
520 Urena, Mendez-Torres, and Thomas
The urinary elevation of several enzymes and proteins has been used as biochemical
markers to document shockwave injury to nephrons and the surrounding soft tissues.
The elevated biochemical markers include proximal tubular enzymes, such as N-acetyl-
β-
D-glucosaminidase and β-galactosidase, renal brush border epithelial cells enzymes,
γ-glutamyltransaminase and angiotensin converting enzyme and renal tubular enzymes
β-microglobulin, as well as urothelial glycosaminoglycan and glucose, proteins, and
immunoglobulin G alterations in cases of diffuse renal trauma (88–101). Although
most studies have found significant elevated levels of these biochemical markers,
Krongrad et al. (102) did not find a statistically significant increase of these tubular
enzymes, suggesting that their elevation was a result of a tubular defect in association
with stone disease and not a response to SWL treatment. Other less specific markers
have also been found to be transiently elevated after SWL, but are not just associated
with shockwave-related injury to the kidney but also to adjacent organs and soft tissues.
These include alkaline phosphatase, lactic dehydrogenase, glutamic-pyruvic transami-
nase, glutamic-oxaloacetic transaminase, C-reactive protein, S-100 protein, and crea-
tinine kinase.
Histopathologic studies in animals and humans have also documented acute changes
in the kidneys and surrounding tissues after SWL. Tubular, vascular, and interstitial
changes have been localized to the plane of the pressure wave, in which disruption of
the renal parenchymal cells have been found, as well as degenerative changes and
accumulation of hemosiderin granules and cast material (103). Dilation of veins with
evidence of endothelial damage and thrombus formation was among the alterations
found within the microvasculature (103). The effect of increasing the number of
shockwaves is translated into a higher rate of damage to the nephrons and especially to
small- and medium-sized blood vessels within the F2 range. This explains why although
electrohydraulic lithotriptors produce a larger lesion, electromagnetic lithotriptors,
because of more cellular destruction at F2, are associated with a higher rate of subcap-
sular hemorrhage.
Retroperitoneal hematomas have been documented radiographically in intraparen-
chymal, subcapsular, and perirenal locations. These hematomas have been found to be
produced primarily as a result of shockwave-induced vascular insult to thin-walled
veins and walls of small arteries and glomerular and peritubular capillaries. Rupture
of these interlobular and arcuate veins located in the corticomedullary junction makes
this region of the kidney more vulnerable to SWL-related intrarenal hematoma and
hemorrhage. Histopathology analysis after SWL has shown that although glomerular
atrophy and sclerosis, as well as interstitial fibrosis and hyalinization of arcuate veins,
are present, the rest of the renal parenchyma appears normal (89,104), suggesting that
SWL-related renal injury is focal and that this does not affect the majority of the renal
parenchyma.
Perirenal and subcapsular fluid collections, either from bleeding or urine, occur in 24–
32% of patients after SWL (78,83,84). Their appearances vary from mild intraparenchy-
mal contusions to large hematomas. Most hematomas are usually asymptomatic, with
symptomatic hematomas being reported in less than 1% of patients (105,106). These
hematomas are more commonly found in hypertensive patients, especially those with
poor blood pressure control at the time of treatment, and among patients on antiplatelet
medication (84,107,108). Other risk factors for increased hemorrhage and also related
to vascular disorders, are advanced arteriosclerosis, primary coagulopathic disorders,
diabetes mellitus, coronary artery disease, and obesity (109,110). No correlation in the