This document provides an overview of pediatric urolithiasis (urinary stones in children). Some key points: - Infection and metabolic abnormalities are major causes of stones in children. - Metabolic evaluation is essential for every child to identify underlying conditions. - Stones are most commonly calcium-containing, struvite, or uric acid. - Common metabolic abnormalities include hypercalciuria, hyperoxaluria, cystinuria, and hypocitraturia. - Treatment involves managing the underlying condition, increasing fluid intake, and sometimes surgery or lithotripsy as in adults. Thorough evaluation is needed to identify causes and guide management.

1. PEDIATRIC
UROLITHIASIS
Elsayed SALIH, MD.

2. Introduction
 Urinary calculi in children, account 2–3% of all
patients with stone disease.
 Infection remains a major aetiological factor
 the proportion of affected children with an
underlying biochemical predisposition appears to
be increasing.
 Metabolic evaluation is essential for every child.
 The rate of stone recurrence is lower in children
compared with adults.
 The majority of stone disease is now managed, as
in adults, by lithotripsy or endourological
techniques
 Open surgery has decreased dramatically.

3. Epidemiology
 Geographical variations in the incidence of stone in
children reflect differences in the prevalence of
environmental, dietary and genetic factors.
 In the UK the incidence of urinary calculi in children is 3
new cases per million of the population per year.
 infective calculi are more common in boys under 5 years
of age
 there is an increased incidence of metabolic
abnormalities.
 The greater frequency of infection in uncircumcised
infants explain the higher incidence of stone in certain
European countries compared with the US where
circumcision remains common.

4. Epidemiology
 stones is twice as high in boys as it is in girls.
 the peak age of presentation is younger in
boys, being 3 years vs 4 years in girls.
 This gender difference reflects in part the role
of bacterial colonisation and subsequent UTI
in uncircumcised boys.
 A geographical ‘stone belt’ extending from the
Balkans across Turkey, Pakistan and northern
India is characterised by a high incidence of
endemic bladder stones in children.

5. Pathology/aetiology
 Urinary calculi are composed of crystalline and
matrix components in varying proportions.
 Matrix, a gelatinous glycoprotein, is a particular
feature of infective stones, which are typically soft
and crumbly in composition.
 Metabolic stones, e.g. cystine and xanthine, are
predominantly crystalline and correspondingly
harder.
 The terminology historically used to describe the
crystalline structure of urinary calculi (‘struvite’,
‘brushite’, ‘weddellite’, etc.) is uninformative
 stones are categorised by chemical composition.

6. Pathophysiology
 Formation of stone
 Urinary volume
 pH
 Presence of promoters or inhibitors of
lithogenesis
 Central event is supersaturation
 Crystallization occurs via homogenous vs.
heterogenous nucleation

7. Pathophysiology
Saturation
Crystal growth
and aggregation
Supersaturation
Crystal
Retention
Stone formation
Nucleation

8. Factors involved in stone
formation
1. Urinary concentration, ionic activity and
solubility of stone-forming constituents.
2. Presence of abnormal urinary metabolites or
pathologically elevated concentration of
normal urinary constituents.
3. Urinary infection
4. Anatomical abnormalities of the urinary tract.
5. Foreign materials.
6. Prematurity.

9. Urinary concentration, ionic activity and
solubility of stone-forming constituents.
 Stone formation is initiated by the precipitation
of urinary constituents from solution, followed
by crystal formation.
 In turn, this process is influenced by the
urinary excretion rate of the stone-forming
substance, the level of hydration and the
urinary pH.

10. Presence of abnormal urinary metabolites or
pathologically elevated concentration of
normal urinary constituents.
 When a metabolite is excreted in high
concentrations its saturation
 point in the urine is exceeded and crystal
deposition occurs, progressing to stone
formation.
 Reduced urinary output, leading to a higher
urinary concentration of the metabolite
 unfavourable urinary pH, will accelerate this
process.

11. Urinary infection
 Proteus, Klebsiella and Pseudomonas, are
capable of the enzymatic splitting of urea to
produce NH3, elevation of the urinary pH and
precipitation of ammonium salts.
 Infection is a factor in the production of the
proteinaceous matrix component of calculi.

