ratios, hazard ratios, or mean differences). To ensure methodological rigor and reliability of the evidence, the risk of bias of each included study was systematically evaluated according to its study design.

RCTs were assessed using the Cochrane Risk-of-Bias tool (RoB 2), which evaluates key domains such as randomization process, deviations from intended interventions, missing outcome data, measurement of outcomes, and selective reporting.

Non-randomized observational studies were evaluated using the ROBINS-I tool (Risk of Bias in Non-randomized Studies of Interventions), which allows structured appraisal of confounding, selection bias, classification of interventions, deviations from intended interventions, missing data, outcome measurement, and reporting bias.

For health-economic evaluations, methodological quality and reporting standards were assessed using the CHEERS (Consolidated Health Economic Evaluation Reporting Standards) checklist, which is specifically designed to ensure transparency, validity, and completeness in economic modeling and cost-effectiveness analyses.

These complementary instruments were selected to provide a rigorous and study-type-appropriate appraisal of bias, thereby increasing the validity and interpretability of the results of this narrative review.

Table 1 summarizes the articles included in this review, and Table 2 outlines the search strategy summary.

Key content and finding

Pathophysiological background: why surgery-and when-matters

In the RCT of Cruzado et al. (8), SPTX resulted in a more substantial decline in circulating parathyroid hormone. Serum phosphate concentrations normalized in almost all recipients and a significant gain in femoral-neck bone mineral density was observed, without discernible differences in vascular calcification between treatment strategies. Gastrointestinal disorders were most common with cinacalcet, whereas postoperative hypocalcemia predominated following surgery.

Economic modelling indicated that PTX becomes the more cost-efficient approach when cinacalcet therapy exceeds approximately 14 months. Graft function was preserved in all patients throughout follow-up. Considering all the above findings, SPTX provided superior biochemical control of hypercalcemia in kidney-transplant recipients with persistent HPT compared with cinacalcet therapy.

Long-term follow-up of Moreno et al. (9) showed that, at 5-year evaluation, recurrence of hypercalcemia was documented exclusively in the cinacalcet cohort. SPTX was associated with a more durable suppression of intact parathyroid hormone (PTH), while renal allograft function and the incidence of fragility fractures remained comparable between treatment groups. These findings indicate that, in kidney-transplant recipients with THPT, biochemical relapse is more likely with cinacalcet therapy than following SPTX. In the comparative cohort evaluated from Dulfer et al. (7), PTX achieved normocalcemia (100% of patients) with PTH normalization, whereas cinacalcet often normalized calcium (67% of patients) without normalizing PTH.

Jung et al. (10) compared two groups of patients with THPT treated with PTX and cinacalcet, respectively, immediately after transplantation. Their analysis showed there was no significant difference in corrected calcium levels between the two groups before treatment. However, these values were higher in the cinacalcet group until follow-up at 3 years after the start of treatment. In addition, normocalcemia was never obtained in the cinacalcet group. PTH levels were higher than the PTX group at all follow-ups at 6 months, 1 year, and 3 years. No difference was found in the estimated glomerular filtration rate (eGFR) values, in the change in BMD between pretreatment and post- treatment periods and in transplant failure rates, cardiovascular events and fractures in the two groups.

Alvarado et al. (11) compared long-term outcomes and survival between cinacalcet and PTX in SHPT treatment, reporting better 5-year survival in the patients undergoing surgery than in the cinacalcet group. The authors emphasize the importance of considering surgical indication particularly in patients with SHPT with PTH levels >1,000 pg/mL.

Zhao et al. (12) in their retrospective analysis evaluated outcomes in patients with THPT after transplantation according to the type of treatment performed (PTX vs. medical treatment). They found in cinacalcet group a 77% higher risk of persistent hypercalcemia and a 73% greater risk of having elevated PTH levels within 3–10 years after the start of treatment than the PTX group.

