Audio-Digest Foundation: urology

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Audio-Digest FoundationUrology


Volume 29, Issue 02
February 1, 2006

The following is an abstracted summary, not a verbatim transcript, of the lectures/discussions on this audio program. If, after reviewing this written summary, you would like to hear the contents and/or earn CME/CE credit, simply visit the Audio-Digest Foundation website

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STONE DISEASE UPDATE

From the Kaiser Permanente Urology Symposium

Margaret S. Pearle, MD, PhD, Professor of Urology and Internal Medicine, University of Texas Southwestern Medical Center, Dallas

DIET IN STONE MANAGEMENT
Diet and stone disease: “stone clinic” effect—refers to reduction in stone formation rates produced by preventive dietary measures; provides baseline for determining relative efficacy of various drug therapies; point—to achieve best therapeutic results, dietary program must be combined with careful metabolic evaluation and follow-up
Fluid intake: basic component of any stone prevention program; data show—high fluid intake markedly reduced stone recurrence rates among calcium oxalate stone formers; coffee, tea, beer, and wine seem to be associated with reduced risk for stone formation
Fruit juice and risk for stone formation: in stone formers with hypocitraturia, administering 2 L/day of lemonade for 1 wk produced mean increase in urinary citrate of 200 mg/day; in normal subjects who received grapefruit juice, small increases in urinary oxalate offset beneficial increase in urinary citrate; cranberry juice—conferred no specific protection against calcium oxalate stone formation; may pose limited risk for stone formation by producing overall net increase in urinary saturation of calcium and oxalate; among normal subjects and stone formers with hypocitraturia, consumption of—orange juice produced beneficial increase in urinary pH and citrate (urinary oxalate also increased slightly); potassium citrate also produced beneficial increase in urinary pH and citrate (small reduction in urinary calcium also occurred)
Protein from red meat, fish, and poultry: increases stone risk by—increasing urinary uric acid via purine load; decreasing urine pH by presenting acid load; increasing urinary calcium via reduction in urine pH; metabolic study data show patients on low-protein diets experienced—reduction in urinary uric acid, calcium, and oxalate; increase in citrate; results of only prospective randomized clinical trial—showed subjects on low-protein diet faced increased risk for stone formation; may have been influenced by confounding factors, ie, subjects in control group had higher mean urine volumes than subjects on low-protein diet
Metabolic study investigating low-carbohydrate and high-protein diets and stone formation: mimicked baseline, induction, and maintenance phases of Atkins diet; during induction and maintenance—decrease in urine pH associated with increased acid excretion and decreased urinary citrate; urinary calcium and uric acid increased; increase in calcium excretion caused overall negative net calcium balance; data suggest institution of low-carbohydrate and high-protein diet— may increase risk for stone formation and bone loss; should be discouraged in stone formers
Dietary sodium: important factor; often overlooked; high sodium intake—increases urinary calcium and pH; decreases urinary citrate; changes in relative saturation ratio proved—significantly increased for brushite and sodium urate stones; insignificant for calcium oxalate stones; points—monitor urinary sodium when treating calcium stone disease, ie, for every 100-mEq increase in urinary sodium, urinary calcium correspondingly increases by 50 mg; to decrease urinary calcium and sodium urate saturation, restrict sodium intake to 2000 to 3000 mg per day
Dietary calcium: dietary calcium believed important because—calcium most common component of urinary stones; hypercalciuria common in stone formers; drugs that reduce urinary calcium also reduce stone recurrence rates; sources of controversy—lack of direct link between hypercalciuria and calcium stone formation; questions concerning impact of low-calcium diet on stone recurrence and bone loss
Protective effect of high calcium intake against incident stone formation: observations from study data—2 prospective cohort studies showed high-calcium diet exerted protective effect against incident stone formation; ineffectiveness of low-calcium diet in preventing stone-occurrence attributed to compensatory increase in urinary oxalate; point— protective effect of high-calcium diet likely due to concurrent greater intake of stone-protective factors, ie, fluids, potassium, magnesium, phosphorous, and alkali; data suggest high calcium intake—increases urinary calcium and relative saturation ratio of calcium and oxalate; may reduce urinary oxalate but does not compensate for effect of increased urinary calcium on relative saturation ratio of calcium oxalate
Urinary oxalate: intestinal absorption—depends on passive diffusion across intestine; greatest activity occurs across colon; rate of diffusion depends on concentration of free oxalate, accessibility of colon, and permeability of membrane to oxalate; amount of oxalate in intestine depends on dietary intake, calcium binding, and presence of fatty acids and bile salts; points—approximately equal amounts of oxalate produced by oxidation of glyoxylate and direct metabolic conversion from ascorbic acid and tryptophan; 25% to 50% of urinary oxalate derived from diet (remainder derived from endogenous production); ascorbic acid—may increase urinary oxalate levels (impact on risk for stone formation unknown); intake should be limited to 1 g daily in patients with stone disease
Interaction between calcium and oxalate in urine: data (obtained using Finlayson stability constant) show—urine concentrations of calcium and oxalate equally important in determining urinary saturation of calcium oxalate; in normal subjects, high calcium intake probably not likely to increase risk for calcium oxalate stone formation; in hypercalciuric stone formers, modest calcium restriction probably indicated, ie, in these individuals, increased calcium intake can produce marked increase in urinary calcium; risk for bone loss remains concern when restricting calcium intake; among patients with absorptive hypercalciuria and recurrent calcium stones, clinical data show combination of thiazide diuretics, potassium citrate, and mild restriction of dietary calcium and oxalate can—reduce hypercalciuria; prevent secondary rise in oxalate generally associated with calcium restriction; decrease urinary saturation of calcium oxalate; reduce stone recurrence rates; stabilize or increase bone density
Conclusions concerning dietary management: high fluid intake can reduce stone recurrence rates; in metabolic studies, consumption of orange juice and lemonade improved stone risk factors; mild salt restriction can help reduce urinary calcium; association between animal protein and increased stone risk not clearly demonstrated in randomized trials; severe calcium restriction should be discouraged; combination of mild calcium and oxalate restriction and thiazide diuretics with or without potassium citrate may be advisable in patients with absorptive hypercalciuria