12. Anatomical abnormalities of the
urinary
tract.
 Stasis of urine within an obstructed or dilated
urinary tract creates an environment in which
stone-forming substances are more likely to
precipitate out of solution and thus initiate
stone formation.
 This process can occur in sterile urine, but not
uncommonly infection and stasis coexist.

13. Foreign materials
 Non-absorbable foreign bodies, usually
surgical in origin act as a nidus of encrustation
and stone formation:
i. stents
ii. fragments of catheters
iii. non-absorbable sutures
iv. staples

14. Prematurity
 premature children are much greater risk of
nephrocalcinosis and nephrolithiasis.
 20% of babies born under 32 weeks gestation
develop nephrocalcinosis and 5–9% have calculi.
 The risks are increased with increasing prematurity
of birth, decreasing birth weight, co-morbidity and
the use of furosemide, thiazides.
 formula-fed babies have increased solute excretion
(e.g. oxalate).
 parenteral nutrition have a higher oxalate and
calcium but lower citrate excretion

15. Frequency
 calcium with phosphate or oxalate (57%),
 struvite (24%),
 uric acid (8%),
 cystine (6%),
 endemic (2%),
 mixed (2%),
 other types (1%).

16. Classification
 Enzyme Disorders
Primary Hyperoxaluria
Type I: glyoxylic aciduria
Type II: glyceric aciduria
Xanthinuria
1,8-Dihydroxyadeniuria
Lesch-Nyhan syndrome

17. Classification
 Renal tubular syndromes
Cystinuria
Renal tubular acidosis
 Hypercalcemic states
HyperPTH
Immobilization

18. Classification
 Uric Acid Lithiasis
 Enteric urolithiasis
 Idiopathic calcium oxalate urolithiasis
Hypercalciuria (Absorptive and Renal)
Hyperoxaluria
Hyperuricosuria
Hypocitraturia
Medications

19. Classification
 Endemic bladder stone formation
 Secondary urolithiasis
Infection
Obstruction
Structural abnormalities
Urinary diversion procedures
Foreign body

20. Metabolic Classification
Calcium Stones Non-Calcium
Hypercalciuria
-Absorptive
-Renal
-Resorptive
Uric Acid
Hyperuricosuria Cystine
Hyperoxaluria
-Primary
-Enteric
Struvite
Hypocitraturia
-RTA I
Amonium Acid Urate
Hypomagnesuria Indinavir

21. Hypercalciuria
Absorptive
GI ABSORPTION
PLASMA CA
PTH URINARY CA

22. Absorptive Hypercalciuria
 Type I (Diet Independent)
 High urinary calcium despite diet
 Type II (Diet dependent)
 Responds to calcium restriction
 Type III (phosphate leak)
 Low serum phosphate with increased Vit D and increased GI
absorption
 Sarcoidosis
 Increased Vit D-->increased GI absorption

23. Hypercalciuria
Renal Leak
Urinary Calcium
PTH
GI Absorption
Bone Resoprtion
Plasma Calcium

24. Hypercalciuria
Resorptive (PTH)
PTH
Urinary Ca
Bone Resorption GI Absorption
Plasma Ca

25. Hypercalciuria
Intestinal
Absorption
Fasting
Urinary Ca
PTH
High
High
High
High
High
High
High
Low-
High
Normal
Low
HighSerum Ca
ResorptiveRenalAbsorptive

26. Hyperuricosuria
 Diet high in purines
 Renal tubular defects
 Defect in renal tubular urate reabsorption
 Chemotherapy
 Recurrent calcium oxalate stones (nidus)
 Chemotherapy
 Catabolic State
 Urine pH <5.5
 Serum uric acid and calcium normal

27. Primary Hyperoxaluria
• Inherited disorder of glyoxylate metabolism
• Type I: Alanine-glyoxylate aminotransferase (1 in
120,000 births)
• Median age at presentation 5 yrs
• Oxalate deposition occurs in bones
• Screen all patients with stones for hyperoxaluria
• Type II
• D-glycerate dehydrogenase
• ESRD less common

