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Abstract: PO2427

Evaluation of Changes in Renal Microperfusion in Hyperuricemic-Induced Kidney Injury by Contrast-Enhanced Ultrasound Imaging

Session Information

Category: CKD (Non-Dialysis)

  • 2102 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • Fan, Ying, Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, China
  • He, Li, Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, China
  • Li, Ze, Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, China
  • Zhou, Ting, Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, China
  • Jia, Junjie, Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, China
  • Wang, Niansong, Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, China
Background

The diagnostic tools for early detection of renal injury caused by hyperuricemia are particularly lacking. Our study investigated the application of contrast-enhanced ultrasound (CEUS) in both hyperuricemic nephropathy (HN) rats and patients with hyperuricemia induced kidney injury.

Methods

Animal study was performed in hyperuricemic rat induced by feeding with a mixture of adenine and potassium oxonate for 4 weeks. In addition, 10 healthy volunteers and 40 patients with hyperuricemia induced kidney injury from CKD 1 to 4 stage were enrolled. CEUS was performed and low acoustic power contrast-specific imaging was used for quantitative analysis. Time-intensity curves (TICs) and quantitative indexes were created by Qlab software.

Results

In HN rat model monitored by CEUS technique, a significant decline in renal cortical perfusion as reflected by lower Peak Intensity (PI) value (25.43±1.31 vs. 37.9±1.75db) and longer time to reach peak (TTP) intensity (34.5±5.9 vs. 8.58±1.6s) was found when compared to control rats one week after administration of adenine and potassium oxonate, with more pronounced decline in HN rats at 4 weeks. Quantitative assessment of PI was well corelated with the serum Kim-1 level as well as the fibrosis scores in hyperuricemic rats from mild to advanced disease stage. Clinically, an early decline of PI in renal cortical perfusion was found in CKD stage 1 patients with hyperuricemia induced kidney injury as compared to the control group (61.1±4.52 vs. 65.80±7.10 db), which became progressively less visible in patients with more severe kidney injury in these patients of CKD 4 stage (40.93±13.36 db). An early increase of TTP could also be detected in HN patients with CKD 1 stage as compared to normal control (15.14±1.75 vs. 14.52±4.75s), which became the most pronounced in these patients of CKD 4 stage (67.32±3.29s). In addition, Peak value measured by CEUS was correlated with renal function in patients with hyperuricemia induced kidney injury.

Conclusion

CEUS is able to detect the renal perfusion in a dynamic way. Renal perfusion measured by CEUS correlates with the renal functional impairment and tubulointerstitial fibrosis, suggesting a sensitive, reliable and non-invasive method that could be applied in the diagnosis of hyperuricemia induced kidney injury in clinical practice.

Funding

  • Government Support – Non-U.S.