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Li X et al, 2014: Shock Wave Induces Biological Renal Damage by Activating Excessive Inflammatory Responses in Rat Model

Li X, Long Q, Cheng X, He D
Department of Urology, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi Province, 710061, China


Abstract

The study was aimed to investigate the potential mechanism of inflammatory renal damage induced by shock wave. A total of 48 rats, with the right kidney cut, are randomly assigned into control group, ESWL group and ESWL + PDTC group. Rats were treated with shock wave at the left kidney. At post-shock wave 3 and 105 days, all the animals were sacrificed for detecting the expression of tumor necrosis factor (TNF)-α, intercellular adhesion molecule (ICAM)-1, and monocyte chemoattractant protein (MCP)-1. The inflammatory responses were evaluated by detecting the level of myeloperoxidase (MPO) and ED-1. The histological renal injury was also examined. Before the animals were sacrificed, the urine samples were collected for measuring the values of malondialdehyde (MDA), β2-microglobulin, interleukin (IL)-6, and IL-18. At post-shock wave 3 days, the higher expression of ICAM-1 and TNF-α were observed in shock wave-treated kidneys. The level of urine TNF-α, IL-6, and IL-18 were also increased significantly. Using PDTC obviously decreased the expression of ICAM-1 and TNF-α. It also effectively inhibited the degree of oxidative stress and neutrophil infiltration. At post-shock wave 105 days, the expression of MCP-1 and the level of urine β2-microglobulin and IL-18 were increased significantly. The histological analysis also indicated more ED-1-positive cells and serious fibrosis in shock wave-treated kidneys. PDTC significantly suppressed MCP-1 and IL-18 expression, decreased monocyte infiltration, and alleviate the degree of interstitium fibrosis. Shock wave triggered excessive inflammatory responses and aggravated renal biological damage. Several inflammatory factors including ICAM-1, MCP-1, and TNF-α were considered to play important role in this type of renal damage.

Inflammation. 2014 Mar 4. [Epub ahead of print]
PMID:24590377[PubMed - as supplied by publisher]

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Comments 1

Peter Alken on Wednesday, 05 February 2014 14:05

This is an extensive study on the shock wave effects on rat kidneys. Reading manuscripts on the experimentally induced SWL renal trauma I think about the discrepancy between these findings and the clinical experience of more than 30 years. The debate on the SWL induced hypertension and diabetes that was initiated by Krambeck et al (Krambeck AE et al. Diabetes Mellitus and Hypertension Associated With Shock Wave Lithotripsy of Renal and Proximal Ureteral Stones at 19 Years of Followup, J.Urol 175, 1742-1747, 2006) has been finished without a proof for these effects in the general patient population. I doubt that the present manuscript is leading us to a better understanding of what we are doing clinically.

See also the article by Alp BF et al. Inhibition of inducible nitric oxide synthase prevents shock wave therapy induced renal injury. Ren Fail. 2014 Feb 10. in the I 2014 reviews.

Peter Alken

This is an extensive study on the shock wave effects on rat kidneys. Reading manuscripts on the experimentally induced SWL renal trauma I think about the discrepancy between these findings and the clinical experience of more than 30 years. The debate on the SWL induced hypertension and diabetes that was initiated by Krambeck et al (Krambeck AE et al. Diabetes Mellitus and Hypertension Associated With Shock Wave Lithotripsy of Renal and Proximal Ureteral Stones at 19 Years of Followup, J.Urol 175, 1742-1747, 2006) has been finished without a proof for these effects in the general patient population. I doubt that the present manuscript is leading us to a better understanding of what we are doing clinically. See also the article by Alp BF et al. Inhibition of inducible nitric oxide synthase prevents shock wave therapy induced renal injury. Ren Fail. 2014 Feb 10. in the I 2014 reviews. Peter Alken
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