28. Primary Hyperoxaluria
• ESRD
• 50% of patients by age 15 and 80% by age 30
• Therapy
• High urinary flow
• Pyridoxine supplements
• Liver/Kidney Transplant

29. Enteric Hyperoxaluria
Bowel Disorder
Fat malabsorption
Excess fats bind to
intestinal Ca
Insufficient calcium to
bind oxalate
Unbound oxalate

30. Hypocitraturia
 Citrate is potent stone inhibitor
 Caused by
 acidosis (RTA)
 Hypokalemia
 High animal protein diet
 UTI

31. RTA
 Type I
 Defect in distal tubule to excrete acid
 Dx with systemic acidosis and urine pH>5.5
 Osteomalacia in children
 Infants: growth retardation/vomitting/diarrhea
 Type II
 Defect in bicarb reabsorption (nephrocalcinosis not
seen)
 Type IV
 Nephrocalcinosis not seen

32. Type I RTA
 May be a secondary manifestation
 Sjogren’s, Wilson’s, Jejunoileal bypass
 Hypokalemic,hyperchloremic metabolic acidosis
 Diagnostic workup indicated when
nephrocalcinosis or recurrent nephrolithiasis
 Ammonium chloride load testing (urinary pH
should fall below 5.5)
 Stones composed of calcium phosphate

33. Calcium Stones Misc
 Immobilization of children is most common
cause of secondary hypercalciuria
 Hypomagnesuria increases solubility of Ca,
phosphate
 Most common cause is IBD

34. Uric Acid Lithiasis
 5% of calculi in pediatric patients
 Orange (can be mistaken for blood)
 Dysfunction of tubular reabsorption
 Wilson’s disease
 Fanconi syndrome
 Overproduction of uric acid
 Lesch-Nyhan (deficiency of hypoxanthine-guanine
phosphoribodyl transferase)
 Neurological disabilties, present between 3-12 “orange sand in
diaper”
 Type I glycogen storage disease
 Myeloproliferative disorders

35. Uric Acid Lithiasis
 Increased intake
 Uricosuric drugs (probenecid, salicylate)
 Chronic diarrheal syndromes (net alkali defecit and
lowered urine volume)
 Treatment
 Increasing oral fluid intake
 Urinary alkalinization pH 6.5 to 7.0
 Allopurinal (but can lead to xanthine stones)

36. Cystinuria
 Autosomal recessive disorder
 1 in 15,000 live births
 1-3% of children with metabolic urolithiasis
 Defective transport of cystine, ornithine, lysine
and arginine
 Treatment
 High fluid intake (<300 mg cystine/L of urine)
 Urinary alkalinzation
 D-peniclliamine or Thiola (better tolerated)
 Captopril

37. Xanthinuria
 Enzymatic deficiency of xanthine
dehydrogenase
 Urolithiasis, arthropathy, myopathy, crystal
nephropathy, or renal failure

38. Infection Stones
 2-3% of stones in pediatric population
 Urinary pH >6.8 (urease)
 Proteus, pseudomonas, klebsiella,
streptococcus, mycoplasma
 Treatment
 Hemiacidrin irrigation
 Acetohydroxamic acid (urease inhibitor)

39. Misc Stones
 Triamterene stones
 Sulfadiazine stones
 Indinavir stones

40. Underlying urological
conditions
 In 20–30% of children with urinary calculi,
 VUR play an aetiological role by promoting
urinary infection
 PUJ obstruction are characteristically small
and multiple (fancifully likened to melon
seeds).
 megaureters
 The use of intestinal segments for bladder
reconstruction (enterocystoplasty)

41. Clinical presentation
1. Age
 Stones may develop from as early as 2–3
months of life.
 a higher prevalence in early childhood (less
than 5 years due to an excess of infective
stones
2. Urinary infection
 older children present with symptoms of UTI
 In infants: vague ill health, low-grade fever and
failure to thrive.

