UROLITHIASIS/UPJ OBSTRUCTION: NEW IDEAS, NEW APPROACHES
From Urology Update: New Ideas, Approaches, and Techniques, presented by the Faculty of Medicine, University of
Toronto
Urolithiasis
| EVALUATION AND TREATMENT: A SIMPLIFIED APPROACH— Margaret S. Pearle, MD, PhD, Professor of Urology
and Internal Medicine, University of Texas, Southwestern Medical Center, Dallas
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| Medical management: number of randomized trials showed benefit of medical and dietary prophylactic regimens in
preventing stone recurrence
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 | Metabolic abnormalities: hypercalciuria—most common risk factor for stone disease; occurs in 35% to 65% of recurrent
stone formers; characterized by intestinal hyperabsorption of calcium; associated with bone loss in 25% of patients;
genetic predisposition for stone disease (putative gene identified; human soluble adenylyl cyclase [hsAC]);
hypocitraturia—leads to enhanced crystallization of stone-forming calcium salts (citrate important inhibitor of stone
disease); in setting of hypercalciuria, formation of soluble calcium-citrate complex reduced, leading to increase in ionized
urinary calcium, which leads to increase in urinary saturation of calcium oxalate; several metabolic, dietary, and
genetic risk factors, all leading to intracellular acidosis; due to altered metabolism and cellular transport of citrate in renal
proximal tubule, as result of low urine pH from intracellular acidosis; gouty diathesis—another important cause of
stone disease; characterized by low urine pH; at pH <5.5, increase in amount of poorly soluble undissociated uric acid
leads to production of uric acid stones; undissociated uric acid also risk factor for calcium stone disease due to hyperuricosuric
calcium nephrolithiasis, which occurs when urine pH <5.5; cause of low pH in gouty diathesis not well understood;
uric acid stones, comprising 6% to 10% of stones in general population, overrepresented in diabetics (34%);
diabetes associated with insulin resistance; study showed inverse relationship between urine pH and body weight; insulin
action peripherally leads to obesity; obesity associated with insulin resistance, which leads to defect in genesis of
ammonia from glutamine in kidney, thereby reducing urinary ammonium, leading to low urine pH and, ultimately, uric
acid stones
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| Dietary factors: citrus fruits—thought to have beneficial effect on stone formation due to alkali load (increases excretion
of urinary citrate [important inhibitor of stone formation]); potassium content of fruit determines amount of alkali delivered
(eg, lemon and cranberry juice contain virtually no potassium, whereas grape juice and orange juice contain
large amounts of potassium); metabolic studies show orange juice provides most benefit and cranberry juice least; lemonade
did not provide benefit; none of juices evaluated in clinical trials; animal protein—increases urinary uric acid
due to purine load; decreases urine pH because of acid load; increases urinary calcium because reduced urinary pH increases
calcium excretion
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| Effect of dietary calcium on stone formation: controversial; urinary saturation of calcium oxalate correlates positively
with urinary calcium and urinary oxalate concentrations; contrary to popular belief, urinary calcium and oxalate contribute
equally to increase in rise of urinary saturation of calcium oxalate; influencing factors—oxalate intake (liberal
or restricted); state of intestinal calcium absorption; type of dietary restriction
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| Program of broad dietary modification: promoted by speaker; consists of modest calcium restriction, oxalate restriction,
≤2 servings meat daily (preferably 1 serving/day), sodium restriction, and high fluid intake; studied in large
number of idiopathic calcium stone formers (group 1, moderate-to-severe hypercalciuria; group 2, mild hypercalciuria;
group 3, normal urinary calcium); results—dietary calcium restriction shown to reduce urinary calcium in those with hypercalciuria
(those with increased intestinal absorption of calcium), but did not lower urinary calcium in those with normal
urinary calcium; no change in urinary oxalate in any group; study suggests that limiting dietary oxalate can prevent
expected rise in urinary oxalate associated with dietary calcium restriction; after dietary modification, relative saturation
ratio of calcium oxalate declined moderately in group 1, modestly in group 2, and no change in group 3;
recommendations—for group 1, dietary calcium restriction and other dietary modifications; for group 2, modest calcium
restriction and other dietary measures; for group 3, liberal calcium intake and other dietary measures
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| Simplified approach to diagnosis and treatment of stone disease: step 1—collect 24-hr urine to check for
stone risk factors and obtain stone analysis and baseline serum chemistries; step 2—assign patients to groups based on
urinary calcium; those with secondary causes of stone disease excluded; step 3—initiate dietary and pharmacologic
treatment; recommendations—for group-1 patients, dietary restriction and initiation of indapamide (or other thiazide diuretic
with hypocalciuric action) and potassium citrate; group-2 patients, modest calcium restriction and potassium citrate
