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Kidney Week

Abstract: FR-PO721

Chronic Exercise Ameliorates the Progression of Renal Dysfunction in Polycystic Kidney Disease Model Rats

Session Information

Category: Genetic Diseases of the Kidneys

  • 1001 Genetic Diseases of the Kidneys: Cystic

Authors

  • Qiu, Jiahe, Tohoku University Graduate School of Medicine, Sendai-shi, Miyagi-ken, Japan
  • Sato, Yoichi, Tohoku University Graduate School of Medicine, Sendai-shi, Miyagi-ken, Japan
  • Miura, Takahiro, Tohoku University Graduate School of Medicine, Sendai-shi, Miyagi-ken, Japan
  • Ito, Osamu, Tohoku Medical Pharmacetical University Faculty of Medicine, Sendai, MIYAGI, Japan
Background

Autosomal Dominant Polycystic Kidney Disease (PKD) is the most frequent hereditary renal disease, but the exact mechanisms of cystogenesis remain to be elucidated. PKD leads to renal dysfunction, and it is a major cause of ESRD. Several clinical studies have shown that chronic exercise (Ex) exerts beneficial effects in CKD patients. However, the beneficial effects of Ex on renal function have not been reported in PKD. The present study investigated the effects of Ex in polycystic kidney (PCK) rats with PKD.

Methods

Five-week-old male PCK rats were divided into the sedentary (Sed) group and Ex group. Ex underwent forced treadmill exercise (28m/min, 60 min/day, 5 days/week) for 12 weeks. Plasma and urinary parameters and renal histology were examined. Expression of Ki67, desmin, TGF-β and PGC-1α and phosphorylation of AMPK were assessed by immunohistochemistry and western blotting.

Results

Ex significantly decreased the body weight, kidney weight, urine volume, urinary protein excretion, plasma creatinine and ameliorated renal cystic formation and interstitial fibrosis. Ex significantly decreased the Ki67 and TGF-β expressions in tubulointerstitial cells and the desmin expression in glomeruli. Ex also increased the PGC-1α expression and stimulated the phosphorylation of AMPK in the kidney.

Conclusion

Chronic exercise ameliorates renal dysfunction with inhibition of cystic formation and podocyte injury via an AMPK-PGC-1α-mediated metabolic switch in PCK rats. Ex may be a novel therapeutic approach for the development of renal dysfunction in PKD patients.

Funding

  • Government Support - Non-U.S.