42. 3. Haematuria
 Macroscopic or microscopic
4. Passage of stone
5. material per urethra
 a fragment or some softer matrix material

43. 6. Pain
 Acute renal colic of the pattern and severity
encountered in adults is not a prominent
feature of the symptomology in children.
 When pain does occur it is often a poorly
localised symptom in a fractious, unwell child.
7. Abdominal mass

44. Differential Diagnoses
1. Hematuria
2. Hemolytic-Uremic Syndrome
3. Hemorrhagic Fever With Renal Failure Syndrome
4. IgA Nephropathy
5. Medullary Sponge Kidney
6. Munchausen Syndrome by Proxy
7. Nephritis
8. Polycystic Kidney Disease
9. Pyelonephritis
10. Renal Cortical Necrosis
11. Urinary Tract Infection
12. Xanthinuria

45. Diagnosis
Two levels.
A. Initial screening for possible calculi
1. Urine analyis
2. Ultrasound
3. Abdominal X-ray
4. Unenhanced spiral computed tomography

46. Diagnosis
2. Evaluation prior to treatment of proven
stone disease
1. DMSA
2. Dynamic renography
3. Intravenous urography
4. Micturating cystography
5. Metabolic investigations
6. Stone screening

47. Ultrasound
 a sensitive modality for the detection of renal
calculi.
 Depending on their physical characteristics
(chemical composition, hardness, etc.), calculi
can be directly visualised on ultrasound.
 Ureteric calculi and small bladder calculi may
sometimes be difficult to detect on ultrasound.

48. Ultrasound appearances of renal calculi,
illustrating ‘acoustic shadow

50. KUB
 mandatory to look for possible calculi in any
child with:
 haematuria.
 urinary infection in boys less than 5 years of
age.
 a documented Proteus urinary infection at any
age

51. KUB
Radiopaque OR Radiolucent
Calcium Oxalate
Uric Acid
Calcium phosphate
Trimaterene
Struvite
Cystine
Silica
Xanthine

52. Plain X-ray revealing multiple infective
calculi in the left kidney.

53. Unenhanced spiral computed
tomography
 provides an accurate diagnosis within minutes,
 avoids the risk of adverse reaction to contrast
media
 Detection of radiolucent calculi
 the radiation dosage is three to five times greater
than that of IVU
 Radiation dosage amounts to only a quarter of the
recommended limit of medical radiation exposure
for a child in a year.
 greater difficulty in interpreting the images of the
collecting system.

54. Unenhanced spiral computed
tomography
 children are 3 to 10 times more radiosensitive
than adults
 Long-term risks of radiation exposure in children
are not completely understood
 a single abdominal CT in a one-year-old imparts
a 1 in 550 risk of subsequent lethal tumor
development
 Recently, there has been interest in development
of low-dose CT techniques for use in the
diagnosis of renal stones.

55. CT renal stones

56. CT with 3D reconstruction volume rendering.
Shows stone configuration in PA, Oblique and AP
view

57. Intravenous urography
 IVU permitting visualisation of nonopaque
stones
 Information on calyceal anatomy for PCNL
and ESWL
 Ureteric calculi are best localised IVU
 detection of anatomical abnormality
predisposing to urolithiasis.

58. Intravenous urogram demonstrating a
calculus in a single (orthotopic) ureterocoele.

59. DMSA
 differential function in the affected kidney(s)
should be documented on DMSA
(dimercaptosuccinic acid), and re-evaluated
after treatment.

60. Dynamic renography
 Dynamic renography, e.g. MAG3
(mercaptoacetyltriglycine), DTPA
(diethylenetriamine pentaacetic acid)
undertaken if obstruction is suspected.
 the diagnosis of obstruction should not be
made in the presence of a large calculus
within the renal pelvis.
 Diagnosis of junction PUJ obstruction can only
be made after a period of time following the
complete removal of the stone.

61. Micturating cystography
 MCU is not routinely required.
 Infection and the passage of stone
material to the bladder may result in
transient VUR
 If ureteric dilatation persists
postoperatively, an MCU should be
performed.

62. METABOLIC EVALUATION
The goals of the metabolic evaluation
 identify children at increased risk for recurrent
stone disease
 diagnose specific treatable metabolic
derangements.