The authors also evaluated the optimal time at which to perform surgery and found that patients undergoing PTX within 1 year of transplantation had a 57% relative risk reduction for kidney stone formation and were 2 times more likely to maintain a normal GFR for 3 to 10 years. They also compared patients undergoing PTX within 6 months with those operated on 1 year after transplantation and found in the group operated on within 6 months a 62% lower risk of hypercalcemia, hyperphosphatemia and kidney stone formation as well as a 57% lower risk of elevated PTH and creatinine. The authors therefore demonstrated the superiority of surgical treatment over medical treatment with cinacalcet (12).

Finally, the evaluation of HBS risk showed that it rises with high pre-operative PTH/alkaline phosphatase (ALP), long dialysis vintage, low pre-op calcium, large gland mass; mitigation includes pre-operative vitamin D repletion, early IV calcium protocols, and close 48–72 h monitoring (13).

Recent comparative studies strengthen the advantages of PTX. A 2025 meta-analysis (14) confirmed that PTX achieves superior biochemical control without compromising graft function. In line with this, Frey et al. (15) demonstrated that PTX does not impair 1-year eGFR or 5-year allograft survival. Finally, Wang et al. (16) showed that treating hypercalcemic THPT, either surgically or with cinacalcet, significantly reduces the risk of allograft failure compared with no treatment. These converging findings underscore both the clinical importance of addressing persistent post-transplant HPT and the safety of surgery when adequately timed.

Taken together, these findings confirm that PTX represents the most effective and durable treatment for THPT in transplant recipients. Comparative studies (17,18) consistently report calcium normalization rates above 90% after PTX, compared with less than 50% in patients treated with cinacalcet. PTX also produces significant reductions in PTH and improvements in bone mineral density, both critical factors in preventing fractures and cardiovascular complications.

Cinacalcet remains a useful alternative for frail or inoperable patients.

However, its efficacy is transient, it requires long-term and costly treatment, and it does not provide durable improvement in bone mass.

However, the optimal timing of PTX remains debated.

Pre- or post KT PTX

A systematic review (19) in which the authors included 47 articles found that surgical treatment of THPT has higher cure rates than medical therapy. After SPTX and TPTX, calcemia normalized in 98.7% and 100%, respectively, while after cinacalcet treatment in 80.8% of patients.

For long-standing THPT, PTX provides more complete and durable biochemical control than cinacalcet, aligning with clinical priorities (hypercalcemia resolution, PTH reduction) and potential downstream benefits (bone, vascular).

Other analyses have explored the influence of surgical timing, evaluating PTX undertaken prior to subsequent to KT. Observational comparative data of Wang et al. (18) suggest no detriment to graft function whether PTX is performed pre- or post-KT, though some series show faster PTH normalization when PTX is done before KT and a reduction in post-KT hypercalcemia/nephrocalcinosis when PTX is conducted within the first 12 months after KT. The authors observed no differences in serum creatinine levels in the two groups at 6 months, 1, 2, 3, 4 and 5 years after KT. Patients in the pre-KT PTX group required more calcium supplements up to 1 year after PTX than those in the post-KT group. With the use of propensity score matching, this difference persisted up to 6 months after PTX.

Callender et al. (20) reported that PTX before KT was associated with lower post-KT graft failure in a large database analysis. The authors, from a total of 913 patients undergoing KT, found that patients who had a diagnosis of uncorrected uremic HPT before kidney transplantation experienced complications in the first-year post-transplant. Their analysis showed that a PTH level greater than 6 times normal was associated with post-kidney transplantation graft failure.

Comparative studies found no adverse effect on allograft function whether PTX was performed before or after KT (2,21); some cohorts even suggested benefits of pre-KT PTX on graft survival metrics (2,22).

As highlighted in the review by Cianciolo et al. (2), PTX should be performed before kidney transplantation to prevent persistent HPT and improve transplant outcomes.

In fact, post-KT PTX was associated with worse outcomes of graft function (decrease in eGFR). This risk would appear to decrease when PTX is performed at 1 year after KT or better before KT.

In patients undergoing post-KT PTX, worsening renal function was correlated with the change in PTH decline before and after surgery: a PTH decrease >80% was followed by a major decrease in creatinine clearance. In addition, post-KT PTX proved to be an independent risk factor for persistent hypocalcemia, due to HBS or hypoparathyroidism, and for a 20% reduction in eGFR at 12–36 months after transplantation.