with or without hypocalciuric agent; group-3 patients, liberal calcium intake and potassium citrate; rationale for treatment
with indapamide—lowers urinary calcium (but also causes hypokalemia, which is why potassium citrate added);
also provides alkali load, increasing urinary citrate and urinary inhibitory activity; study results—pharmacologic (thiazide
diuretic and potassium citrate) and dietary (calcium and oxalate restriction) therapy evaluated in 28 hypercalciuric
(groups 1 and 2) stone formers; significant reduction in urinary calcium, with no change in urinary oxalate; overall result,
significant decrease in urinary saturation of calcium oxalate; rationale for treatment of group 3 with potassium citrate—
provides alkali load, thereby increasing urinary pH and citrate and modestly reducing urine calcium; may prevent bone
loss by inhibiting bone resorption (and perhaps by enhancing bone formation); Barcelo et al—showed 75% reduction in
new-stone formation in those taking potassium citrate
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| Questions and answers: which patients should be evaluated?—anyone with recurrent stones, with family history of
stones, who is a child, or has chronic diarrheal syndrome, urinary tract infections, or bone disease; obtain baseline blood
work, urinalysis, and analysis of stones; also if patient needs dietary modification, obtain 24-hr urine; speaker tries not to
commit low-risk first-time stone former to long-term medication but prefers to recommend broad dietary changes; is calcium
supplementation problematic in patients who develop stones late in life?—for most part, not a problem; older patients,
in general, have poor intestinal absorption of calcium, so supplementation not issue (urinary calcium low);
problem occurs in patients with absorptive hypercalciuria (increased calcium intake causes marked increase in urinary
calcium); speaker recommends thiazide diuretic or indapamide to lower urinary calcium (allows relatively liberal calcium
intake); calcium supplementation added, as guided by urinary calcium; necessary to monitor patient closely with
bone density and serial 24-hr urine analyses; importance of fluid intake?—high fluid intake important in preventing
stone formation because it lowers urinary saturation of stone-forming salts; randomized trial showed stone formation
twice as high when urine output <2 L daily; how to manage stone formation during pregnancy?—urinary calcium and citrate
both increase markedly during pregnancy; supposedly, likelihood of forming stones no greater during pregnancy;
high fluid intake recommended for pregnant patients; speaker generally does not maintain medications during pregnancy;
taking potassium citrate (Urocit-K) probably not helpful because urine citrates increased significantly during pregnancy;
speaker generally does not recommend thiazide diuretics during pregnancy if patient taking for stones; fluid best protective
factor; what is recommended dose of potassium citrate for calcium stone formers?—for uric acid stone former,
speaker generally does not monitor urine pH but follows patient with 24-hr urine; start at 20 mEq bid and increase as
needed to maintain pH >5.5; for calcium oxalate stone formers, start with dose of 20 mEq bid, based on maintaining normal
serum potassium and normal urinary citrate; if patient on low dose of thiazide diuretic, dose 10 mEq bid; if on higher
dose of indapamide or thiazide diuretic, use higher dose; urine pH also monitored; if urine pH high with normal urinary
citrate, speaker gives thiazide diuretic and potassium chloride supplement (not potassium citrate)
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| SHOCK WAVE LITHOTRIPSY: CAN WE IMPROVE PRESENT TECHNOLOGY ?—Kenneth Pace, MD, MSc, Assistant
Professor of Urology, Department of Surgery, St. Michael’s Hospital, and Faculty of Medicine, University of Toronto,
ON
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| Success rate: shock wave lithotripsy revolutionized treatment of kidney stones, but not 100% effective; stone size and
success rate—for larger stones, one treatment not effective; for larger stones (particularly 2-cm stones) in ureter, single
shock wave lithotripsy treatment insufficient; alternatives include percutaneous nephrolithotomy and ureteroscopy
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| Ways to improve lithotripsy: better lithotriptor; original machines reported better outcomes than second- or third-
generation machines; how to make existing machines work better—maximize standard clinical practice by hitting stone
with maximum (but safe) voltage and maximum number of safe shocks; also, optimize targeting to minimize respiratory
movement and keep stone in focal zone for duration of treatment
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| Treatment rate: first-generation lithotriptors synchronized to electrocardiography (ECG); treatment carried out at rate of 60
to 80 shocks/min; subsequently determined that faster rates safe; treatment rates increased to 120 shocks/min; second- and
third-generation machines not as effective as first-generation gated machines, partly due to design differences, differences in
peak pressure, and focal zone size; also may be due to change in rate
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| Methods of fragmentation: spalling—application of tensile force to stone (tears it apart); related to peak pressure
