Dumitru D. Branisteanu

Background: Bone disease remains a major long-term complication after kidney transplantation. However, the relationship between circulating bone turnover markers (BTMs) and densitometric skeletal parameters in kidney transplant recipients (KTRs) remains incompletely understood. Methods: This single-center, cross-sectional comparative study included 50 stable adult KTRs and 56 non-transplanted individuals with dual-energy X-ray absorptiometry (DXA)-confirmed osteopenia or osteoporosis. Serum bone formation markers, bone-specific alkaline phosphatase (BALP) and procollagen type I N-terminal propeptide (P1NP), and bone resorption markers, β-C-terminal telopeptide of type I collagen (β-CTX) and tartrate-resistant acid phosphatase 5b (TRAP5b), were quantified by enzyme-linked immunosorbent assay (ELISA). Bone mineral density (BMD), Z-scores, and Fracture Risk Assessment Tool (FRAX) estimates were obtained by DXA. Between-group comparisons were adjusted for age, sex, body mass index (BMI) and postmenopausal status, with sensitivity analyses restricted to participants with low bone mass. An exploratory receiver operating characteristic (ROC) analysis was performed to assess the association of BTMs with KTR status. Results: KTRs showed lower DXA-derived Z-scores at the total hip, femoral neck and lumbar spine despite being younger. After adjustment for age, sex, BMI and postmenopausal status, KTRs had significantly higher BALP (adjusted Δ = 129.96 ng/mL, p < 0.001) and PTH, and lower eGFR and magnesium than the reference group, whereas unadjusted differences in P1NP and lumbar spine BMD did not persist; β-CTX and TRAP5b did not differ between groups. BALP remained significantly higher in KTRs across the low-bone-mass restricted and propensity-score overlap analyses. BTMs showed no significant correlations with DXA parameters in KTRs. In the exploratory ROC analysis of study-group status, BALP showed the strongest separation between KTRs and the reference group (AUC = 0.808, p < 0.001). Conclusions: Long-term KTRs exhibit a distinct bone remodeling profile characterized most consistently by elevated BALP, which remained significant after adjustment and showed the strongest separation regarding KTR status. The limited BTM–DXA associations require confirmation in longitudinal studies.

Background: The nipple–areolar complex (NAC) necrosis is a rare yet significant complication following breast reduction surgery, primarily linked to compromised vascularization of the NAC, particularly in nipple-sparing techniques. While multiple therapeutic strategies have been described in the postoperative setting, their application remains limited in clinical practice. Case series: We report on three patients that developed early NAC venous distress following bilateral breast reduction. Following discussion of therapeutic options—ranging from conventional methods such as scarification and local heparin therapy to off-label pharmacologic treatment—all three patients received oral sildenafil citrate (20 mg every 6 h), after excluding contraindications and obtaining informed consent. In two patients, sildenafil alone was sufficient to restore venous outflow and salvage the NAC. In one case, adjunct scarification and heparin therapy were necessary due to partial response. No arterial damage or major adverse effects related to sildenafil were observed during the postoperative period. Conclusions: This small series supports the potential use of off-label sildenafil citrate as a valuable, non-invasive pharmacologic option for treating postoperative areolar venous congestion. Its favorable safety profile, widespread hospital availability, and mechanism of enhancing microvascular circulation make it a promising adjunct in managing this complication. Further studies are warranted to standardize its use and determine its place within a broader postoperative management spectrum of compromised vascularization in breast surgery.

Parathyroid carcinoma (PC) associated with primary hyperparathyroidism (PHPT) has been well investigated in recent years. Data regarding PC evolution in secondary hyperparathyroidism (SHPT) due to chronic kidney disease (CKD) are, however, scarce. Most features that raise the suspicion of PC in PHPT are part of the usual SHPT evolution in CKD, mirroring the natural changes undergone by the parathyroid glands. Therefore, pre-surgically establishing the malignant or benign character of the lesions is cumbersome. We present two cases of PC in end-stage renal disease, one of which was bilateral, diagnosed after total parathyroidectomy in a high-volume parathyroid surgery center. A literature review of the data was also performed. A systematic search of the PubMed/MEDLINE database until January 2024 identified 42 cases of PC associated with SHPT. Understanding the PC features in CKD might improve associated bone and mineral disease management, and reduce the risk of metastasis, parathyromatosis, or recurrence. Irradiation, prolonged immunosuppression, long dialysis vintage, and genotype may predispose to the malignant transformation of chronically stimulated parathyroids. Despite postsurgical diagnosis, favorable outcomes occurred when distant metastases were absent, even without “en bloc” resection. Further research is warranted to delineate specific diagnostic and therapeutic approaches tailored to this particular patient subpopulation.

While chronic kidney disease-associated mineral and bone disorders (CKD-MBD) prevail in the endocrinological assessment of CKD patients, other endocrine abnormalities are usually overlooked. CKD is associated with significant thyroid, adrenal and gonadal dysfunction, while persistent and de novo endocrinological abnormalities are frequent among kidney transplant recipients (KTR). Low T3 levels prior to transplantation may help identify those at risk for delayed graft function and are often found in KTR. Thyroid surveillance after kidney transplantation should be considered due to structural anomalies that may occur. Despite the rapid recovery of gonadal hormonal secretion after renal transplantation, fertility is not completely restored. Testosterone may improve anemia and general symptoms in KTR with persistent hypogonadism. Female KTR may still experience abnormal uterine bleeding, for which estroprogestative administration may be beneficial. Glucocorticoid administration suppresses the hypothalamic-pituitary–adrenal axis in KTR, leading to metabolic syndrome. Patients should be informed about signs and symptoms of hypoadrenalism that may occur after glucocorticoid withdrawal, prompting adrenal function assessment. Clinicians should be more aware of the endocrine abnormalities experienced by their KTR patients, as these may significantly impact the quality of life. In clinical practice, awareness of the specific endocrine dysfunctions experienced by KTR patients ensures the correct management of these complications in a multidisciplinary team, while avoiding unnecessary treatment.