Changes in the sodium and potassium transporters in the course of chronic renal failure

Se Joong Kim, Nam Ju Heo, Ji Yong Jung, Min Jeong Son, Hye Ryoun Jang, Jay Wook Lee, Yun Kyu Oh, Ki Young Na, Kwon-Wook Joo, Jin Suk Han

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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-α 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. Conclusion: 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.

Original languageEnglish
Pages (from-to)p31-p41
JournalNephron - Physiology
Issue number4
StatePublished - 1 Jul 2010


  • Chronic renal failure
  • Membrane transport proteins
  • Potassium
  • Sodium

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