63. Metabolic evaluation

64. Spot’, i.e. untimed, urine sample 2–5 ml (divided
in the laboratory into two aliquots)
 First aliquot acidified and analysed for
creatinine, calcium, magnesium, cystine,
oxalate
 Second aliquot alkalinised and analysed for
creatinine and uric acid

65. URINALYSIS/CULTURE
 The urine pH can suggest the types of crystals
that are most likely to form.
 A low urine pH, associated with uric acid
stones.
 A high pH associated with infection stones and
renal tubular acidosis.
 urine pH varies over the course of the day
 Microscopic urinalysis may identify distinctive
crystal structure, such as the flat hexagonal
crystals formed by cystine stones.

66.  Urinary leukocytes, nitrites, and leukocyte
esterase may suggest the presence of infection.
 A urine culture should be obtained to investigate
bacterial colonization of the urinary tract.
 A calcium-to-creatinine ratio can be derived from a
single specimen and is often used as an initial
screening test for hypercalciuria.
 If hypercalciuria is suspected based on a random
spot sample this should be confirmed with a 24-h
urine collection.
 If cystiunuria is suspected, a nitroprusside test
can verify the presence of cystine

67. Calcium oxalate monohydrate

68. Calcium oxalate dihydrate

69. Calcium phosphate brushite

70. Uric acid

71. Struvite

72. Cystine

73. SERUM TESTING
 not as informative as urine studies,
 Provide information for interpretation of urine test
results.
 Serum creatinine can identify renal insufficiency
and is used to calculate the expected excretion
of creatinine in a given urine sample.
 Bicarbonate and pH levels can help diagnose
and classify renal tubular acidosis.
 Serum calcium and phosphate levels are used to
evaluate for hypercalcemic conditions.

74. SERUM TESTING
 If abnormal, specific investigation of
parathyroid function (i.e. PTH) should be
obtained.
 Irregularities of serum potassium and
magnesium can be associated with
abnormalities of urinary stone inhibitors.
 Elevated serum urate found with
abnormalities in the metabolism of
purines.

75. 24-H URINALYSIS
 Because of variation in diet and fluid intake,
results from two separate 24-h urine
collections, ideally six weeks after the patient
achieves a stone-free status, should be used
to guide treatment.
 To ensure that there is a complete 24-h
collection of urine, a total creatinine should be
greater than 15-20 mg/kg.
 When interpreting 24-h urine results, it is
important to remember that adult reference
values are not necessarily applicable to the
pediatric population.

76. Adult and pediatric reference values for 24-
hour urinalysis

77. Bonn risk index (BRI)
 better predict recurrent calcium oxalate stone
formation.
 The BRI is the ratio of ionized urinary calcium
to the amount of ammonium oxalate required
to induce calcium oxalate crystallization in 200
ml of urine.
 BRI values in children with renal stones are
15-fold higher when compared to healthy
children.
 Future research on the BRI is required to
define its potential as a predictor of stone
formation in asymptomatic children.

78. Management
 The overall goals of care are as follows:
1. To prevent additional renal damage, which
may lead to loss of renal parenchyma
2. To manage pain associated current stone(s)
3. To expedite passage or removal of any
stones present
4. To prevent new stones from forming.
 may include medical approaches, surgical
interventions, and dietary modification.

79. Conservative Treatment
 Medical care largely depends on the type of
presentation.
 Care may range from observation to emergency
treatment.
 An obstructed infected portion of the urinary tract is a
surgical emergency
 A child presenting with acute colic and gross
hematuria can be managed with analgesics.
 Narcotics may be required, as well as enteral or
parenteral hydration.
 When a stone is small and at the ureteropelvic or
ureterovesical junction, it may pass spontaneously; a
few days of observation for spontaneous passage
may be indicated prior to more aggressive
intervention.

80.  A stone that completely obstructs the bladder
outlet should be treated with catheterization
using a Foley catheter.
 Children with asymptomatic stones detected
while screening for another problem should
have blood and urine testing performed to
identify underlying metabolic abnormalities.

