Histopathologic effects of extracorporeal shock wave lithotripsy on rabbit kidney

Abstract

Despite the widespread clinical use of the lithotriptor, the margin of safety for the kidney during shock wave application is substantially unknown. Although a series of pilot studies have been performed in laboratory animals, long-term follow-up is mandatory to establish the effect of extracorporeal shock wave lithotripsy (ESWL) and subsequent dose-dependent changes on the kidneys. An experimental study was performed in 45 rabbits; to define and compare the early and late complications of ESWL in the kidneys. The rabbits were divided into three groups of 15 animals each that received 1000, 1500 or 3000 shock waves respectively at 15-20 kV. The rabbits in each group were killed and necropsy performed within 24 h for the first 5 animals, 1 week for the second 5 animals and 2 months post-ESWL for the last 5 animals. Dose-dependent moderate damage (subcapsular hemorrhage, interstitial hemorrhage, capsular tension and perirenal hemorrhage) were noted in all kidneys at 24 h after treatment. Evidence of permanent changes (some fibrosis, tubular and glomerular damage, chronic inflammatory alterations) was noted in long-term follow up. Complete necrosis of the treated kidney was not encountered in this study.

Renal Trauma and the Risk of Long-Term Complications in Shock Wave Lithotripsy

“…The vast majority of studies show that SW cause renal damage, but there is a broad spectrum to the severity of injury described in this literature. Earlier studies in dogs showed minimal-or-no injury [9], while more recent work with dogs [10, 11, 12, 13, 14, 15, 16], rats [17, 18], pigs [19, 20, 21, 22, 23], and rabbits [24, 25] demonstrated substantial morphologic and functional alterations following SWL. These apparent contradictions resolve when one recognizes that the kidney is sensitive to the dose of SW insult (i.e., number of SWs, SW voltage, rate of SW administration) [11, 14, 16, 26] and that the magnitude of SW injury is dependent on the size of the kidney [27].…”

“…In the pig we see neutrophils, macrophages, and platelets lining injured vessels and within the perivascular and peritubular interstitium as early as 30 min following a clinical dose of SW. The literature suggests that inflammation is a consistent feature of SWL injury when the kidney is treated with a clinical dose of SW [2, 10, 11, 13, 24, 25, 32, 33, 34], but may be absent or minimal in extent at lower, subclinical SW doses [9]. Since inflammation is intimately involved in directing tissue repair toward fibrogenesis and scar formation [35] this may explain why some animal studies of SWL-induced injury have shown limited or no scar formation.…”

“…Several animal studies have examined the site of SW treatment 1–2 weeks to 3–6 months after SWL to determine the outcome of the reparative process and have found striking evidence of chronic damage including diffuse interstitial fibrosis, and focal areas of calcification, nephron loss, dilated veins, hyalinized to acellular scars running from the cortex to the medulla, perivascular fibrosis, focal glomerulonephritis to chronic tubulointerstitial disease [2, 10, 11, 13, 24, 25, 32, 33, 34]. In addition, Banner et al [23] have described progressive deposition of complement 3 and traces of immunoglobulin G in glomeruli of SWL-treated pig kidneys.…”

Effects of Previous Unsuccessful Extracorporeal Shockwave Lithotripsy Treatment on the Performance and Outcome of Percutaneous Nephrolithotomy

“…The appearance of detrimental effects after intense ESWL applications has been confirmed in many studies. [26,27] Stoller et al [28] retrospectively reviewed their cases and showed that previous ESWL history had no effect on bleeding in subsequent PCNLs.…”

Morphological changes induced in the pig kidney by extracorporeal shock wave lithotripsy: Nephron injury

“…The traumatic lesions caused by SWL have been studied in human kidneys (Kaude et al, 1985;Brewer et al, 1988;Rigatti et al, 1989;Umekawa et al, 1992;Lechevallier et al, 1993;Roessler et al, 1993) and in animal models, such as the dog (Newman et al, 1987;Abrahams et al, 1988;Delius et al, 1988;Jaeger et al, 1988;Karlsen et al, 1991;Rassweiler et al, 1993;Koga et al, 1996), rat (Neuerburg et al, 1989;Recker et al, 1989;Weber et al, 1992), rabbit (Fajardo et al, 1990;Kaji et al, 1991;Karalezli et al, 1993), and pig (Banner et al, 1991;El-Damanhoury et al, 1991;Evan et al, 1998;Connors et al, 2000). The majority of these studies documented extensive damage to blood vessels in the path of the shock waves, and suggested that the primary injury occurs in vascular tissue.…”