THE LOWER-POLE RENAL STONE: OPTIMAL MANAGEMENT
Extracorporeal shock wave lithotripsy (ESWL): outcome depends on location of stone in kidney, ie, highest stone-free rates (SFRs) achieved in renal pelvis or ureteropelvic junction (UPJ); lower pole of kidney—relatively unique anatomic region for stone management; gravity-dependent lower pole calices associated with lowest SFRs after ESWL; factors favoring use of ESWL to manage lower-pole stones—only available noninvasive treatment option; high patient acceptance rate; relatively low complication rate; ability to readily salvage failed percutaneous nephrolithotomy (PCNL) or ureteroscopy; maneuvers suggested to facilitate clearance of fragments from lower pole of kidney—percussion, diuresis, and inversion (PDI) therapy (effective maneuver for improving stone clearance); vibration massage-initiated post-ESWL; placement of retrograde catheter or nephrostomy tube to permit continuous irrigation during treatment; pharmacotherapy, ie, data suggest administration of potassium citrate (Urocit-K) can reduce aggregation of stone fragments and facilitates discharge of fragments after ESWL
Percutaneous nephrolithotomy: advantages of procedure—SFR in general does not depend on stone size or location (ie, SFRs uniformly high, regardless of stone size); generally easy to perform (lower pole usually contains isolated stone); relatively safe (procedure usually performed below 12th rib); compared to ESWL, PCNL—achieves superior SFRs overall; requires longer duration of hospitalization and has higher complication rates; has lower retreatment and auxiliary procedure rates; achieves superior SFRs when used to treat >1-cm stones (ESWL reasonable for <1-cm stones)
Factors affecting SFRs after ESWL
Anatomy: 3 factors that may correlate with favorable outcome after ESWL—angle between renal pelvis and lower pole infundibulum; infundibular width; spatial arrangement of lower pole calices; additional data suggest favorable anatomic factors include—infundibulopelvic angle >90°; infundibulum <3 cm in length and >5 mm in width; based on clinical experience with individuals who have 15-mm stones in lower pole—ESWL reasonable when infundibulopelvic angle >70°, or when infundibulopelvic angle between 40° and 70° and infundibular length and width favorable; PCNL treatment of choice when infundibulopelvic angle <40° or when other anatomic factors do not favor ESWL; bottom line— anatomic factors probably play some role in clearance of stone fragments; specific anatomic factors of concern yet to be definitively identified; other factors in descending order that proved helpful in predicting clearance of stone fragments (determined by using artificial neural network)—dynamic urinary transport; infundibuloureteropelvic angle; caliceal pelvic height; body mass index (BMI); SFRs
Ureteroscopy: advantages—clinical efficacy; can be performed on outpatient basis; minimal morbidity; efficacy against small-to-moderately sized stones; can be used whenever patient fails ESWL or when trying to avoid percutaneous approach; modern ureteroscopes—use 2-way deflection; active deflection occurs at tip with movement of lever; passive deflection facilitates access to lower pole by using natural bend that occurs 5 to 10 cm from tip of ureteroscope; access to lower pole of kidney can be achieved in patient with—small minimally dilated collecting system and relatively shallow infundibulopelvic angle, by using active deflection of standard ureteroscope; well dilated collecting system with sharp infundibulopelvic angle, by using standard ureteroscopy and combination of active and passive deflection performed under fluoroscopic control; measures to facilitate access to lower pole—placing patient prone with head down (approach provides broadest angle of entry into lower pole calyx and achieved 88% stone-free rate); new ureteroscopes with dual active primary and/or secondary deflection; when unsure whether stone can be reached—schedule patient for ureteroscopy and possible PCNL; treat patient in prone position; if ureteroscopy fails, perform PCNL
Maximum deflection of ureteroscope: essential, ie, 104° to 175° deflection necessary to access lower pole calyx; passage of instruments through ureteroscope can reduce deflection by 86° and push instrument out of lower pole; pointers—make sure shaft of scope as straight as possible (back tension helps straighten shaft); to keep shaft from buckling in bladder, pass scope through ureteral access sheath (cystoscope sheath contraindicated); when shaft tip lacks sufficient stiffness to maneuver through lower pole calyx, pass superstiff guidewire in antegrade fashion through ureteroscope to location near tip; to protect working channel, straighten tip of ureteroscope to <30°
Nitinol retrieving devices: important advance in ureteroscopic treatment of lower-pole stones; passage results in 10° loss of deflection in scope; data showed—1.6 F electrohydraulic lithotripsy (EHL) probe, Nitinol basket, and 200-µm laser fiber produced minimal deflection through DUR-8 Elite flexible ureteroscope; flexibility of 200-µm laser fibers varies with manufacturer; to achieve maximum deflection when using DUR-8 Elite scopes, perform primary deflection initially
Repositioning stone from lower pole of kidney into more accessible middle or upper pole calyx: proven effective for larger stones; uses Nitinol device to facilitate treatment of large stones with laser fiber; procedure—route ureteroscope into steep infundibulopelvic angle and use secondary deflection to enter lower pole calyx; engage stone with Nitinol retrieval device; once stone repositioned into upper pole calyx, place patient in Trendelenburg position (approach uses upper pole calyx as backstop to facilitate stone clearance); pass laser fiber through scope and fragment stone; anesthesia—general endotracheal anesthesia recommended during treatment; to increase accuracy of stone fragmentation, periodically ask anesthesiologist to suspend patient’s respiration (especially when dealing with small fragments); injection of autologous blood through ureteroscope and into lower pole calyx and infundibulum—reasonably effective approach; uses clot formation to prevent reaccumulation of stone fragments in lower pole calyx and improve clearance of fragments from upper pole calyx; clot formation may extend beyond calices
Algorithm derived from phase 1 and 2 lower-pole stone data: for <1-cm stones, ESWL and ureteroscopy achieve disappointingly low SFRs (ESWL favored from patient standpoint); for >2-cm stones, PCNL preferred; for <10-mm stones— evaluate anatomic factors to determine whether ESWL reasonable option; if situation inappropriate for ESWL, consider ureteroscopic procedure; for stones between 1 and 2 cm—PCNL achieves highest SFRs; ESWL and ureteroscopy have poor SFRs (over time, some anatomic factors may be used to select subgroup of patients that can be treated with ESWL; newer maneuvers for manually retrieving stone fragments from kidney may make ureteroscopy reasonable alternative); points—algorithm can change over time; as technology improves, endoscopic management may increase in importance

