Abstract
Dear Editor:
We thank the author of the editorial comment 1 for his remarks on our article. In response, we fully agree that, ultimately, in vivo studies are critical and essential. However, as noted also by the editorial comment author, there are a large number of variables and intertwined responses, rendering current in vivo studies difficult and inconclusive. It is, therefore, preferable to compare, first, different stents and specific factors under well-controlled in vitro conditions, following the standard scientific practice of study from the bench to live models and to human exposure.
The author of the editorial comment asks: how can we design a truly accurate model for stented ureters ex vivo? Our response is that, given the nature of organ, tissue, and muscle behavior, we (currently, at least) cannot! However, there is much to be learned from ex vivo (in vitro) systems, and such studies are fundamental prerequisites to subsequent in vivo studies. In vitro systems allow identification, isolation, and quantification of specific components of complex (kidney/ureter/stent/bladder/obstruction) systems. We, therefore, argue that it is not “unfortunate” that we used all man-made materials in our current experiments, and disagree with the author's doubts that our measurements and conclusions can be translated to live tissue and clinical scenarios. Indeed, we focused on underlying essentially mechanical aspects of stent functioning and incorporated basic, well-established aspects of fluid dynamics. Our experiments, conducted under a scientifically strict and sound methodology, tested different stents under identical conditions.
The literature to date that addresses stent failure—defined as the inability of fluid to pass through a stented ureter—in the presence of extrinsic obstruction has focused on mechanical aspects and compression of stents. In our study, for the first time, we tested different sizes of stents, placed within artificial ureters, and measured actual fluid flow through these systems under various configurations of deformation and compression (to simulate the presence of an extrinsic obstruction). In terms of isolating key properties, we show that—contrary to many statements and assumptions in the literature 2 –5 —stent failure will occur in only rare circumstances purely from deformation and mechanical compression, particularly under physiologically realistic compression forces. We thank the author of the editorial comment for commending our contribution, which we see as another step in developing a more complete understanding of controls on stent behavior and failure.