Localization of renal oxidative stress and inflammatory response after lithotripsy

• Published in: BJU international 2009-06, Vol.103 (11), p.1562-1568
• Main Authors: Clark, Daniel L., Connors, Bret A., Evan, Andrew P., Willis, Lynn R., Handa, Rajash K., Gao, Sujuan
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Enzyme-Linked Immunosorbent Assay; Female; Heme Oxygenase (Decyclizing) - metabolism; heme‐oxygenase; inflammation; Interleukin-6 - metabolism; Ischemia - pathology; kidney; Kidney - blood supply; Kidney - injuries; Kidney - pathology; Kidney Calculi - therapy; Lithotripsy - adverse effects; Medical sciences; Nephrology. Urinary tract diseases; oxidative stress; Oxidative Stress - physiology; shock wave lithotripsy; Swine
• ISSN: 1464-4096; 1464-410X
• DOI: 10.1111/j.1464-410X.2008.08260.x

OBJECTIVE To determine if the acute renal oxidative stress and inflammation after extracorporeal shock wave lithotripsy (ESWL), thought to be mediated by ischaemia, is most severe in the portion of the kidney within the focal zone of the lithotripter, and if these effects result primarily from ischaemic injury. MATERIALS AND METHODS Pigs (7–8‐weeks old) received either 2000 shock waves at 24 kV to the lower‐pole calyx of one kidney or unilateral renal ischaemia for 1 h. A third group (sham) received no treatment. Timed urine and blood samples were taken for analysis of lipid peroxidation and the inflammatory cytokines, tumour necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6). At 4 h after treatment, kidneys were removed and samples of cortex and medulla were frozen for analysis of cytokines and heme oxygenase‐1 (HO‐1). RESULTS ESWL did not affect urinary excretion of malondialdehyde, but did elicit an eight‐fold induction of HO‐1 in the portion of the renal medulla within the focal zone of the lithotripter (F2), while remaining unchanged elsewhere in the treated kidney. There was no induction of HO‐1 in renal tissue after ischaemia‐reperfusion. Urinary excretion of TNF‐α increased from the lithotripsy‐treated kidney by 1 h after treatment, but was unaffected by ischaemia‐reperfusion. As with the HO‐1 response after lithotripsy, IL‐6 increased only in the renal medulla at F2. By contrast, ischaemia‐reperfusion increased IL‐6 in all samples from the treated kidney. CONCLUSION These findings show that the acute oxidative stress and inflammatory responses to ESWL are localized to the renal medulla at F2. Furthermore, the differing patterns of markers of injury for ESWL and ischaemia‐reperfusion suggest that ischaemia is not the principal cause of the injury response after ESWL.