Microdialysis assessment of shock wave lithotripsy-induced renal injury.

Published

Journal Article

OBJECTIVES: Shock wave lithotripsy (SWL) is the primary treatment modality for managing the majority of symptomatic renal calculi. However, the fundamental mechanisms for stone fragmentation and the resultant morphologic changes that occur are not fully understood. Furthermore, a thorough understanding of the complex biologic pathways involved in SWL-induced renal injury does not exist at present. To elucidate the biologic processes involved in tissue injury after SWL, an animal model was designed to mimic the pathogenesis of high-energy SWL in humans. METHODS: Juvenile female swine were anesthetized, and a midline laparotomy incision was performed to expose the right kidney. Using an introducer apparatus, a microdialysis probe was placed into the renal parenchyma of the right kidney lower pole and a tunnel was generated to exit the distal ends of the inlet and outlet tubing outside the body. After a 72-hour postoperative recovery period, SWL was performed to the lower pole renal region of the kidney, as a microdialysis pump continuously infused dialysate through the inlet tubing. Microdialysis fluids were collected during SWL, and lipid peroxidation, as measured by conjugated diene concentrations, was monitored. RESULTS: All microdialysis probes remained patent for a total of 2000 shock waves. A significant elevation in conjugated diene levels was observed in the SWL versus untreated kidneys after 1000 shock waves were administered (P <0.02). CONCLUSIONS: This animal model is unique in that it represents the first system for the real-time collection of renal interstitial fluids during SWL. Analysis of this fluid may provide insight into the physiologic mechanisms responsible for shock wave-induced renal injury.

Full Text

Duke Authors

Cited Authors

  • Brown, SA; Munver, R; Delvecchio, FC; Kuo, RL; Zhong, P; Preminger, GM

Published Date

  • September 2000

Published In

Volume / Issue

  • 56 / 3

Start / End Page

  • 364 - 368

PubMed ID

  • 10962295

Pubmed Central ID

  • 10962295

Electronic International Standard Serial Number (EISSN)

  • 1527-9995

International Standard Serial Number (ISSN)

  • 0090-4295

Digital Object Identifier (DOI)

  • 10.1016/s0090-4295(00)00694-4

Language

  • eng