generated by machine; cavitation—related to bubble dynamics and bubbles forming on surface of stone; directly related
to rate; bubbles form and implode on surface of stone, creating microfissures; bubbles get into cracks and enlarge them;
to avoid, perform lithotripsy in viscous environment, increase hydrostatic pressure so bubbles unable to form, or place
thin membrane on surface of stone so bubbles not in contact with stone; negative effects of cavitation—breaking of
blood vessels, leading to tissue damage; shock wave energy does not transmit effectively through gaseous environment or
air, so bubbles along blast path of shock wave inhibit energy transmission and perhaps affect fragmentation; rate affects
cavitation; cavitation plays role in renal injury; in porcine experiments, with blood vessel damage, whole area injured by
shock wave energy with normal cavitation; but if cavitation suppressed and lithotripsy performed, no injury (tissue cavitation
not good); slower rates protective in 2 ways (minimize tissue injury and minimize number of shocks needed to
fragment stone); in vitro experiments showed slower rates better; Honey showed better fragmentation obtained with
fewer shocks at slower rate; for renal calculi, treatment at 60 shocks/min (single-treatment success rate 70%) better than
120 shocks/min (success rate 23%), particularly for bigger stones; ureteral stones—similar study design; at 2 wk and 3
mo, stone-free rates higher for patients treated with 60 shocks/min; fewer shocks needed to fragment stone; treatment
time longer; no difference in complication rates; lower retreatment rate for those treated at 60 vs 120 shocks/min; slowing
rate appears to have same benefit for ureteral stones as it does for renal stones
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| Conclusion: lithotripsy viable treatment option if effectiveness maximized, particularly for renal calculi and upper ureteral
stones; several parameters can be changed to optimize lithotripsy, eg, dual-firing generators, computed tomography
(CT) targeting, better respiratory gating techniques; tailor treatment selection to patient preferences and stones; for larger
stones, use slower rates; larger ureteral stones would probably benefit from primary endoscopic therapy; smaller stones,
particularly renal stones, benefit from lithotripsy
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Ureteropelvic Junction (UPJ) Obstruction
| ENDOPYELOTOMY: IS THERE A ROLE ?—Dr. Pearle
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| Treatment options for management of UPJ obstruction: endopyelotomy (EP; antegrade and retrograde); laparoscopic
pyeloplasty; percutaneous endopyeloplasty; open pyeloplasty (reserved for laparoscopic failures)
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| Outcomes: antegrade EP—large series from Long Island Jewish Medical Center had overall success rate of 85%; other
large series had average success rate of 81% with follow-up of 3 to 120 mo; retrograde EP—series vary in type of
cutting device utilized; overall success rate ≈85%; Acucise EP—overall success rate ≈87%; long-term outcomes—80
patients underwent antegrade EP with mean follow-up of 40 mo; overall success rate 67%; 18 failures (15 found at
pyeloplasty to have crossing vessel); another study of 80 patients who underwent Acucise EP, with mean follow-up of
6.1 yr; success rate 54% in patients with primary UPJ obstruction and 50% for secondary UPJ obstruction; earlier success
rates 76% to 78%; long-term durability of EP—reviewed series of antegrade EPs and compared to outcomes from
laparoscopic and open pyeloplasty from 1988 to 2004; recurrence-free survival for pyeloplasty group at 3, 5, and 10 yr
85%, 80%, and 75%, respectively, and 61%, 55%, and 41% for EP; concluded that success rates for EP and pyeloplasty
declined over time, with decline more marked in EP
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| Anatomic factors that affect success of EP
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| Hydronephrosis: Gupta et al—found that for patients who underwent antegrade or retrograde EP, increase in hydronephrosis
led to decline in success rates
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| Crossing vessel: even greater influence on outcome; if present, success rate only 33%; if absent, success rate 82%; overall,
subgroup with poorest outcome those with crossing vessel and high-grade hydronephrosis; additional studies concluded
still worth doing EP, even if crossing vessel present
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| Renal function: Gupta et al—found direct correlation between success and renal function; when renal function <25%,
success rate 50% to 60%
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| Anatomy of UPJ: study—compared outcomes with antegrade and retrograde EP in those with dependent UPJ vs those
with high insertion; found no significant difference between groups, regardless of anatomy of UPJ (although overall
success rates higher in retrograde EP); Clayman et al—high success rates (90%), when antegrade EP performed on
those with high insertion, 63% with retrograde approach; therefore, best to use ureteroscopic retrograde approach or
antegrade approach; EP for UPJ obstruction after previous failed EP—no significantly large series in literature; average
success rates 52%; speaker recommends another treatment, rather than repeat EP
