View clinical trials related to Hyperparathyroidism, Secondary.
Filter by:Patients with end-stage kidney disease (ESKD) have an increased risk of cardiovascular mortality. High parathyroid hormone (PTH) from secondary hyperparathyroidism leads to increased efflux of phosphate and calcium from bone, which exacerbates vascular calcification and increases the risk of bone fractures. The main driving factor for secondary hyperparathyroidism is hypocalcaemia caused by low levels of 1,25-dihydroxy vitamin D and pharmacological supplementation with activated vitamin D and oral calcium-containing phosphate-binders are used to control secondary hyperparathyroidism. The amount of calcium used in this context is controversial, as higher calcium load in blood may theoretically increase vascular calcification. Conversely, by alleviating the efflux of phosphate and calcium from bone due to secondary hyperparathyroidism, increasing the load of calcium might actually prevent vascular calcification. To study this further, we wish to conduct a randomised double-blinded controlled clinical trial of increasing dialysate Ca from 1.25 mmol/L (standard dialysate concentration) to 1.50 mmol/L in patients with ESKD and secondary hyperparathyroidism on maintenance haemodialysis (HD). The overall effect of increased dialysate calcium will be gauged by its effect on serum calcification propensity (T50) and on markers of bone turnover.
The purpose of this study is to characterize the quality of life change in patients undergoing parathyroidectomy with secondary hyperparathyroidism due to end-stage renal failure.
The study is being conducted to evaluate the efficacy, and safety of Paricalcitol for secondary hyperparathyroidism with stage 3 and stage 4 chronic kidney disease in adults.
Through multi-center randomized controlled trial studies on preemptive surgical intervention in patients with chronic kidney disease (CKD) - secondary hyperparathyroidism (SHPT), to precisely evaluate the safety and effectiveness during perioperative period, and the long-term outcomes by 1-year follow-up. The follow-ups include the evaluation of the overall quality of life, calcium and phosphorus metabolism, hyperparathyroidism level, vitamin D metabolism, bone mineral density, soft tissue and vascular calcification.
Currently, the indications used for MA (Marketing Authorization) Cinacalcet in France are hyperparathyroidism (hyperPTH) in adults, whether primary (for patients in whom parathyroidectomy is theoretically indicated but in whom it is contraindicated or not is not clinically appropriate) or secondary to a chronic kidney disease, and parathyroid carcinomas. In pediatric patients, data on its use are restricted due to its recent marketing authorization (2017) and limited to dialysis patients suffering from secondary hyperPTH. Nevertheless, some patients with phosphocalcic pathologies without renal insufficiency must be treated off-label by cinacalcet in the presence of severe hyperPTH, without any other chronic treatment available to date. The objective of this study is therefore to evaluate the use in France of cinacalcet in phosphocalcic pathologies without renal insufficiency, in order to obtain efficacy and safety data in order to improve our knowledge on the management of these orphan diseases.
The purpose of this study is to compare short-term and long-term efficacy of total parathyroidectomy with autotransplantation and total parathyroidectomy without autotransplantation for Secondary hyperparathyroidism.
This is a single arm, open-labelled study to determine the effectiveness of combination Cinacalcet with Vitamin D analogue in the treatment of severe hyperparathyroidism in patients with ESRF on haemodialysis. Patients will be started on PO Cinacalcet 25mg OD + PO/IV active Vitamin D analogues adjusted by increments/decrements in steps of 1 mcg 3x per week every 1-4 weeks until the corrected calcium level is within 2.4-2.54 mmol/L. After iPTH has reached 2-9x ULN, patient enters maintenance phase. If serum calcium falls below 2.1mmol/L, active Vit D dose will be increased and if it is above 2.54 mmol/L, the dose will be decreased. Percentage reduction of iPTH levels from baseline at 6,12 and 24 months treatment and Percentage of patients achieving iPTH levels within the target range of 2-9x upper limit normal at 6, 12 and 24 months will be determined