title: Correction of hyperphosphatemia suppresses cardiac remodeling in uremic rats.
abstract: BACKGROUND
  Hyperphosphatemia is associated with cardiovascular disease in patients with chronic kidney disease. To examine the effects of correction of hyperphosphatemia, we investigated the association between phosphate metabolism and cardiac remodeling in uremic rats.
  
  
  METHODS
  Four groups were studied for 8 weeks: (1) control (sham), (2) 5/6 nephrectomized (Nx) rats fed a normal phosphate regular diet (Nx + NP), (3) Nx rats fed a high phosphate (1.2 %) diet (Nx + HP), and (4) Nx rats fed a high phosphate diet containing 2 % lanthanum carbonate (Nx + HP + La). The relationship between phosphate metabolism and cardiac remodeling was analyzed.
  
  
  RESULTS
  Nx + HP rats showed a significant increase in serum phosphate and PTH compared with Nx + NP rats, while Nx + HP + La rats showed slight decreases in these levels. Both Nx + HP and Nx + HP + La rats showed a significant increase in fibroblast growth factor-23 (FGF23) compared with Nx + NP rats. Urinary phosphate excretion showed a similar trend to that of FGF23. Nx + HP rats showed a significant increase in LV weight and matrix deposition compared with Nx + NP rats, and this increase was also significantly suppressed in Nx + HP + La rats. Serum phosphate levels and PTH were significantly correlated with LV weight and matrix deposition, but FGF23 levels did not show the correlation. FGF23 had a high correlation with urinary phosphate excretion.
  
  
  CONCLUSIONS
  These results suggest that correction of hyperphosphatemia by lanthanum carbonate could suppress cardiac remodeling independently of changes in FGF23.
authors.affiliation: Division of Nephrology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
authors.forename: Ai
authors.initials: A
authors.lastname: Yamazaki-Nakazawa
authors.forename: Masahide
authors.initials: M
authors.lastname: Mizobuchi
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Ogata
authors.forename: Chiaki
authors.initials: C
authors.lastname: Kumata
authors.forename: Fumiko
authors.initials: F
authors.lastname: Kondo
authors.forename: Naoko
authors.initials: N
authors.lastname: Ono
authors.forename: Fumihiko
authors.initials: F
authors.lastname: Koiwa
authors.forename: Susumu
authors.initials: S
authors.lastname: Uda
authors.forename: Eriko
authors.initials: E
authors.lastname: Kinugasa
authors.forename: Tadao
authors.initials: T
authors.lastname: Akizawa
mesh_terms: D000818:Animals; D002614:Chelating Agents / Q000494:pharmacology*; D004032:Diet; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000378:metabolism; D005346:Fibroblast Growth Factors / Q000097:blood; D006352:Heart Ventricles / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D054559:Hyperphosphatemia / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D007811:Lanthanum / Q000494:pharmacology*; D008297:Male; D009392:Nephrectomy; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates; D017207:Rats, Sprague-Dawley; D014511:Uremia / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D016277:Ventricular Function, Left / Q000187:drug effects*; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D002614:Chelating Agents; C505605:Fgf23 protein, rat; D010281:Parathyroid Hormone; D010710:Phosphates; C119467:lanthanum carbonate; D005346:Fibroblast Growth Factors; D007811:Lanthanum