If KT is imminent (<6–12 months) it appears reasonable to defer PTX and reassess at 6–12 months post-KT because a subset of patients normalizes spontaneously (1,2,23).

If wait-time to KT is uncertain/prolonged or SHPT is severe (very high PTH/ALP, symptomatic, calcifications), the PTX performed before KT prevents THPT and post-KT hypercalcemia (2).

Finally, if THPT persists after the KT, the evidence consistently supports performing PTX within 12–18 months, particularly in hypercalcemic or symptomatic patients (2,23,24).

In another recent study (18) that analyzed 1,554 patients undergoing KT, the authors found 75% persistent HPT after KT and it was found to be associated with an increased risk of allograft failure.

Nakamura et al. (25) argue that in KT recipients with THPT, PTX can improve biochemical control without harming graft function.

The authors recommend PTX before KT for advanced SHPT; for other, less advanced forms of SHPT, the indication should be reevaluated at 1 year after KT when the frequency of post-transplant complications and acute rejection decreases.

For candidates with severe SHPT and uncertain KT timing, pre-KT PTX is favored to prevent refractory post-KT hypercalcemia/THPT and may even improve graft outcomes (20).

For candidates with imminent KT (≤6–12 months) or modest biochemical activity, deferring surgery and reassessing at 3–12 months after KT is reasonable because a proportion of patients will normalize.

If THPT persists at 12 months (especially with hypercalcemia), it is recommended to proceed to PTX by 12–18 months (2).

In confirmed THPT, PTX outperforms cinacalcet for durable biochemical control (normal calcium and substantial PTH reduction) and likely confers QoL advantages. Economic models indicate PTX is cost-effective when calcimimetic therapy would otherwise extend beyond ~9 months (8,26).

We also asked the present review about the question of balancing HBS risk. The literature confirmed that pre-KT PTX in very severe SHPT (PTH >800–1,000 pg/mL, high ALP) carries HBS risk (2,8,27).

However, some areas of uncertainty remain, as heterogeneity in timing definitions, variable use of cinacalcet pre/post-KT, and selection bias (more severe patients referred for surgery) limit certainty.

Nonetheless, converging signals support (I) pre-KT PTX for severe SHPT or long wait-time, and (II) post-KT PTX by 12–18 months in persistent THPT, especially with hypercalcemia or target-organ involvement (18).

Observational cohort studies (25,28) suggest that pre KT surgery reduces the likelihood of persistent HPT after transplantation and lowers the risk of cardiovascular and skeletal events. This strategy also stabilizes calcium-phosphate balance before transplantation, limiting the risk of post-transplant hypercalcemia.

On the other hand, an often-cited argument against pre-transplant PTX is that a substantial proportion of patients (up to 20–30%) experience spontaneous regression of HPT following KT, owing to recovery of renal function and normalization of mineral metabolism.

According to this view, waiting 6–12 months post-KT can avoid potentially unnecessary surgery and its associated risks such as severe hypocalcemia and complications correlated to surgery (29,30).

Recent data (26) add an important perspective: beyond 12–18 months after transplantation, persistent HPT is associated with increased risk of vascular calcifications, nephrocalcinosis, and progressive renal dysfunction. Deferring PTX beyond this therapeutic window exposes patients to irreversible complications.

Nephrocalcinosis is a devastating post-transplant complication; hypercalcemia due to THPT can cause tubular or parenchymal deposition of calcium crystals in the transplanted kidney causing atrophy and, in the long run, reducing the lifespan of the transplanted kidney or, in the worst cases, loss of the transplanted organ (12).

These results support systematic screening for post-transplant HPT and early surgical decision making when hypercalcemia persists despite optimized medical therapy.

Economic considerations

In a recent study of Wang et al. (26), economic modelling demonstrated that PTX is the dominant strategy when compared with cinacalcet, offering both lower overall costs and greater health-related QoL.

Surgical management yielded superior gains relative to prolonged pharmacological therapy, whose cumulative expenses increase rapidly over time.

Sensitivity analyses indicated that, beyond a certain duration of cinacalcet use (more than 9 months), medical therapy loses cost-effectiveness, whereas surgery consistently maintains a more favourable economic profile.

