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Early Detection of Drug-Induced Renal Hemodynamic Dysfunction Using Sonographic Technology in Rats
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Early Detection of Drug-Induced Renal Hemodynamic Dysfunction Using Sonographic Technology in Rats

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Expression of salt and urea transporters in rat kidney during cisplatin-induced polyuria

C A Ecelbarger1, J M Sands, J J Doran

  • 1Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University, Washington D.C., USA.

Kidney International
|December 12, 2001
PubMed
Abstract

Insights

Cisplatin causes polyuria by altering kidney salt and urea transporters. While protein levels remained unchanged, qualitative modifications in urea transporter proteins may explain the reduced kidney function.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Renal Physiology

Background:

  • Cisplatin-induced polyuria in rats is linked to reduced medullary hypertonicity.
  • This reduction is associated with impaired function of thick ascending limb salt transporters and collecting duct urea transporters.

Purpose of the Study:

  • To investigate the molecular mechanisms behind cisplatin-induced polyuria.
  • To determine the protein abundance of key salt and urea transporter isoforms in rat kidneys.

Main Methods:

  • Male Sprague-Dawley rats received either cisplatin (CP) or saline injection.
  • Kidneys, urine, and blood were collected and analyzed five days post-injection.
  • Western blot analysis was used to assess protein abundance of specific transporters.

Main Results:

  • Cisplatin-treated rats exhibited polyuric acute renal failure, indicated by increased BUN and urine volume, and decreased urine osmolality.
  • A significant reduction in the bumetanide-sensitive Na-K-2Cl cotransporter protein was observed in the kidney cortex, but not the outer medulla.
  • No significant changes in protein abundance were found for ROMK, NHE3, Na,K-ATPase, or urea transporter isoforms (UT-A1, UT-A2, UT-A4).
  • Qualitative differences in UT-A2 and UT-A4 protein patterns were noted in the outer medulla of cisplatin-treated rats.

Conclusions:

  • Reduced medullary hypertonicity in cisplatin-induced polyuria is unlikely due to changes in the abundance of medullary salt or urea transporters.
  • Qualitative modifications in urea transporter proteins may play a role in the observed functional impairment.

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