This chapter will take approximately 21 minutes to read.

  1. Sydney Children's Hospital, Sydney, NSW, Australia
  2. Department of Paediatric Surgery, Queensland Children's Hospital, Brisbane, QLD, Australia
  3. Department of Paediatric Surgery and Urolgy, Sydney Childrens Hosptial, Randwick, NSW Australia, Randwick, NSW, Australia
  4. School of Womens and Childrens Health, University of New South Wales, Randwick, NSW, Australia
  5. School of Medicine, Western Sydney University, Randwick, NSW, Australia


‘Urinary stones’ is a malady known to humans since early times; evident from the findings of urinary stones in Egyptian mummies. Sir G E Smith found a bladder calculus, dated to 4800 BC, in the mummy of the pelvis of a 16-years old in 1901 in El Amrah, Egypt. The calculus had concentric laminations of calcium oxalate, ammonium magnesium phosphate around a uric acid nucleus.1,2,3 Sushruta, India, 600 BC, in his medical text, Sushruta Samhita, described formation of bladder stones and perineal lithotomy! Urinary stone disease finds its mention in Ancient Greek texts and recognition by Hippocrates. Ancient Arabic medicine has perineal lithotomy described in a book by Al-Razi in 841–926 AD.4

Historical urinary stone disease literature is fascinating with the morbidity of the disease, the mortality of the surgical attempted cures, and the descriptions of “lithotmus, stein-schnieider, clysters, lithotryptors to crush stone!


The incidence in adults is understood to be at 10-12% lifetime risk. Though it was thought to be a male predominant disease, the gender bias seems to be equalizing. The cost of management of urinary stone disease is thought to be over 2 billion dollars in 2010 to over $10 billion annually.5 There has been over a doubling of incidence (from 7.9 to 18.5 per 100,000 children) in just over a decade in South Carolina..6,7,8 A Chinese meta-analysis has a similar observation.9

Geographic distribution of stone disease has been well known. The ‘stone belt’ in the southern USA is an example. In the middle and far east, there is endemicity for bladder stones. In the UK, ‘stone districts’ such as Norfolk, were common during the 19th century, with subsequent decline in the endemic bladder stone incidence with improved nutrition. Colonel McCarrison noted the endemicity of bladder stones in India and its similarity in the UK.

Urinary stone disease may be related to many factors including diet, environment, geographical location, metabolic and genetic factors. The geographical variability is multifactorial with arid climates, water intake, salt intake, diet including protein load, fruits and vegetable intake.

Bladder calculi could be idiopathic/endemic, secondary and migrant. The incidence of bladder calculi is less in the developed world as compared to the developing world and may be attributed to a diet lacking in animal proteins. There is an overall decrease in the incidence of endemic stones ‘the stone wave’. The incidence of bladder calculi in Pakistan has reduced from 70% in 1984 to 18% in 2007 and similarly from Satpura ranges in central India.10 Still, the Afro-Asian endemic bladder calculi belt continues to be a cause of morbidity from endemic urinary stone disease. An epidemiological study reveals the disease in Asia in the 20th century is similar to that in Europe in the nineteenth century.11 The endemic bladder calculi are commonly see in children between 1-5 years, with a peak at 3 years, likely due to weaning period and single cereal diet.10 They are more common in males with M:F = 10:1, this may presumably be due to differences in urethral anatomy.12

It is unclear if augmentation cystoplasty stone disease incidence follows the geographic distribution of urolithiasis.

Stone formation is also related to UTIs and anatomic urological anomalies. One study found 18/54 children with calculi had associated genitourinary anomalies and another found calculi associated with genitourinary anomalies in 35.9% children.13,14 80% of children with stones associated with infections are male. Infection related stones are found usually under 5 years of age.

Bacterial infections with proteus, pseudomonas, klebsiella and enterococci are strongly associated with stone formation, as the urease breaks down urea to form ammonium and bicarbonate, favorable for struvite stones. Matrix concretion, a soft radiolucent mucoid substance produced with infection may calcify ready and account for rapid formation of infection related stones. In one study, frequency of hypercalciuria and hyperuricosuria was higher in children with VUR.15 Eight to eighteen percent of children with VUR have stone disease and some may present later in adulthood.16,17

Obesity and weight gain are independent factors in the development of urinary stones in adults and yet less evident in children. In one study, BMI of more than 30 had an odds ratio of 1.7 as compared to BMI of 18.5 to 24.9 kg/m.218 The disease may be changing from a disease of poorly nourished to be one associated with obesity.19

Bladder Augmentation

Bladder augmentation was first described in the canine model by Tizzoni and Foggi in 1888 and von Mikulicz described it in humans a year later.20 The number of botox injections to the bladder have progressively increased since 2006, going from a few hundred to over 4,000 in UK and it is not surprising that the number of bladder augmentations is reducing, as reported in the study by Biers et al.20 The reduction in the incidence of augmentation may also be related to availability of anticholinergics, CIC but also decreasing incidence of anomalies such as spina bifida. Though ileocystoplasty is the commonest augmentation, there are many other segments of the bowel from stomach to the sigmoid colon, including ileocecal segments that are used. Also, autoaugmentation and ureterocystoplasty are other modalities of augmenting the hostile bladder.21,22 Augmentation helped us move away from incontinent reservoirs to continent reservoirs. It has replaced urinary diversion as the preferred surgical method for neurogenic bladder or congenital bladder issues. The indications are incontinence or renal damage in presence of a small capacity high pressure bladder. This move towards augmentation was facilitated by works of Bramble and Adams in the late 80s.23,24 It was encouraged by the advent of CISC and 10-75% of patients require it to empty the bladder. Combination of anticholinergics and CISC increase the rate of continence with cystoplasty with low bladder filling pressures and preservation of renal function. Augmentation cystoplasty also remains an important tool in preserving the renal function post-transplant in patients with hostile bladders. There is no confirmation yet that the best graft survival remains in non-augmented bladders.25,26