In kidney-transplant recipients with THPT, PTX therefore emerges as the more cost-effective option when long-term cinacalcet therapy would otherwise be required.

More specifically, delaying PTX beyond 12–18 months post-KT is associated with more complications (e.g., persistent hypercalcemia, nephrocalcinosis) (22).

Furthermore, PTX can be economically favorable if cinacalcet is otherwise needed beyond ~9 months (26). These findings underscore the importance of discussing economic implications as part of shared decision-making.

Cost-effectiveness was also analyzed. Decision-analytic evaluations consistently indicate that cinacalcet monotherapy represents the least cost-effective management strategy. In contrast, PTX becomes the economically preferred option when calcimimetic therapy is expected to be maintained beyond approximately 9–12 months, owing to the progressive accumulation of drug-related costs and the more durable biochemical control achieved with surgery (7,26,31).

Sa et al. (32) have analyzed costs and final outcomes of three main surgical treatment options of SHPT (subtotal, total with autotrasplatation and TPTX) and found that PTX as the first-line treatment for ESRD secondary to refractory HPT is considered to have the highest cost-effectiveness.

QoL

Another evidence underlined in the present review was the QoL improvement in the patients who underwent surgery. Morandi et al. (28) in their analysis conducted on 34 patients underwent PTX for THPT found significant and sustained QoL gains.

The authors using PAS and SF-36 questionnaires, found an improvement in some symptoms including bone pain, fatigue, mood disturbances and in the ability to perform normal activities without being hindered by the symptoms of the disease (28).

Wang et al. also emphasized that untreated or treatment-resistant SHPT results in complications that negatively affect QoL (26).

Practical algorithm for surgical decision-making

Arguments supporting early PTX include:

• More rapid and durable metabolic control, with consistent evidence that PTX results in faster and more stable normalization of serum calcium and PTH compared with calcimimetic therapy (3,7,8).
• Skeletal benefits, including significant improvement in femoral-neck bone mineral density and reduction of high-turnover bone disease after surgery (8,27).
• Economic advantages, as PTX becomes more cost-effective when prolonged calcimimetic treatment is anticipated, particularly beyond 9–12 months (26).

Conversely, several arguments support delaying PTX after kidney transplantation:

• A proportion of patients exhibit spontaneous regression of HPT within 6–12 months post-transplantation as renal function improves and mineral metabolism normalizes (1,2). Avoiding unnecessary surgery during this window is therefore considered reasonable, particularly in light of perioperative risks such as postoperative hypocalcemia.
• The early post-transplant period is also characterized by instability of calcium-phosphate homeostasis, which may predispose to clinically significant hypocalcemia and HBS following PTX (2,27).
• Contemporary CKD-MBD guidelines support a staged approach, emphasizing biochemical reassessment after transplantation before proceeding to surgery (1).

Based on the current evidence, a stepwise approach could be proposed:

• Pre-transplant PTX in patients with severe SHPT (PTH >800 pg/mL, clinical symptoms, or extensive bone/cardiovascular involvement).
• Close monitoring of PTH and calcium at 3, 6, and 12 months after transplantation.
• SPTX within 12–18 months post-transplant if persistent HPT with hypercalcemia >2.7 mmol/L or symptomatic disease.
• Long-term medical therapy reserved for frail and/or inoperable patients or those awaiting delayed intervention.

A recently published article supports the importance of surgery especially in patients refractory to medical therapy by emphasizing that the surgery also alleviates symptoms associated with SHPT including bone pain, muscle weakness and fatigue (33).

The authors therefore included 36 patients undergoing SPTX who were refractory to medical therapy. Of these, 23 patients (63.9%) experienced symptomatic hypocalcemia and 14 patients (38.9%) developed HBS. The cure rate was 91.6%. The authors found a statistically significant reduction in mean levels of PTH (P<0.0001) and serum calcium (P<0.01) at 36 months after surgery.

The authors emphasized the importance of surgery as a viable option to achieve biochemical balance in patients with refractory SHPT and chronic renal failure, ultimately improving their QoL (33).

