Andrew P. Evan - evan@anatomy.iupui.edu
Indiana University School of Medicine
Indianapolis, IN
Popular version of paper 3aPAa2
Presented Wednesday morning, 15 May 1996
Acoustical Society of America, Indianapolis, Indiana
Embargoed until 15 May 1996
Over the past 11 years, shock wave lithotripsy (SWL) has changed the way Urologists have managed urinary tract calculi. Owing to its wide applicability, noninvasive nature, low morbidity, and cost effectiveness, SWL has become popular among treating physicians and has received unprecedented patient endorsement. However, the popularity of SWL is also based on the false perception that the technology is entirely safe and free of adverse long-term effects. In fact, numerous clinical studies have now shown SWL to induce acute structural changes in the treated kidney of a majority, if not all, SWL patients. Similar data have been reported in animal models treated with SWL. The acute renal lesion associated with SWL has been reported to mimic that of blunt renal trauma. This structural injury is thought to resolve without the development of long-term functional complications suggesting that the morphological changes are reversible. However, irreversible forms of injury have been reported that result in permanent alterations in kidney structure. At this point is not clear if such changes will lead to chronic changes in renal function. While the level of acute structural injury induced by SWL may not cause a significant health risk to most stone patients, there are several clinical and experimental studies suggesting that there may be pre-existing risk factors that would predispose a kidney to increased renal trauma following SWL treatment. The concern for these patients is that the increased damage to the renal tubule and vasculature would result in permanent alterations in renal hemodynamics or function. The risk factors that have been reported include pre-existing hypertension, kidney size, number of kidneys, and the number of kidneys treated per same sessions. These observations have led us to formulate a hypothesis for the investigation of the renal bioeffect of SWL. The hypothesis states: 1) that stone comminution is dependent on the physical features of the shock wave; 2) that acute cellular injury in the kidney alters renal function transiently; and 3) that pre-existing risk factors predispose the SWL-treated kidney to chronic complications.
To test this hypothesis, our laboratory has initiated a series of controlled experiments on the pig kidney. In these studies, F2 of a unmodified Dornier HM3 lithotripter was on the right kidney (lower and/or upper pole calyx) and treated with 2,000 shocks at 24kV. A series of control animals were also studied. Each animal was subjected to a set of pre-SWL, one and four hour post-SWL evaluations which included inulin and P-aminohippurate (PAH) clearances and extractions. At the end of the study, both kidneys were perfused with glutaraldehyde and routinely processed for detailed morphological examination. Two different risk factors were investigated: 1) the effect of kidney size, adult vs juvenile pig, and 2) number of treatments to one kidney per same session.
At autopsy, all treated kidneys showed areas of histological change that corresponded to the region of F2. A more severe lesion was induced in the small (juvenile) vs the large (adult) kidney and in the kidneys that received 2000 shock to both the upper and lower poles vs lower pole only. The most obvious lesion included sites of intraparenchymal hemorrhage/edema and subcapsular hematomas. These lesions appeared as focal regions of injury but were multiple in number at F2. Careful examination of intrarenal arteries and veins revealed an unusual observation that being actual breaks/tears in the wall of these structures which permitted uncontrolled bleeding. Injury to the nephron also included lacerations of the tubular wall and necrosis of some cells. Many of these morphological changes represent irreversible sites of injury. This means scar tissue will form at these sites because the tubule or vessel injury cannot be repaired.
When we analyzed the renal hemodynamic and tubular functional changes in the adult vs juvenile kidneys treated with a single dose of shock waves, no detectable acute alterations were noted in the adult kidney, however; significant changes were seen in the GFR and RPF values of the juvenile (small) kidney. In addition, a fall in tubular function (PAH extraction) was also seen acutely in the small kidneys. When the small kidney received treatment to both the upper and lower poles in the same session, a further fall in tubular function occurred.
The conclusion we have formed from these data are: 1) a clinical dose of shock waves always induces a tubular and vascular injury, 2) kidney size make place a kidney at-risk for increased functional changes, 3) a reduction in renal plasma flow is the most pronounced functional change seen immediately following SWL and 4) double SWL treatment causes a further decrease in tubular function.