Stone formation is common after bladder augmentation. It is reported from 3-40% but was reported in over 50% in the series by Palmer et al.27,28,29,30,31,32,33,34,35

The mean time for stone formation was found to be 30.3 months and most stone formation occurred within 3 years of the augmentation as reported by Zhang H et al.36 The stone formation is reported from 25 months to 39 months.29,37 In another report, the median time for stone formation in adults with a history of augmentation cystoplasty was reported to be 16 years, a range of 5–38 years.38

Stone Composition in Children

  • Calcium oxalate: 45–65 %
  • Calcium phosphate: 14–30%
  • Struvite: 13%
  • Cystine: 5%
  • Uric acid: 4%
  • Miscellaneous: 4%

The metabolic derangements that lead to increased incidence of stone formation in children without augmentation are hypophosphaturia, hypomagnesuria, hypocitraturia, hypercalciuria, hyperoxaluria, hyperuricosuria, xanthinuria, cystinuria.

In patients with augmented bladders, infectious stones are most likely to be struvite, followed by carbonate apatite, ammonium acid ureate or mixed, while non-infectious stones are most likely to be calcium phosphate followed by calcium oxalate and uric acid.39

Stones are less common in Augmentation cystoplasties who can void spontaneously and efficiently and occur in less than 2% of patients. The incidence is 5 times more if CISC is used per urethra but rises to 10 times if using a Mitrofanoff channel. This finding implies a role of stasis.40

The addition of bladder neck procedure, catheterizable channel or both with augmentation significantly increased the risk of stone formation as compared to augmentation alone..41 A stoma created at time of AC was associated with an increased hazard of bladder stones. The 10 year cumulative risk of developing lower tract stones was expected to be 13–36%.42

Hensle et al reported over 10 percent incidence in their study and were concerned that sedentary habitus in spina bifida patients would lead to more stones.34 They subsequently in other study showed that the patients with immobility and sensory impairment were worse off and similar to Nurse et al finding reservoir calculi in 66% as compared to 15% those who used native urethra.34,40 Bladder stones occur about 10 times more often in SB patients than in the population and approximately 1% of patients with spina bifida develop stones annually after augmentation.43 The predicted ‘lifetime incidence’ was 2.25 episodes per 1,000 patient-years. 14/260 patients (5.4%) spina bifida patients were found to have bladder stones in a retrospective study by Veenboer et al.44

Stones are commonly triple phosphate implying that bacteriuria with urease producing bacteria (proteus, klebsiella) may be the cause as found in many reports. In one study, patients with augmented bladders were typically linked to metabolic abnormalities and were non-infectious.39

Uric acid stone formation has been reported in bladder augmentation using stomach.45

Cloacal exstrophy patients may be prone to metabolic abnormalities that increases the stone risk and affect composition of stones. Szymanski et al found cloacal exstrophy patients to have uric acid stones significantly more than other types.39

Metabolic factors in patients with augmentation cystoplasty that have been associated with stone formation like hypocitraturia and high calcium phosphate ratio in bladder mucus may also predispose to stone formation.46

Up to 60% of bladder stones in post enteric bladder augmentation are due to metabolic factors. The loss of bowel length and ileal volume, malabsorption of bile salts leading to steatorrhea, relative dehydration due to diarrhea, loss of enteric bicarbonate, and eventual metabolic acidosis resulting into hyperoxaluria, hyperuricosuria and hypocitraturia. Mobilization of the calcium phosphate from the bony stores due to immobilization or to buffer the metabolic acidosis may also lead to hypercalciuria.38,47

Metallic staples used in the operation are known to be associated with stone formation.48 Even absorbable staples used for approximating reconfigured bowel segments have been found to be associated with the stone formation with a ghost of the staple found in the calculus mass![]

Stones seen in exstrophy bladder augmentation may be due to the keratine elements including at the time of repair.49 Unintentional inclusion of the para-exstrophy skin, squamous metaplasia in the bladder mucosa de novo or down the suprapubic tract sites were found to be the site of stone formation.50

Though the above multiple factors such as augmentation with bowel, presence of mucous, bacteria, nidus from non-absorbable material are all found to have a role in development of stones, it is still unclear which factor is most important.

Seromuscular bladder augmentation is an alternative to ileocystoplasty and may be associated with lesser stone formation due to lack of bladder mucous. Though Odeh et al did not find any stone formation in SMBA in the 10 patients as compared to the other 30 who underwent standard ileocystoplasty it was not significant.51

In 1998 it was expected advances in tissue engineering and alternatives to methods of augmentation will relegate the stone formation to “arena of historical significance”![]

Evaluation and Diagnosis


  • Presenting features can include:
    • Pain or discomfort in suprapubic or hypogastric region
      • Pain can be referred to the penis
    • Frequency or urgency
    • Turbid sandy urine
    • Nocturnal enuresis
    • Dribbling of urine
    • Terminal dysuria
    • Hematuria
    • Strangury and urinary retention
    • Non-specific signs particularly in endemic stones include anemia, malnutrition, conjunctival hemorrhage due to straining, fever secondary to UTI, dehydration, rectal prolapse

