Hyperparathyroidism (HPT) with hypercalcemia, often deemed irreversible and detrimental to graft survival post-kidney transplantation (KT), prompts pre-transplant parathyroidectomy in hypercalcemic patients. In this retrospective analysis of 1212 kidney transplant recipients (KTRs) between 2006 and 2019, the incidence and effect of persistent HPT and hypercalcemia on graft and patient survival, and risk factors for persistence were analyzed until 60 months of follow up (FU). At KT, 5.7% (n = 69) had no HPT, 32.7% (n = 396) had HPT without hypercalcemia and 37.0% (n = 448) had HPT with hypercalcemia. At 2 years FU, 26.4% (n = 320) of patients had no HPT and 6% (n = 73) had HPT with hypercalcemia. Dialysis and dialysis duration were linked to HPT development, while dialysis, KT waiting time and donor type correlated with persisting hypercalcemia after KT. KTRs with normalized PTH and recovered hypercalcemia had improved death-censored graft survival (p < 0.001) and overall patient survival (p < 0.001). HPT with hypercalcemia is frequent at time of KT with normalization of PTH and calcium in a substantial proportion of patients after a KT. These findings question the routine pre-KT parathyroidectomy for suspected parathyroid autonomy. Persisting HPT, especially with hypercalcemia, adversely affects graft and patient survival, suggesting the need for more aggressive treatment of HPT, especially in cases of persisting hypercalcemia.

UNASSIGNED: Primary hyperparathyroidism (PHPT) increases the risk of bone loss, debilitating fractures, kidney stones, impaired renal function, and neurocognitive symptoms. Studies describing the natural history of PHPT have been limited to small samples, single institutions, or specific populations.
UNASSIGNED: We assessed the natural history of PHPT through a large, diverse national cohort from an electronic health record dataset representing more than 100 million patients.
UNASSIGNED: The TriNetX database was queried for adult patients with PHPT. We extracted demographics, comorbidities, and longitudinal biochemistries. Primary outcomes included major osteoporotic fracture (MOF) and chronic kidney disease (CKD). Outcomes were stratified by treatment strategy (surgical parathyroidectomy [PTX] vs nonsurgical) and age.
UNASSIGNED: Among 50 958 patients with PHPT, 26.5% were treated surgically at a median of 0.3 years postdiagnosis. At diagnosis, median age was 65 years, 74.0% were female, and median calcium level was 10.9 mg/dL. Black and older patients underwent PTX less frequently than White and younger patients. MOF 10-year incidence was 5.20% (PTX) and 7.91% (nonsurgical), with median 1.7-year delay with PTX compared to nonsurgical. PTX-associated MOF absolute risk reduction was 0.83% (age < 65 years) and 3.33% (age ≥ 65 years). CKD 10-year incidence was 21.2% (PTX) and 33.6% (nonsurgical), with median 1.9-year delay with PTX. PTX-associated CKD absolute risk reduction was 12.2% (age < 65 years) and 9.5% (age ≥ 65 years).
UNASSIGNED: We report 1 of the largest, representative, population-based natural histories of PHPT with different management strategies. A minority of patients underwent PTX, especially in older age. Patients managed surgically had lower incidence of fracture and CKD, and older patients experienced differential benefit.

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An 11-year-old neutered male large crossbreed dog was presented for investigation because of a 10-day history of progressive lethargy, hyporexia, and pyrexia. Physical and dermatological examinations were unremarkable. Blood biochemical analysis identified a marked total and ionized hypercalcemia and increased C-reactive protein concentration. Bicavitary computed tomography screening for causes of the dog\'s clinical and biochemical abnormalities identified a diffuse panniculitis. Histopathological examination of full-thickness skin biopsies was consistent with pyogranulomatous inflammation. Extensive histochemical staining revealed no infectious etiology. Complete clinical and biochemical remissions were observed after starting immunosuppressive, followed by tapering, doses of prednisolone, supporting an immune-mediated etiology. Key clinical message: Sterile, immune-mediated pyogranulomatous inflammation should remain a differential diagnosis for hypercalcemia in dogs. Significant dermatological disease may occur without visible abnormalities.
Panniculite pyogranulomateuse à médiation immunitaire avec hypercalcémie chez un chienUn grand chien croisé mâle castré de 11 ans a été présenté pour examen en raison d’antécédents de léthargie progressive, d’hyporexie et de pyrexie depuis 10 jours. Les examens physiques et dermatologiques étaient sans particularité. L’analyse biochimique du sang présentait une hypercalcémie totale et ionisée marquée et une concentration accrue de protéine C-réactive. Le dépistage par tomodensitométrie bicavitaire des causes des anomalies cliniques et biochimiques du chien a identifié une panniculite diffuse. L’examen histopathologique des biopsies cutanées de pleine épaisseur était compatible avec une inflammation pyogranulomateuse. Un examen par coloration histochimique extensive n’a révélé aucune étiologie infectieuse. Les rémissions cliniques et biochimiques complètes ont été observées après le début du traitement immunosuppresseur, suivies d’une diminution progressive des doses de prednisolone, confirmant une étiologie à médiation immunitaire.Message clinique clé:L’inflammation pyogranulomateuse stérile à médiation immunitaire doit rester un diagnostic différentiel de l’hypercalcémie chez le chien. Une maladie dermatologique importante peut survenir sans anomalies visibles.(Traduit par Dr Serge Messier).