Educational Objectives

The goal of this program is to educate the listener about the management of stone disease. After hearing and assimilating this program, the clinician will be better able to:
1. Identify dietary factors that contribute to the development of stone disease.
2. Determine the impact of dietary calcium levels on stone formation.
3. Assess the relative effect of calcium and oxalate on calcium oxalate saturation.
4. Discuss current techniques for managing lower-pole renal stones.
5. Individualize the management approach based on the size of lower-pole stone being treated.

Discussed on This Program

Potassium citrate [Urocit-K]

Suggested Reading

Borghi L et al: Urinary volume, water, and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study. J Urol 155:839, 1996; Elbahnasy AM et al: Lower caliceal stone clearance after shockwave lithotripsy or ureteroscopy: the impact of lower pole radiographic anatomy. J Urol 159:676, 1998; Kourambas J et al: Nitinol stone retrieval- assisted ureteroscopic management of lower pole renal calculi. Urology 56:953, 2000; Pearle MS et al: Prospective, randomized trial comparing shock wave lithotripsy and ureteroscopy for lower pole caliceal calculi 1 cm or less. J Urol 173:2005, 2005; Seiner R et al: The efficacy of dietary intervention on urinary risk factors for stone formation in recurrent calcium oxalate stone patients. J Urol 173:1601, 2005; Straub M, Hautmann RE: Developments in stone prevention. Curr Opin Urol 15:119, 2005; Taylor EN et al: Obesity, weight gain, and the risk of kidney stones. JAMA 293:455, 2005.

Faculty Disclosure

In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported nothing to disclose.


Dr. Pearle gave her scientific presentation at the Kaiser Permanente Urology Symposium 2005, presented October 21-23, 2005, in Santa Barbara, California, by the Southern California Permanente Medical Group. The Audio-Digest Foundation thanks Dr. Pearle and the Southern California Permanente Medical Group for their cooperation in the production of this program.


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