History and Examination

  • Exclude underlying structural abnormalities of the kidney and urinary tract
  • Diet (excessive salt, ketogenic, excess animal protein, low calcium, cereal, calcium), fluid intake (inadequate, fructose rich drinks),
  • Medications—anticonvulsants (topiramate, zonisamide), antibiotics (ceftriaxone), diuretics (frusemide, acetazolamide), vitamin C and D intoxication, uricosuric acid agents, corticosteroids, protease inhibitors (indinavir)
  • Family history of calculi, hematuria, or renal failure. Parents and siblings have a positive history in 50–75% cases. Consanguinity (increases occurrence of cystinuria and hyperoxaluria)
  • Predisposing conditions—UTI (especially proteus or klebsiella), intestinal malabsorption (inflammatory bowel disease, short gut, cystic fibrosis), prematurity, Dent’s disease, primary hyperoxaluria, resistant epilepsy on ketogenic diet, prolonged immobilization
  • Examination—palpable bladder, dysmorphic features of William syndrome, rickets, tetany and gout, rectal prolapse52


  • Initial workup
    • Serum
      • Full blood count
      • Creatinine
        • Dehydration due to vomiting and prerenal
        • More severe elevation with solidary kidney, bilateral obstruction, advanced chronic kidney disease
      • Calcium, phosphorous, bicarbonate, magnesium, and uric acid levels are effective in screening
      • Parathyroid hormone—if hypercalcemia and hypophosphatemia
      • 25-hydroxyvitamin D level—in hypercalcemia
    • Urinalysis and culture—presence of hematuria or infection
      • Proteinuria and glucosuria—worrying for tubular dysfunction as a complication for prolonged or severe nephrolithiasis
  • Metabolic evaluation
    • Urine osmolality
    • Urine pH
    • Most appropriate method of urine collection is still a matter of debate
      • 24 h urine collection can be achieved in toilet trained children
        • Analyzed for calcium, oxalate, uric acid, sodium, citrate, creatinine levels, volume, pH, and cystine
      • Not toilet trained—solute/creatinine ratio in single spot urine
        • Ratio of calcium, uric acid, citrate and oxalate levels to creatinine level in random urine sample
    • Microscopic urinalysis for crystalluria - not diagnostic unless hexagonal crystals (cystine) or coffin lid–shaped triple phosphate crystals (struvite) are seen
    • Stone analysis
      • Stone composition can change over time, therefore recurrent stones should be analyzed as well
      • Methods of analysis—radiograph diffraction, infrared
    • Spot urine beta-2-microgloblulin—screening for Dent disease in recurrent calcium-based calculi
  • Imaging
    • Role in:
      • Establishing diagnosis,
      • Elucidating size location and burden of stones,
      • Identifying urinary tract abnormalities
      • Detecting complications
    • Plain abdominal x-ray53
      • Sensitivity in detection of renal calculi 45–58%, can pick up 50% of bladder calculi
      • While many stones are radio-opaque, calculi comprising of uric acid, cystine, xanthine
    • Non contrast CT if US non-diagnostic despite clinical suspicion or when anatomical details needed to guide surgical planning

Treatment Options and Their Outcomes

Medical Treatment

Acute management

  • Adequate pain relief—paracetamol, NSAIDs, opioids—equally effective, combination therapy being superior to single agents
  • Parenteral hydration if not tolerating fluid
  • Treat for UTI if suspected
  • Strain urine for stone
  • Medical dissolution therapy rarely used


Goals are to prevent formation of new stones and expansion of existing ones.

Recurrent stone disease in augmentation cystoplasty is an ongoing concern. Cohen et al reported 63% recurrence after 5 year follow-up.54 Thomas et al found 38% recurrence in their review.55

Higher risk patients are those who are sedentary, wheelchair bound and with closed bladder necks. These patients require a more concentrated effort towards prevention with the use of irrigation and mucous clearance.

  1. General
    • Increasing urine volume—in all types of stones
      • No matter the crystallized solute, role for decreasing solute concentration and therefore supersaturation, allowing for a lower concentration for nucleation and growth
      • Especially important in warmer climates and during summer
    • Decreasing salt consumption
      • Excess salt intake is couples with increased excretion of urinary calcium
    • In endemic bladder calculi, improving nutritional status, preventing diarrhea and fever, frequent voiding to avoid prolonged stasis of urine in the bladder
  2. Specific
    • Calcium stones
      • Hypercalcinuria and hypocitraturia
        • Urine ca can be reduced by decreasing dietary sodium
        • Dietary ca should not be restricted—decreases intestinal oxalate absorption, necessary for growing bones
        • Fruits and vegetables high in citrate can be an effective part of dietary regimen to prevent stones
        • Potassium citrate—dual advantage of decreasing urinary calcium and increasing urine citrate
        • When diet not successful alone then thiazide diuretics—reduce urinary calcium excretion by increasing calcium absorption in proximal tubule
        • Potassium sparing diuretics (amiloride)—enhance calcium reabsorption
      • Hyperoxaluria
        • Avoid high oxalate foods—spinach, rhubarb, nuts, chocolate, coffee, dark tea
        • Pyridoxine (vitamin B6)—decreases urine oxalate
        • Oxalobacter formigenes—oral intestinal colonization degrades intestinal oxalate, resulting in decreased blood and urine oxalate levels— novel therapy56
    • Cystinuria
      • Significantly increase fluid intake
      • Maintain urine pH between 7–7.5—cystine solubility increases dramatically in alkaline urine—with the use of potassium citrate and potassium bicarbonate
      • D-pencillamine and tipronin—sulfhydryl compounds, cleave cystine into two cysteine-disulfide moieties that are 50 times more soluble than cystine
        • If D-penicillamine used long term then should be supplemented with pyridoxine (vitamin B6
    • Captopril—also sulfhydryl agent, used with mixed results
    • Infection related stones
      • Formed in presence of bacteria which produce urease, causing breakdown of urea to ammonium and bicarbonate—results in alkaline urine which promotes formation of struvite and carbonate apatite stones
      • Prevention includes
        • Sterilization of urinary tract—only possible after infected stone has been removed
        • Correction of underlying anatomic abnormalities
        • Protection from infection
        • Urine acidification
        • Acetohydroxamic acid, a urease inhibitor, successful in adults, has not been used in children
    • Uric acid stones
      • Urine alkalization—potassium citrate - increases solubility of uric acid
      • Dietary purine restriction
        • Meat increases uric acid excretion but should not be limited in growing children unless excessive in patient with uric acid stones
      • If needed, allopurinol can be added, as it reduces uric acid levels.57

