title: Phosphate handling by end-stage kidneys and benefits of residual renal function on phosphate removal in patients on haemodialysis.
abstract: OBJECTIVE
  We investigated the handling of phosphate by end-stage kidneys and the contribution of residual renal function (RRF) to phosphate homeostasis in haemodialysis patients.
  
  
  METHODS
  Blood and 24 h urinary specimens were obtained from 79 consecutive chronic haemodialysis patients with a urinary output greater than 100 mL/day. Thirty-five patients with a glomerular filtration rate (GFR) ≥ 3.0 mL/min were included as group A, and 44 patients with GFR < 3.0 mL/min as group B. Additionally, the whole dialysed fluids during a session of haemodialysis were collected from another nine patients. Concentrations of phosphate, creatinine, urea nitrogen, intact parathyroid hormone (iPTH) and fibroblast growth factor 23 (FGF-23) were measured.
  
  
  RESULTS
  Twenty-four hour urinary phosphate excretion (UPE) was 283 ± 115 and 139 ± 57 mg/day (9.1 ± 3.5 and 4.5 ± 1.8 mmol/day) in groups A and B, respectively. Tubular reabsorption of phosphate (TRP) was 39.2 ± 13.3 and 31.7 ± 13.6% in groups A and B, respectively (P = 0.02). UPE significantly correlated with GFR (r = 0.85, P < 0.001) and PTH (r = 0.44, P < 0.001), but not with FGF-23, in the entire patient population. The correlation between UPE and intact PTH levels was absent in group B. Weekly UPE in group A was significantly greater (P < 0.001), while that in group B was similar to the amount of phosphate removed by a haemodialysis session.
  
  
  CONCLUSIONS
  Urinary phosphate excretion by end-stage kidneys depends more on GFR than diminishing TRP. The action of PTH on the kidneys remains until GFR decreases to as low as 3 mL/min. Residual renal function plays a significant role in phosphate elimination, and it is possible that FGF-23 no longer acts effectively to excrete phosphate in the urine in these patients.
authors: Department of Nephrology, Tokyo Medical University, Tokyo, Japan.
authors: Hideaki
authors: H
authors: Iwasawa
authors: Toshiyuki
authors: T
authors: Nakao
authors: Hiroshi
authors: H
authors: Matsumoto
authors: Tomonari
authors: T
authors: Okada
authors: Yume
authors: Y
authors: Nagaoka
authors: Toshikazu
authors: T
authors: Wada
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood; D005919:Glomerular Filtration Rate; D006706:Homeostasis; D006801:Humans; D007668:Kidney / Q000378:metabolism* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology / Q000628:therapy* / Q000652:urine; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates / Q000097:blood / Q000378:metabolism* / Q000652:urine; D006435:Renal Dialysis; D012189:Retrospective Studies; D013997:Time Factors
chemical_list: D015415:Biomarkers; C000717427:FGF23 protein, human; C470125:PTH protein, human; D010281:Parathyroid Hormone; D010710:Phosphates; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; D003404:Creatinine