Experimental basis of shockwave-induced renal trauma in the model of the canine kidney

Abstract

Using the new electromagnetic shockwave source of the Modulith SL 20 shockwave-induced renal trauma was evaluated by acute and chronic studies in the the canine kidney model. In a further study the electromagnetic shockwave source of the Lithostar Plus Overhead module was tested. Overall, 92 kidneys were exposed to shock waves coupled either by water bath (Modulith lab type) or by water cushion (Modulith prototype, Lithostar Overhead) under ultrasound localization. The generator voltage ranged between 11 and 21 kV, the number of impulses between 25 and 2500. After application of 1500/2500 shocks the extent of the renal lesion depended strictly on the applied generator voltage and was classified into 4 grades: Grade 0, no macroscopic trauma detectable (at 11-12 kV); grade 1, petechial medullary bleeding (at 13 kV); grade 2, cortical hematoma (at 14-16 kV); and grade 3, perirenal hematoma (17-20 kV). Whereas at low and medium energy levels the number of shocks played only a minor role, at maximal generator voltage (20 kV) even 25 impulses induced a grade 2 and 600 shocks a grade 3 lesion, emphasizing the importance of shockwave limitation in the upper energy range. In shockwave-induced renal trauma a vascular lesion was predominant and cellular necrosis was secondary. Coupling with a water cushion resulted in a 15%-20% decrease in the disintegrative and traumatic effect, which was compensated for by increasing the generator voltage by 2 kV. Long-term studies showed complete restitution following grade 1 and 2 trauma, whereas after a grade 3 lesion a small segmental and capsular fibrosis without hyperplasia of the juxtaglomerular apparatus was observed. Based on the characteristic ultrasound pattern found in the first study, the threshold for induction of grade 1 lesion was investigated. With both lithotripters a wide range for induction of a grade 1 lesion (Modulith 234-411, Lithostar Plus 220-740) and also a significant overlapping with grade 0 and 2 lesions was seen at low energy settings (levels 2-4). In contrast, the range of shocks (Modulith 96-150, Lithostar Plus 90-142) and overlapping was minimal when high energy was used (levels 7-9). Finally, the disintegration-trauma coefficient combining the results obtained in a standard stone model with those of the canine kidney model was introduced.

Improving the lens design and performance of a contemporary electromagnetic shock wave lithotripter

“…6D) surfaces of the kidneys did not show any gross hematoma, nor was gross injury observed in other tissues (retro peritoneum, pancreas, spleen, and liver) near the kidney along the LSW blast path. These would all be a grade 0 based on a previously described grading scale for SWL injuries (34). From histology of the cortical area within the lithotripter beam focus (Fig.…”

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

“…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]. Some early animal studies [1] showed that SWL did not produce significant renal injury, but those findings were based on low SW dosage (i.e., a maximum of 500 SW were adininistered).…”

“…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.…”

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.…”