Bladder Irrigation

Bladder irrigation protocols with saline and gentamicin, reducing the mucus and bacteriuria are shown to be helpful in reducing the incidence of stones.34 Use of hemiacidrin in bladder irrigation was thought to have an adjunctive role in decreasing particles after stone removal.29

  • High volume (250 mL) daily washout with saline reduces recurrence of stone formation compared to 120 mL / 60 mL washout. Also reduces bacterial load and recurrent UTI.58 With daily high volume irrigation the incidence is < 5% over 10 years follow up.38
  • Hensle et al reduced the incidence of stone occurrence from 36 to 7% incidence with a bladder washout irrigation regime. They used 120–240 mL saline with a flush of Gentamicin once a week.34
  • Kronner et al also reported a 7% incidence of stone formation after the use of a washout regime.41
  • Recurrent stone formers—use of mucolytic has been trialled, however has not been shown to benefit, although it is still advocated by some in the event of severe mucous production.38
  • Washout with acetylcysteine solution (10 mL in 20% acetylcyteine solution with 40 mL saline) 2–4 times per day for severe mucous.59 They did a high frequency follow up to ensure compliance. 28 children included with formation of stones in 7%.

Type of Augment

  • Seromuscular bladder augmentation recorded no calculi after an average 75 month follow up (range 36–120 months).51
  • Stone development is rarely seen with gastrocystoplasties as it could be attributed to less mucus, acidic pH and less bacteriuria.32,41
  • It is advisable to not use non absorbable staples or wires in surgeries involving the urine reservoir-exstrophy bladder pubis closures or bowel for augmentation.
  • New technology with autologous and tissue engineered augments are still in the experimental phase of development and may show some promise against the development of stones.60


Fruits and vegetables containing magnesium, potassium, phytates and citrate may contribute to reducing the calcium load and thus calcium stone formation, but this action may be mitigated due to the oxalate content in some vegetables. Increasing fruit and vegetable intake in children with hypocitraturia is protective.61

Animal proteins, red meat and poultry, with sulphur containing amino acids (methionine, cystine, homocysteine and taurine) can result in net acidemia with resultant hypocitraturia and those rich in purines can lead to hyperuricosuria. Both hypocitraturia and hyperuricosuria can result in stone disease.62

The daily recommended sodium intake is recommended to be less than 1.5 g for children aged 1–3 years, less than 1.9 g for ages 4–8 years, less than 2.2 g for ages 9–13 years and less than 2.3 g for ages 14–18 years.

Low calcium intake does not correlate with low stone formation, rather high calcium intake may bind with enteral oxalate, reducing oxalate absorption and thus reducing urinary oxalate excretion.63

The dietary approach to stop hypertension (DASH) encourages low fat dairy products, lean meats, fish and poultry, whole grains, legumes, fruits and vegetables. DASH helps in reducing red meat and fructose intake, adequate calcium intake and increasing the urinary citrate. It may risk increasing the oxalate intake. In one study, participants with highest DASH scores had a low relative risk of urinary stone disease.64

Surgical Treatment

Traditional surgical management of bladder stones relate to the size and type of stones. Large stones either require open surgery or endoscopic or percutaneous litholapaxy. The added difficulty in the augmented bladder is risk of bladder rupture and access to the bladder. Often these children have conditions that made urethral access difficult, such as those with structural anomalies or surgically closed bladder necks.

Treatment is classified as below

  • Endoscopic
    • Electrohydraulic (less common due to mobility of stones)
    • Ballistic / pneumatic
    • Ultrasonic
    • Combination
    • Laser Holmium YAG
    • Last Thulium
  • Extracorporeal Shock Wave Lithotripsy (ESWL)
  • Open


Endoscopic technology in the late 1990s emerged to allow better access for the pediatric population. Endoscopic management including dilation of the urethra in selected older patients was performed, with electrohydraulic lithotripsy or simple extraction with forceps or basket retrieval.65

Access to the bladder can be achieved via the urethra, or if present, via the Mitrofanoff or Monti channel.

