Urinary concentration defect and renal glycosuria in cyclosporine-treated ratsopen access
- Authors
- Lee, Jun Han; Kim, Su A; Jo, Chor Ho; Lee, Chang Hwa; Kim, Gheun-Ho
- Issue Date
- Jun-2020
- Publisher
- Korean Society of Electrolyte and Blood Pressure Research
- Keywords
- Aquaporin-2; Cyclosporine; GLUT2; Osmotic diuresis; Water diuresis
- Citation
- Electrolyte and Blood Pressure, v.18, no.1, pp.1 - 9
- Indexed
- SCOPUS
KCI
- Journal Title
- Electrolyte and Blood Pressure
- Volume
- 18
- Number
- 1
- Start Page
- 1
- End Page
- 9
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/9723
- DOI
- 10.5049/EBP.2020.18.1.1
- ISSN
- 1738-5997
- Abstract
- Background: Urinary concentration impairment is a major feature of cyclosporine nephrotoxicity.
Methods: We explored two possible mechanisms that may underlie cyclosporine-induced polyuria; water, and/or osmotic diuresis. Cyclosporine was subcutaneously injected to normal salt-fed Sprague-Dawley rats at a daily dose of 25 mg/kg for 2 weeks (Experiment I) and 7.5 mg/kg for 6 weeks (Experiment II).
Results: In Experiment I, cyclosporine treatment caused an increase in urine volume (2.7±0.5 vs. 10.3±1.13 mL/d/100 g BW, p<0.001) and a decrease in urine osmolality (2,831±554 vs. 1,379±478 mOsm/kg H2O, p<0.05). Aquaporin-2 (AQP2) protein expression decreased in cyclosporine-treated rat kidneys (cortex, 78±8%, p<0.05; medulla, 80±1%, p<0.05). Experiment II also showed that urine volume was increased by cyclosporine treatment (4.97±0.66 vs. 9.65±1.76 mL/d/100 g BW, p<0.05). Whereas urine osmolality was not affected, urinary excretion of osmoles was increased (7.5±0.4 vs. 14.9±1.4 mosmoles/d/100 g BW, p<0.005). Notably, urinary excretion of glucose increased in cyclosporine-treated rats (7±1 vs. 10,932±2,462 mg/d/100 g BW, p<0.005) without a significant elevation in plasma glucose. In both Experiment I and II, GLUT2 protein expression in the renal cortex was decreased by cyclosporine treatment (Experiment I, 55±6%, p<0.005; Experiment II, 88 ±3%, p<0.05).
Conclusion: Both water diuresis and osmotic diuresis are induced by cyclosporine nephrotoxicity. AQP2 and GLUT2 downregulation may underlie water and osmotic diuresis, respectively.
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