Document Type : Original Article
Authors
1
internal medicine, faculty of mrdicine, Minia University
2
Endocrinology and Diabetes unit, Internal medicine department, Faculty of medicine, Minia university
3
Internal Medicine , Faculty of Medicine, Minia University
4
Department of Internal Medicine, Faculty of Medicine, Minia University, Minia, Egypt
Abstract
Background:Chronic kidney disease (CKD) is further compounded by the presence of either one or a combination of biochemical abnormalities, such as inappropriate calcium,phosphate,parathyroid hormone,or vitamin D metabolism.Additionally,CKD is associated with bone abnormalities,including abnormal bone turnover,mineralization,volume, linear growth,or strength.Furthermore,CKD can lead to the development of vascular or other soft tissue calcification. In recent times, there has been an increased understanding of the underlying pathophysiology, which has shown a more intricate nature. It has been discovered that fibroblast growth factor 23 (FGF23),a-Klotho,and the Wnt-b-catenin signaling pathway also have significant involvement in this process.Aim of work:to assess PTH in different treatment strategies for secondary hyperparathyroidism in haemodialysis patients
Patients and Methods:We selected our patients from renal dialysis unit at El-Minya and Aswan university hospital.We divided them into 4 groups: Group 1:20 patients undergo parathyroidectomy.Group 2:10 patients who receive calcimimetics. Group 3:10 patients who receive phosphate binders(sevelamer).Group 4:10 patients who receive vit D analogues (Alfacalcidol).
Results: there was significant decrease in serum parathormone level in group I in comparison with other groups in all serial measurements as intial level of parathormone was 1755.0 pg/ml,1225.0 pg/ml,820.0 pg/ml,813.5 pg/ml in goup I,II,III and IV respectively.Also there was significant decrease in serum parathormone in all groups in serial measurements.Conclusion:There has been a substantial expansion in the range of treatment options for managing renal hyperparathyroidism,and in most cases,these drugs can effectively regulate PTH levels.Nevertheless,there is currently insufficient evidence to support the notion that these interventions have substantial positive effects on critical clinical outcomes,such as fracture prevention,cardiovascular events,or survival.
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