Percutaneous Access with Cystoscopic Guidance

Percutaneous access is also feasible, and seems to compare favorably when compared to the open group, without the complications of open surgery.66 Percutaneous cystolitholapaxy has become the treatment of choice for children, due to difficulty with the size restrictions of the male urethra.67

A guidewire is placed percutaneously with cystoscopic visualization, and the tract dilated to allow insertion of an access sheath such as the Amplatz sheath (Cook Medical, US) in various sizes. A nephroscope can then be used for direct stone retrieval or litholapaxy.68 Other instruments for percutaneous access are also possible such as a laparoscopic port.49 In order to prevent trauma to the bladder with lithotripsy equipment a laparoscopic entrapment bag can be used to capture the stones before fragmentation and extraction.69

Transvesical laparoendoscopic single site surgery has been described for primary bladder stones, however not in patients with augmented bladders.70

Mitrofanoff / Monti Channel Access

Complete stone retrieval is possible via the catheterizable channel. This requires serial dilation and the use of a sheath such as the Amplatz. This method has been shown to be safe without significant trauma to the catheterizable channel.55

More recently smaller scopes such as a 12 Fr mini PCNL kit have been reported with successful outcomes.71

Open surgery may still be required for large stones that are not amenable for minimally invasive access.72 This occurrence is less likely with current surveillance regimes and with prevention strategies outlined below.

Open Surgery

In a recent systematic review of > 1,000 cases Davis et al found that open surgery, transurethral and percutaneous cystolitholapaxy has comparable stone free rates, and ESWL was less effective.73

Suggested Follow-Up

  • In the augmented patient, annual abdominal radiograph and ultrasound is suggested to surveillance.74


Bladder stones are a long-known issue that has troubled us for millennia. Most are associated with bacterial infection and 80% in male patients. Bladder augmentation using small or large bowel is associated with stone formation, from infection and mucous production. Urine composition can be altered either with diet, medication or flushing to help prevent the stones from forming. Surgical treatment is mainly endoscopic, with the ability to access the bladder percutaneously for excellent clearance without damage to the urethra.

Key Points

  1. Urinary stones occur in augmented bladder in up to 50%, with increased incidence if catheterizable channel is used within 3 years of augmentation, and sedentary patients.
  2. Infection, metabolic factors, type of operation and staples play a role in stone formation. Stones are largely calcium oxalate and calcium phosphate or struvite if infection related.
  3. Diet management, medical therapy and bladder washout may reduce the risk of stone formation
  4. Continuous surveillance is necessary.
  5. Multimodality treatment with use of endoscopic, laser, shockwave lithotripsy all has a role in individualized management of this children.