BACKGROUND: Plasma total magnesium concentration (tMg) is a prognostic indicator in cats with chronic kidney disease (CKD), shorter survival time being associated with hypomagnesemia. Whether this risk factor is modifiable with dietary magnesium supplementation remains unexplored.
OBJECTIVE: Evaluate effects of a magnesium-enriched phosphate-restricted diet (PRD) on CKD-mineral bone disorder (CKD-MBD) variables.
METHODS: Sixty euthyroid client-owned cats with azotemic CKD, with 27 and 33 allocated to magnesium-enriched PRD or control PRD, respectively.
METHODS: Prospective double-blind, parallel-group randomized trial. Cats with CKD, stabilized on a PRD, without hypermagnesemia (tMg >2.43 mg/dL) or hypercalcemia (plasma ionized calcium concentration, (iCa) >6 mg/dL), were recruited. Both intention-to-treat and per-protocol (eating ≥50% of study diet) analyses were performed; effects of dietary magnesium supplementation on clinicopathological variables were evaluated using linear mixed effects models.
RESULTS: In the per-protocol analysis, tMg increased in cats consuming a magnesium-enriched PRD (β, 0.25 ± .07 mg/dL/month; P < .001). Five magnesium supplemented cats had tMg >2.92 mg/dL, but none experienced adverse effects. Rate of change in iCa differed between groups (P = .01), with decreasing and increasing trends observed in cats fed magnesium-enriched PRD and control PRD, respectively. Four control cats developed ionized hypercalcemia versus none in the magnesium supplemented group. Log-transformed plasma fibroblast growth factor-23 concentration (FGF23) increased significantly in controls (β, 0.14 ± .05 pg/mL/month; P = .01), but remained stable in the magnesium supplemented group (β, 0.05±.06 pg/mL/month; P =.37).
CONCLUSIONS: Magnesium-enriched PRD is a novel therapeutic strategy for managing feline CKD-MBD in cats, further stabilizing plasma FGF23 and preventing hypercalcemia.

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Secondary hyperparathyroidism (SHPT) often arises from kidney disease and is characterized by elevated parathyroid hormone (PTH) levels. The reported optimal PTH level to balance the compensatory physiologic response in SHPT with the pathologic morbidity and mortality has changed over time with our evolving understanding. Parathyroidectomy for kidney-related hyperparathyroidism requires consideration of the patient\'s dialysis status, potential for kidney transplantation, and medical history. Extent of parathyroidectomy and intraoperative decision-making requires consideration to maximize cure with the risk of permanent hypoparathyroidism. Parathyroidectomy for kidney-related hyperparathyroidism can provide a reduction in morbidity, mortality, and improved kidney allograft function and survival.

Primary hyperparathyroidism (PHPT) is caused by the overproduction of parathyroid hormone by 1 or more parathyroid glands resulting in hypercalcemia and its downstream clinical consequences. The definitive management of PHPT is surgery. Approaches to successful surgery include bilateral exploration or focused parathyroidectomy with intraoperative parathyroid hormone monitoring, which in experienced hands are both associated with a low risk of complications.

Primary hyperparathyroidism (PHPT) is a disorder characterized by the autonomous overproduction of parathyroid hormone (PTH) that leads to hypercalcemia, multiple clinical sequelae, and heterogenous presentation. Whether PHPT is caused by a single benign adenoma (85%), multiglandular disease (15%), or parathyroid carcinoma (1%), surgery is the definitive treatment.