Phosphate Balance and CKD–Mineral Bone Disease
| Autor: | Daniel W. Coyne, Stuart M. Sprague, Kevin J. Martin |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Fibroblast growth factor 23
medicine.medical_specialty chronic kidney disease mineral bone disorder medicine.medical_treatment 030232 urology & nephrology Parathyroid hormone Review 030204 cardiovascular system & hematology Intestinal absorption fibroblast growth factor 23 03 medical and health sciences chemistry.chemical_compound Hyperphosphatemia 0302 clinical medicine Internal medicine medicine Vitamin D and neurology parathyroid hormone hyperphosphatemia Tenapanor phosphate absorption Dialysis business.industry Phosphate medicine.disease Endocrinology chemistry vascular calcification Nephrology business |
| Zdroj: | Kidney International Reports |
| ISSN: | 2468-0249 |
| DOI: | 10.1016/j.ekir.2021.05.012 |
| Popis: | Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common comorbidity in patients with CKD. Characterized by laboratory abnormalities, bone abnormality, and vascular calcification, CKD-MBD encompasses a group of mineral and hormone disturbances that are strongly associated with increased cardiovascular (CV) morbidity and mortality. Abnormal serum phosphate concentrations are an independent risk factor for CV morbidity and mortality, and overall mortality. Phosphate retention plays a central role in initiating and driving many other disturbances in CKD-MBD (e.g., increased parathyroid hormone and fibroblast growth factor 23 concentrations, hypocalcemia, low vitamin D) that are also linked to increased CV risk. Thus, effective phosphate control is a logical therapeutic target for CKD-MBD treatment. Current phosphate management strategies (dietary restrictions, dialysis, phosphate binders) are insufficient to consistently achieve and maintain target phosphate concentrations in patients on dialysis. Phosphate binders reduce available phosphate for intestinal absorption but do not impair the dominant phosphate absorption pathway. Novel therapies that consider new mechanistic understandings of intestinal phosphate absorption are needed. One such therapy is tenapanor, a targeted sodium-hydrogen exchanger isoform 3 inhibitor that has been shown to reduce serum phosphate concentrations in multiple clinical trials. Tenapanor has a novel mechanism of action that reduces intestinal phosphate absorption in the primary paracellular phosphate absorption pathway. |
| Databáze: | OpenAIRE |
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