  1. Ellis H. A History of Bladder Stone. J R Soc Med 1979; 72 (4): 248–251. DOI: 10.1177/014107687907200403.
  2. Stevenson A. Predynastic Egyptian Figurines. Oxford Handbooks Online 1905. DOI: 10.1093/oxfordhb/9780199675616.013.004.
  3. Schwartz BF, Stoller ML. The Vesical Calculus. vol. 27, Urologic Clinics of North America; 2000, DOI: 10.1016/b978-1-4832-0048-4.50016-3.
  4. López M, Hoppe B. History, epidemiology and regional diversities of urolithiasis. Pediatr Nephrol 2010; 25 (1): 49–59. DOI: 10.1007/s00467-008-0960-5.
  5. Bowen DK, Tasian GE. Pediatric Stone Disease. vol. 45, Urologic Clinics of North America; 2018, DOI: 10.1007/s11934-009-0025-8.
  6. Sas DJ, Hulsey TC, Shatat IF, Orak JK. Increasing Incidence of Kidney Stones in Children Evaluated in the Emergency Department. J Pediatr 2010; 157 (1): 132–137. DOI: 10.1016/j.jpeds.2010.02.004.
  7. Ang AJS, Sharma AA, Sharma A. Nephrolithiasis: Approach to Diagnosis and Management. Indian J Pediatr 2020; 87 (9): 716–725. DOI: 10.1007/s12098-020-03424-7.
  8. Kusumi K, Becknell B, Schwaderer A. Trends in pediatric urolithiasis: patient characteristics, associated diagnoses, and financial burden. Pediatr Nephrol 2015; 30 (5): 805–810. DOI: 10.1007/s00467-014-3012-3.
  9. Wang W, Fan J, Huang G, Li J, Zhu X, Tian Y, et al.. Prevalence of kidney stones in mainland China: A systematic review. Sci Rep 2017; 7 (1): 41630. DOI: 10.1038/srep41630.
  10. Soliman NA, Rizvi SAH. Endemic bladder calculi in children. Pediatr Nephrol 2017; 32 (9): 1489–1499. DOI: 10.1007/s00467-016-3492-4.
  11. Asper R. Epidemiology and socioeconomic aspects of urolithiasis. Urol Res 1984; 12 (1): 1–5. DOI: 10.1007/bf00256301.
  12. Philippou P, Moraitis K, Masood J, Junaid I, Buchholz N. The Management of Bladder Lithiasis in the Modern Era of Endourology. Urology 2012; 79 (5): 980–986. DOI: 10.1016/j.urology.2011.09.014.
  13. Sinno K, Boyce WH, Resnick MI. Childhood Urolithiasis. J Urol 1979; 121 (5): 662–664. DOI: 10.1016/s0022-5347(17)56932-3.
  14. Marquardt H, Nagel R. Urolithiasis in childhood. Urology 1982; 9 (6): 627–629. DOI: 10.1016/0090-4295(77)90307-7.
  15. Madani A, Kermani N, Ataei N, Esfahani ST, Hajizadeh N, Khazaeipour Z, et al.. Urinary calcium and uric acid excretion in children with vesicoureteral reflux. Pediatr Nephrol 2012; 27 (1): 95–99. DOI: 10.1007/s00467-011-1936-4.
  16. Garcia-Nieto V. Urinary calcium excretion in children with vesicoureteral reflux. Nephrol Dial Transplant 2003; 18 (3): 507–511. DOI: 10.1093/ndt/18.3.507.
  17. ROBERTS JP, ATWELL JD. Vesicoureteric Reflux and Urinary Calculi in Children. Br J Urol 1989; 64 (1): 10–12. DOI: 10.1111/j.1464-410x.1989.tb05514.x.
  18. Kokorowski PJ, Routh JC, Hubert KC, Graham DA, Nelson CP. Association of Urolithiasis with Systemic Conditions Among Pediatric Patients at Children’s Hospitals. J Urol 2012; 188 (4s): 1618–1622. DOI: 10.1016/j.juro.2012.02.019.
  19. Cambareri GM, Kovacevic L, Bayne AP, Giel D, Corbett S, Schurtz E, et al.. National multi-institutional cooperative on urolithiasis in children: Age is a significant predictor of urine abnormalities. J Pediatr Urol 2015; 11 (4): 218–223. DOI: 10.1016/j.jpurol.2015.04.021.
  20. Biers SM, Venn SN, Greenwell TJ. The past, present and future of augmentation cystoplasty. BJU Int 2012; 109 (9): 1280–1293. DOI: 10.1111/j.1464-410x.2011.10650.x.
  21. Cartwright PC, Snow BW. Bladder Autoaugmentation: Early Clinical Experience. J Urol 1989; 142 (2 Part 2): 505–508. DOI: 10.1016/s0022-5347(17)38798-0.
  22. Churchill BM, Aliabadi H, Landau EH, McLorie GA, Steckler RE, McKenna PH, et al.. Ureteral Bladder Augmentation. J Urol 1993; 150 (2 Part 2): 716–720. DOI: 10.1016/s0022-5347(17)35596-9.
  23. Bramble FJ. The Treatment of Adult Enuresis and Urge Incontinence by Enterocystoplasty. Br J Urol 1982; 54 (6): 693–696. DOI: 10.1111/j.1464-410x.1982.tb13626.x.
  24. Adams MC, Mitchell ME, Rink RC. Gastrocystoplasty: An Alternative Solution to the Problem of Urological Reconstruction in the Severely Compromised Patient. J Urol 1988; 140 (5 Part 2): 1152–1156. DOI: 10.1016/s0022-5347(17)41986-0.
  25. Basiri A, Hosseini Moghaddam SMM, Khoddam R. Augmentation cystoplasty before and after renal transplantation: long-term results. Transplant Proc 2002; 34 (6): 2106–2108. DOI: 10.1016/s0041-1345(02)02869-5.
  26. Rigamonti W, Capizzi A, Zacchello G, Capizzi V, Zanon GF, Montini G, et al.. Kidney Transplantation into Bladder Augmentation or Urinary Diversion: Long-Term Results. Transplantation 2005; 80 (10): 1435–1440. DOI: 10.1097/
  27. Lebowitz RL, Vargas B. Stones in the urinary bladder in children and young adults. AJR Am J Roentgenol 1987; 148 (3): 491–495. DOI: 10.2214/ajr.148.3.491.
  28. Hendren WH, Hendren RB. Bladder Augmentation: Experience with 129 Children and Young Adults. J Urol 1990; 144 (2 Part 2): 445–453. DOI: 10.1016/s0022-5347(17)39486-7.
