title: Renal phosphate loss in long-term kidney transplantation.
abstract: OBJECTIVE
  Renal phosphate wasting occurs early postkidney transplantation as a result of an accumulation of parathyroid hormone and fibroblast growth factor 23 from the CKD period. Serum phosphate, parathyroid hormone, and fibroblast growth factor 23 return to baseline 1 year postkidney transplantation. What happens beyond this period is unknown.
  
  
  METHODS
  Mineral parameters were obtained from 229 kidney transplant recipients at least 1 year posttransplantation; 46 normal subjects and 202 CKD patients with similar GFR served as controls. Factors associated with phosphate metabolism were analyzed.
  
  
  RESULTS
  Despite the reduced graft function, most kidney transplant recipients had lower serum phosphate than normal subjects accompanied by renal phosphate loss. Fibroblast growth factor 23 was mostly lower or comparable with normal subjects, whereas parathyroid hormone was elevated in most patients. Hyperparathyroidism is also more common among kidney transplant recipients compared with CKD patients. Both parathyroid hormone and fibroblast growth factor 23 showed relationships with renal phosphate excretion, but only parathyroid hormone displayed an independent association. Parathyroid hormone showed the highest area under the curve in predicting renal phosphate leak. When patients were categorized according to parathyroid hormone and fibroblast growth factor 23 levels, only subset of patients with high parathyroid hormone had an increased renal phosphate excretion.
  
  
  CONCLUSIONS
  Relatively low serum phosphate from renal phosphate leak continued to present in long-term kidney transplantation. Both parathyroid hormone and fibroblast growth factor 23 participated in renal tubular phosphate handling, but persistent hyperparathyroidism seemed to have a greater influence in this setting.
authors: Division of Nephrology, Department of Medicine, Ramathibodi Hospital, Mahidol University, Phayathai, Bangkok, 10400 Thailand.
authors: Supinda
authors: S
authors: Sirilak
authors: Kamonwan
authors: K
authors: Chatsrisak
authors: Atiporn
authors: A
authors: Ingsathit
authors: Surasak
authors: S
authors: Kantachuvesiri
authors: Vasant
authors: V
authors: Sumethkul
authors: Wasana
authors: W
authors: Stitchantrakul
authors: Piyanuch
authors: P
authors: Radinahamed
authors: Sinee
authors: S
authors: Disthabanchong
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood; D005919:Glomerular Filtration Rate; D006801:Humans; D006961:Hyperparathyroidism / Q000209:etiology / Q000378:metabolism; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007668:Kidney / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery*; D016030:Kidney Transplantation / Q000009:adverse effects*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates / Q000097:blood / Q000378:metabolism*; D013785:Thailand; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D007166:Immunosuppressive Agents; C470125:PTH protein, human; D010281:Parathyroid Hormone; D010710:Phosphates; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23