title: Changes in the sodium and potassium transporters in the course of chronic renal failure.
abstract: BACKGROUND
  In chronic renal failure (CRF), residual nephrons can increase their excretion of sodium (Na) and potassium (K). However, the mechanisms of renal Na and K regulation in late-stage CRF have not been clearly investigated.
  
  
  METHODS
  We examined altered expression of major renal Na and K transporters in Sprague-Dawley rats at 4 and 12 weeks after a 5/6 nephrectomy.
  
  
  RESULTS
  CRF rats were azotemic and had gradually increased levels of urinary Na and K excretion over time. At 4 weeks, the abundance of Na-K-2Cl cotransporter (NKCC2), and Na-Cl cotransporter (NCC) in CRF rats increased significantly (477 and 222% of the control, respectively). In contrast, expression of NKCC2 and NCC decreased markedly at 12 weeks (55.4 and 30.8%, respectively). Expression of epithelial Na channel-alpha increased throughout the whole period. The abundance of renal outer medullary K-channel (ROMK) and Na-K-ATPase did not decrease at 4 weeks, but it was reduced at 12 weeks.
  
  
  CONCLUSIONS
  We suggest that increased urinary Na excretion in late-stage CRF may be associated with decreased expression of renal Na transporters except ENaC compared to early-stage CRF, and that increased urinary K excretion in the late stage of CRF may not be related to expression of ROMK.
authors.affiliation: Department of Internal Medicine, Gachon University of Medicine and Science, Incheon, Korea.
authors.forename: Sejoong
authors.initials: S
authors.lastname: Kim
authors.forename: Nam Ju
authors.initials: NJ
authors.lastname: Heo
authors.forename: Ji Yong
authors.initials: JY
authors.lastname: Jung
authors.forename: Min-Jeong
authors.initials: MJ
authors.lastname: Son
authors.forename: Hye Ryoun
authors.initials: HR
authors.lastname: Jang
authors.forename: Jay Wook
authors.initials: JW
authors.lastname: Lee
authors.forename: Yun Kyu
authors.initials: YK
authors.lastname: Oh
authors.forename: Ki Young
authors.initials: KY
authors.lastname: Na
authors.forename: Kwon Wook
authors.initials: KW
authors.lastname: Joo
authors.forename: Jin Suk
authors.initials: JS
authors.lastname: Han
mesh_terms: D000818:Animals; D053503:Epithelial Sodium Channels / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D049992:Sodium Chloride Symporters / Q000378:metabolism*; D028021:Sodium-Potassium-Chloride Symporters / Q000378:metabolism*; D064466:Solute Carrier Family 12, Member 1; D014018:Tissue Distribution
chemical_list: D053503:Epithelial Sodium Channels; C510692:Kcnj1 protein, rat; D024661:Potassium Channels, Inwardly Rectifying; C578716:Slc12a1 protein, rat; D049992:Sodium Chloride Symporters; D028021:Sodium-Potassium-Chloride Symporters; D064466:Solute Carrier Family 12, Member 1