  29. Blyth B, Ewalt DH, Duckett JW, Snyder HM. Lithogenic Properties of Enterocystoplasty. J Urol 1992; 148 (2 Part 2): 575–577. DOI: 10.1016/s0022-5347(17)36657-0.
  30. DeFOOR WILLIAM, MINEVICH EUGENE, REDDY PRAMOD, SEKHON DAVINDER, POLSKY ETHAN, WACKSMAN JEFFREY, et al.. Bladder Calculi After Augmentation Cystoplasty: Risk Factors And Prevention Strategies. J Urol 2004; 172 (5): 1964–1966. DOI: 10.1097/01.ju.0000140911.43898.15.
  31. Edlund C, Peeker R, Fall M. Clam Ileocystoplasty: Successful Treatment of Severe Bladder Overactivity. Scand J Urol Nephrol 2001; 35 (3): 190–195. DOI: 10.1080/003655901750291944.
  32. KAEFER MARTIN, HENDREN WHARDY, BAUER STUARTB, GOLDENBLATT PETER, PETERS CRAIGA, ATALA ANTHONY, et al.. Reservoir Calculi: A Comparison Of Reservoirs Constructed From Stomach And Other Enteric Segments. J Urol 1998; 160 (6 Part 1): 2187–2190. DOI: 10.1016/s0022-5347(01)62290-0.
  33. Obermayr F, Szavay P, Schaefer J, Fuchs J. Outcome of Augmentation Cystoplasty and Bladder Substitution in a Pediatric Age Group. Eur J Pediatr Surg 2011; 21 (02): 116–119. DOI: 10.1055/s-0030-1267223.
  34. Hensle TW, Bingham J, Lam J, Shabsigh A. Preventing reservoir calculi after augmentation cystoplasty and continent urinary diversion: the influence of an irrigation protocol. BJU Int 2004; 93 (4): 585–587. DOI: 10.1111/j.1464-410x.2003.04664.x.
  35. Palmer LS, Franco I, Kogan SJ, Reda E, Gill B, Levitt SB. Urolithiasis in Children Following Augmentation Cystoplasty. J Urol 1993; 150 (2 Part 2): 726–729. DOI: 10.1016/s0022-5347(17)35598-2.
  36. Zhang H, Yamataka A, Koga H, Kobayashi H, Lane GJ, Miyano T. Bladder stone formation after sigmoidocolocystoplasty: statistical analysis of risk factors. J Pediatr Surg 2005; 40 (2): 407–411. DOI: 10.1016/j.jpedsurg.2004.10.012.
  37. Mathoera RB, Kok DJ, Nijman RJM. Bladder calculi in augmentation cystoplasty in children. Urology 2000; 56 (3): 482–487. DOI: 10.1016/s0090-4295(00)00663-4.
  38. Husmann DA. Lessons learned from the management of adults who have undergone augmentation for spina bifida and bladder exstrophy: Incidence and management of the non-lethal complications of bladder augmentation. Int J Urol 2018; 25 (2): 94–101. DOI: 10.1111/iju.13417.
  39. Szymanski KM, Misseri R, Whittam B, Lingeman JE, Amstutz S, Ring JD, et al.. Bladder stones after bladder augmentation are not what they seem. J Pediatr Urol 2016; 12 (2): 98.e1–98.e6. DOI: 10.1016/j.jpurol.2015.06.021.
  40. Nurse DE, McInerney PD, Thomas PJ, Mundy AR. Stones in enterocystoplasties. BJU Int 1996; 77 (5): 684–687. DOI: 10.1046/j.1464-410x.1996.97311.x.
  41. KRONNER KEVINM, CASALE ANTHONYJ, CAIN MARKP, ZERIN MICHAELJ, KEATING MICHAELA, RINK RICHARDC. Bladder Calculi In The Pediatric Augmented Bladder. J Urol 1998; 160 (3 Pt 2): 1096–1098. DOI: 10.1097/00005392-199809020-00035.
  42. Schlomer BJ, Copp HL. Cumulative incidence of outcomes and urologic procedures after augmentation cystoplasty. J Pediatr Urol 2014; 10 (6): 1043–1050. DOI: 10.1016/j.jpurol.2014.03.007.
  43. Salama AK, Misseri R, Hollowell N, Hahney B, Whittam B, Kaefer M, et al.. Incidence of nephrolithiasis after bladder augmentation in people with spina bifida. J Pediatr Urol 2021; 17 (4): 521.e1–521.e7. DOI: 10.1016/j.jpurol.2021.03.012.
  44. Veenboer PW, Ruud Bosch JLH, Asbeck FWA van, Kort LMO de. Urolithiasis in adult spina bifida patients: study in 260 patients and discussion of the literature. Int Urol Nephrol 2013; 45 (3): 695–702. DOI: 10.1007/s11255-013-0445-8.
  45. Garzotto MG, Walker RD. Uric Acid Stone and Gastric Bladder Augmentation. J Urol 1995; 153 (6): 1976. DOI: 10.1097/00005392-199506000-00083.
  46. Holcomb GW. Stone formation after augmentation cystoplasty: The role of intestinal mucus. J Pediatr Surg 1997; 33 (5): 805. DOI: 10.1016/s0022-3468(98)90260-3.
  47. Hamid R, Robertson WG, Woodhouse CRJ. Comparison of biochemistry and diet in patients with enterocystoplasty who do and do not form stones. BJU Int 2008; 101 (11): 1427–1432. DOI: 10.1111/j.1464-410x.2008.07492.x.
  48. Dangman BC, Lebowitz RL. Urinary tract calculi that form on surgical staples: a characteristic radiologic appearance. AJR Am J Roentgenol 1991; 157 (1): 115–117. DOI: 10.2214/ajr.157.1.2048508.
  49. Chatterjee US, Chatterjee I. Percutaneous cystolithotomy in augmented bladders. J Indian Assoc Pediatr Surg 2021; 26 (4): 250. DOI: 10.4103/jiaps.jiaps_128_20.
  50. Silver RI, Gros D-AC, Jeffs RD, Gearhart JP. Urolithiasis in the Exstrophy-Epispadias Complex. J Urol 1997; 158 (3 Pt 2): 1322–1326. DOI: 10.1097/00005392-199709000-00175.
  51. Kaefer M. Commentary to ‘Outcomes of Seromuscular Bladder Augmentation versus Standard Ileocystoplasty: A Single Institution Experience over 14 years.’ J Pediatr Urol 2017; 13 (2): 200 1–200 5. DOI: 10.1016/j.jpurol.2016.05.030.