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| Cost: important factor; Gettman et al—found that retrograde EP least costly treatment modality, followed by Acucise EP,
antegrade EP, and laparoscopic pyeloplasty
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| Algorithm: used in speaker’s institution; includes diuretic renal scan to document ipsilateral renal function and presence of
UPJ obstruction; if renal function poor, perform laparoscopic pyeloplasty; if renal function reasonable, any of 3 modalities; if
no crossing vessel present on CT arteriography, any treatment modality reasonable; if crossing vessel present, laparoscopic
pyeloplasty; if high-grade hydronephrosis present, patient undergoes laparoscopic pyeloplasty; if low or moderate-grade hydronephrosis,
any treatment modality; if stones present, antegrade EP or laparoscopic pyeloplasty (if stones accessible with
flexible endoscope through laparoscopic port); if no stones, any treatment modality option; if high insertion UPJ present, retrograde
or antegrade EP; if dependent UPJ, any treatment option
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| Management of secondary UPJ obstruction: failed EP, go on to laparoscopic pyeloplasty; failed laparoscopic or
open pyeloplasty, perform EP; failed laparoscopic pyeloplasty and EP, perform open pyeloplasty; how long to follow
patient—for EP, data suggest follow-up up to 10 yr, less for pyeloplasty
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Suggested Readings
Elbahnasy AM et al: Lower caliceal stone clearance after shock wave lithotripsy or ureteroscopy: the impact of lower
pole radiographic anatomy. J Urol 159:676, 1998; Gettman MT et al: Effect of cranberry juice consumption on urinary
stone risk factors. J Urol 174:590, 2005; Gill IS et al: Laparoscopic ureterocalicostomy: initial experience. J Urol
171:1227, 2004; Gupta M et al: Open surgical exploration after failed endopyelotomy: a 12-year perspective. J Urol
157:1613, 1997; Heller HJ et al: Effect of dietary calcium on stone forming propensity. J Urol 169:470, 2003; Krumholtz
JS et al: Extracorporeal shock wave lithotripsy of the right kidney after liver transplantation. J Urol 163:230, 2000;
Lotan Y et al: Cost-effectiveness of medical management strategies for nephrolithiasis. J Urol 172:2275, 2004; Matsumoto
ED et al: Effect of high and low calcium diets on stone forming risk during liberal oxalate intake. J Urol 176:132,
2006; Nakada SY et al: Ureteropelvic junction obstruction. Retrograde endopyelotomy. Urol Clin North Am 27:677,
2000; Pak CY et al: Biochemical and physicochemical presentations of patients with brushite stones. J Urol 171:1046,
2004; Pak CY et al: Elucidation of factors determining formation of calcium phosphate stones. J Urol 172:2267, 2004;
Pak CY et al: Physicochemical metabolic characteristics for calcium oxalate stone formation in patients with gouty diathesis.
J Urol 173:1606, 2005; Pak CY et al: Predictive value of kidney stone composition in the detection of metabolic
abnormalities. Am J Med 115:26, 2003; Pak CY et al: Prevention of spinal bone loss by potassium citrate in cases of calcium
urolithiasis. J Urol 168:31, 2002; Pak CY et al: Prevention of stone formation and bone loss in absorptive hypercalciuria
by combined dietary and pharmacological interventions. J Urol 169:465, 2003; Pearle MS et al: Optimal
method of urgent decompression of the collecting system for obstruction and infection due to ureteral calculi. J Urol
160:1260, 1998; Shalhav AL et al: Adult endopyelotomy: impact of etiology and antegrade versus retrograde approach
on outcome. J Urol 160:685, 1998; Traxer O et al: Effect of ascorbic acid consumption on urinary stone risk factors. J
Urol 170:397, 2003; Van Cangh PJ et al: Endopyelotomy. Prognostic factors and patient selection. Urol Clin North
Am 25:281, 1998; Van Cangh PJ: Endopyelotomy--a panacea for ureteropelvic junction obstruction? J Urol 159:66,
1998
Educational Objectives
| The goal of this program is to improve the management of urolithiasis and ureteropelvic (UPJ) obstruction. After hearing
and assimilating this program, the clinician will be better able to:
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| 1. Discuss the metabolic abnormalities and dietary factors involved in the pathophysiology of urolithiasis.
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| 2. Explain the association between uric acid stones and diabetes.
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| 3. Utilize the program of broad dietary modification based on the patient’s urinary calcium.
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| 4. Determine when to perform shockwave lithotripsy.
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| 5. Utilize the algorithm for the management of primary UPJ obstruction.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose relevant
financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts
were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial
interest. For this program, the faculty reported nothing to disclose.
Acknowledgements
Drs. Pearle and Pace were recorded at Urology Update 2006: New Ideas, Approaches, and Techniques, presented November
3-4, 2006, in Toronto, ON, and sponsored by the Faculty of Medicine, University of Toronto. The Audio-Digest Foundation
thanks the speakers and the Faculty of Medicine, University of Toronto for their cooperation in the production of this
program.
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