Abstract
I read with interest the article from Shilo and colleagues and I keep asking myself the same questions every time we place a stent: How do stents drain and how do they obstruct? Do they drain through the stent, around the stent, or both? Does the width of stent matter? Does stent design or material matter? When we say “stent failure” what does that actually mean? Obstruction? Infection? Calcification? Kinking? Compression? Buckling? Urologists have been struggling with these questions since the mid-1960s when Ziskind first reported human use of silicone rubber stents in cases of ureteral obstruction. 1 We have also been faced with the challenge of trying to figure out how to study stents and their roles/functions in the urinary tract. Because studying in vivo is invasive, scientists are continuously working on models to mimic urinary obstruction without overwhelming success. How can we design a truly accurate model ex vivo? If we do not understand the tissue changes proximal and distal to the obstruction, the flow characteristics through the stented ureter nor the real effects of peristalsis and drainage through the obstruction; if we do not understand what changes occur in the obstructed ureter as far as muscle hypertrophy, muscle recruitment in the ureteral wall, and muscle pliability in different clinical situations; and if we cannot measure these changes, we will never really understand how to design devices to alter them. Unfortunately, the authors utilized all man-made materials for this experiment and it is doubtful that much of the data derived can truly be translated to live tissue and actual clinical scenarios. The peristaltic pump is a machine-generated static device controlling water flow to the “kidney,” which is a firm rigid enclosure. This in turn gives rise to a silicone tubing “ureter,” which is stented. The tubing drains into the “bladder,” which is a zero-pressure beaker. What we are not taking into consideration are the arterial inflow pressures through the Loop of Henle and the rest of the collecting system; pliability of the renal pelvis and surrounding tissue; the true nature of the ureter and what its abilities and deficiencies are in times of urinary obstruction; and the effects of the bladder on the upper urinary tract especially in men with an element of bladder outlet obstruction. All of these unknowns, in addition to urine composition, muscle physiology, and stent performance make ex vivo artificial testing fraught with error, or at the least pure hypothesis. Although it is invasive, real-time monitoring has been described for many years and in many other specialties. 2 With today's communication and sensing technologies and abilities, I feel it is time to push the envelope to help understand ureteral obstruction, stent function, and stent dysfunction from the “inside looking out.” We need to understand in real time the environment of obstruction, how it affects relevant tissue, and what designs will help preserve more renal units. The other possibilities are endless and can include insights into renal pelvis, bladder, and urethral function as well. All this being said, I commend the authors on contributing more information to the obstructed stent theory and hopefully their work can be built upon. Perhaps an implantable device to get in vivo data.