  52. Levitt SB. Editorial: Options For Management Of Reservoir Calculi. J Urol 1998; 160 (6 Part 1): 2191–2191. DOI: 10.1016/s0022-5347(01)62291-2.
  53. Copelovitch L. Urolithiasis in Children. vol. 59, Pediatric Clinics of North America; 2012, DOI: 10.1007/978-94-011-5396-6_46.
  54. Mandeville JA, Gnessin E, Lingeman JE. Imaging Evaluation in the Patient With Renal Stone Disease. Semin Nephrol 2011; 31 (3): 254–258. DOI: 10.1016/j.semnephrol.2011.05.006.
  55. Cohen TD, Streem SB, Lammert G. Long-Term Incidence and Risks for Recurrent Stones Following Contemporary Management of Upper Tract Calculi in Patients with a Urinary Diversion. J Urol 1996; 155 (1): 62–65. DOI: 10.1097/00005392-199601000-00019.
  56. Canning DA. Re: Paediatric Cystolitholapaxy through the Mitrofanoff/Monti Channel. J Urol 2018; 204 (3): 606–606. DOI: 10.1097/ju.0000000000001169.04.
  57. Alon US. Medical treatment of pediatric urolithiasis. Pediatr Nephrol 2009; 24 (11): 2129–2135. DOI: 10.1007/s00467-007-0740-7.
  58. Scoffone CM, Cracco CM. Pediatric calculi. Curr Opin Urol 2018; 28 (5): 428–432. DOI: 10.1097/mou.0000000000000520.
  59. Meschi T, Maggiore U, Fiaccadori E, Schianchi T, Bosi S, Adorni G, et al.. The effect of fruits and vegetables on urinary stone risk factors. Kidney Int 2004; 66 (6): 2402–2410. DOI: 10.1111/j.1523-1755.2004.66029.x.
  60. Borofsky MS, Bird VG. A Prospective Study of Dietary Calcium and Other Nutrients and the Risk of Symptomatic Kidney Stones. 50 Studies Every Urologist Should Know 1993; 328 (12): 189–192. DOI: 10.1093/med/9780190655341.003.0033.
  61. Ali A, Khan Q, Jafar TH. Kidney Stones and Chronic Kidney Disease. Urolithiasis 2016; 2: 587–593. DOI: 10.1007/978-1-4471-4387-1_74.
  62. Taylor EN, Fung TT, Curhan GC. DASH-Style Diet Associates with Reduced Risk for Kidney Stones. J Am Soc Nephrol 2009; 20 (10): 2253–2259. DOI: 10.1681/asn.2009030276.
  63. Palmer LS, Franco I, Reda EF, Kogan SJ, Levitt SB. Endoscopic management of bladder calculi following augmentation cystoplasty. Urology 1994; 44 (6): 902–904. DOI: 10.1016/s0090-4295(94)80179-7.
  64. Docimo SG, Orth CR, Schulam PG. Faculty Opinions recommendation of Cumulative incidence of outcomes and urologic procedures after augmentation cystoplasty. Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature 1998; 4 (1): 43–45. DOI: 10.3410/f.718363797.793514373.
  65. Salah MA, Holman E, Khan AM, Toth C. Percutaneous cystolithotomy for pediatric endemic bladder stone: experience with 155 cases from 2 developing countries. J Pediatr Surg 2005; 40 (10): 1628–1631. DOI: 10.1016/j.jpedsurg.2005.06.039.
  66. Ahmadnia H, Kamalati A, Younesi M, Imani MM, Moradi M, Esmaeili M. Percutaneous treatment of bladder stones in children: 10 years experience, is blind access safe? Pediatr Surg Int 2013; 29 (7): 725–728. DOI: 10.1007/s00383-013-3320-x.
  67. Tan YK, Gupta DM, Weinberg A, Matteis AJ, Kotwal S, Gupta M. Minimally Invasive Percutaneous Management of Large Bladder Stones with a Laparoscopic Entrapment Bag. J Endourol 2014; 28 (1): 61–64. DOI: 10.1089/end.2013.0127.
  68. Roslan M, Przudzik M, Borowik M. Endoscopic intact removal of medium-size- or multiple bladder stones with the use of transvesical laparoendoscopic single-site surgery. World J Urol 2019; 37 (2): 373–378. DOI: 10.1007/s00345-018-2358-8.
  69. Sakly A, Zakhama W, Mahjoubi Z, Sidhom W, Lahouel Y, Mnasser A, et al.. Paediatric cystolitholapaxy using mini PCNL-kit through the Mitrofanoff stoma. Ann Med Surg (Lond) 2021; 62: 88–91. DOI: 10.1016/j.amsu.2021.01.007.
  70. Nang R, Hinchi H, Lafia T, Rami M, Belkacem R. Giant vesical lithiasis, complication of enterocystoplasty: case report. Pan Afr Med J 2018; 31: 132. DOI: 10.11604/pamj.2018.31.132.15995.
  71. Davis ND, Donaldson J, Neisius A, Petrik A, Seitz C, Thomas K, et al.. Treatment outcomes of bladder stones in children: A systematic review of >1000 cases on behalf of the European Association of Urology Urolithiasis Guideline Panel. Eur Urol 2021; 79: S451. DOI: 10.1016/s0302-2838(21)00697-7.
  72. Walker RD. The management of the failed bladder neck procedure in patients with spina bifida. BJU Int 2016; 92 (1): 35–37. DOI: 10.1046/j.1464-410x.92.s1.13.x.
  73. Heijkant M van den, Haider N, Taylor C, Subramaniam R. Efficacy of bladder irrigation and surveillance program in prevention of urinary tract infections and bladder calculi in children with an ileocystoplasty and bladder neck repair. Pediatr Surg Int 2011; 27 (7): 781–785. DOI: 10.1007/s00383-011-2913-5.
  74. The Kelalis-King-Belman textbook of clinical pediatric urology. Sixth edition, Boca Raton: CRC Press; 2017, DOI: 10.1111/j.1464-410x.2007.06893.x.
  75. Coplen DE. Cutting for Stone in Augmented Bladders–What is the Risk of Recurrence and is it Impacted by Treatment Modality? Yearbook of Urology 2014; 2014 (5): 278–279. DOI: 10.1016/j.yuro.2014.07.035.

Last updated: 2023-02-22 15:40