Strengths and limitations

The present review has several limitations: most published studies remain retrospective, with heterogeneous definitions of THPT (different PTH thresholds) and potential selection bias (more severe patients undergoing surgery). Few RCTs are available, limiting the strength of evidence. Follow-up durations are often short (1–3 years), making it difficult to assess long-term graft survival.

To provide a comprehensive overview of the topic, we also included narrative reviews. Finally, although heterogeneity in timing definitions and variability in pre- and post-transplant cinacalcet use reduces the overall certainty of evidence, several converging signals emerge: pre-KT PTX appears appropriate in cases of severe SHPT or prolonged waiting time, while post-KT PTX within 12–18 months seems advisable for persistent THPT, particularly in the presence of hypercalcemia or target-organ involvement.

Moreover, it may lay the groundwork for future research directions.

Prospective randomized trials could be needed to directly compare pre- versus post-transplant PTX and evaluate their impact on graft survival, long-term bone health, and QoL. The use of innovative biomarkers (FGF-23, coronary calcification scores, quantitative bone densitometry) may help refine patient stratification. Development of minimally invasive PTX techniques and assessment of novel calcimimetic agents (e.g., etelcalcetide) represent promising areas of research.

Despite these limitations, this review provides a comprehensive and clinically integrated synthesis of the available evidence, combining observational studies, comparative cohorts, cost-effectiveness analyses, and expert-based recommendations across the pre- and post-transplant continuum. Moreover, by examining economic implications, this review offers a multidimensional assessment of surgical timing that reflects real-world clinical decision-making. The incorporation of cost-effectiveness models strengthens the analysis by contextualizing surgical decisions within healthcare resource utilization, an increasingly relevant dimension for transplant and endocrine surgery practice.

The review objectively contrasts PTX with calcimimetic therapy, integrating evidence from both interventional and medical management pathways, thus offering a balanced perspective on competing treatment strategies. By synthesizing heterogeneous data into clinically meaningful time intervals (e.g., 6–12 months and 12–18 months post-transplant), the review provides actionable guidance that aligns with biochemical recovery patterns and graft physiology.

This review also integrates data from a wide variety of study designs-retrospective cohorts, population-based studies, and microsimulation models-enhancing its relevance to real-world practice where randomized trials are scarce. Although the literature is heterogeneous, this review identifies converging signals that reliably support specific indications for pre- and post-transplant PTX.

Conclusions

The literature highlights the need for a personalized, multidisciplinary approach. Systematic screening, close biochemical monitoring, and joint decision-making among nephrologists, endocrinologists, and surgeons optimize surgical timing, maximize metabolic benefit, and preserve graft function. Importantly, the significant improvement in QoL reported after PTX justifies a proactive strategy for managing persistent HPT in kidney transplant recipients.

Evidence increasingly supports early PTX (<12–18 months post-transplant) in cases of persistent HPT, in order to prevent metabolic and skeletal complications, while accepting transient hypocalcemia as a manageable side effect.

Overall, PTX demonstrates clear superiority over medical therapy in achieving durable control of calcium-phosphate metabolism. Surgical timing (pre- or post-transplant) has not shown significant difference as regards short-term graft function, anyway early PTX provides superior biochemical outcomes and fewer hospitalizations.

Ideally, surgical timing should be individualized, with a therapeutic window within 12–18 months post-transplant if the indication has not already been established.

THPT in kidney transplant recipients thus represents a major metabolic and surgical challenge. Recent literature confirms that PTX improves biochemical and skeletal parameters without compromising graft survival. Optimal timing depends on biochemical severity and transplant interval. Standardized decision algorithms could help harmonize practices and reduce inter-center variability.

A multidisciplinary approach involving nephrologists, surgeons, and endocrinologists remains essential to optimize metabolic outcomes, preserve graft function, and enhance patient QoL.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://gs.amegroups.com/article/view/10.21037/gs-2025-1-556/rc

Peer Review File: Available at https://gs.amegroups.com/article/view/10.21037/gs-2025-1-556/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://gs.amegroups.com/article/view/10.21037/gs-2025-1-556/coif). N.C.P. serves as an unpaid editorial board member of Gland Surgery from April 2024 to March 2026. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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