81. Treatment Options
 ESWL
 Up to 75-98% stone free rates at 3 months with
stones up to 2.5 cm
 Children can pass larger stone fragments than adults
 Long term functional studies on pediatric patients
show no change in RPF or height after 4 yrs
 Abdominal/flank discomfort in early post-op period
should have eval for hematoma/obstruction
 Hemoptysis in small stature and skeletal deformities
 Prone positioning may be necessary

82. Treatment Options
 ESWL relative contraindications
 Morbid obesity
 Large stone burden
 Increased stone density
 Congenital skeletal/renal abnormalities
 Previously failed ESWL

83. Treatment Options
 Ureteroscopy
 First reported in 1929 by Young
 2 types of ureteroscopes: mini-rigid and flexible
 Varying lengths
 Distal tip as small as 4.7 Fr
 Working channel 3.6 Fr

84. Treatment Options
 Ureteroscopy: Instruments
 Stone retrieval devices can vary
 Size, position, and condition (impacted?)
 Grasping forceps will disengage from a stone if it
is lodged (more effective for solitary stone)
 Helical basket for steinstrasse
 Nitinol baskets for caliceal stones and lower pole
stones

85. Treatment Options
 Intracorporeal lithotripsy
 Ultrasonic lithotripsy (1953)
 Ballistic (pneumatic)
 Electrohydraulic (EHL)
 Laser (1992)

86. Treatment Options
 Ureteroscopy technique
 Dilation required in up to 30%
 Graduated single shaft dilator from 6 to 10 Fr (dilate to 2 Fr
sizes greater than diameter of endoscope)
 May require passive dilation with stent
 Smallest access sheath 9.5 Fr
 Presence of previous reimplant can require initial
cannulation with actively deflecting guidewire
 Recurrent reflux after URS has never been reported
 Intrarenal access after UPJ repair is straightforward
 Impacted stones may require dislodging into proximal
dilated ureter for lithotripsy

87. Treatment Options
 Percutaneous Endourology
 11 Fr and 15 Fr peel away sheaths have been used
 A 24 Fr adult defect equals a 72 Fr defect in a child
 A larger sheath is necessary for treatment of larger
stones >3 cm
 Multiple punctures may be needed
 Upper pole access can cause pneumo/hydrothorax
 Uncontrolled hemorrhage refractory to a tamponade
balloon requires angiography
 Dilutional hyponatremia is possible

88. Treatment Strategies
 Renal Calculi
 ESWL for stones <2 cm
 Contraindication with UPJ obstruction, caliceal
diverticulum, or infundibular stenosis
 Less effective for ectopic or horseshoe kidneys
 Overall, best suited for solitary renal stones <1.5 cm
not contained within an abnormal lower pole calyx or
abnormal renal anatomy

89. Treatment Strategies
 Renal Calculi
 Percutaneous approach
 Intrarenal stones >2cm, multiple large calculi, urinary
tract malformations, previous reconstruction
 Sandwich approach
 Laparoscopy with failure of percutaneous access

90. Treatment Strategies
 Ureteral calculi
 ESWL effective 54-100%
 Ureteroscopic lithotripsy is 77-100%
 Orifice dilation only necessary 33%
 Becoming first line for ureteral stones
 Percutaneous approach with impacted stones,
significant hydro, or urosepsis

91. Treatment Strategies
 Bladder Calculi
 Open cystolithotomy
 Cystolithopaxy
 EHL can perf augmented bladder
 Percutaneous approach

92. MET in children
 MET in children cannot be recommended due
to the limited data in this specific population
(small study).
 Alpha-1 adrenergic blocker agents, such as
doxazosin (0.03 mg/kg/day), have been used
as medical expulsive treatment in children with
distal uretral stones

93. Treatment (cont.)
 In children with hypercalciuria:
- Some reduction in calcium and sodium
intake is necessary
-Thiazide diuretics also reduce renal
calcium
excretion.
-Addition of potassium citrate, an inhibitor
of calcium stones, with a dosage of
1-2 mEq/kg/24hr is beneficial.

94. Treatment (cont.)
 In patients with uric acid stones:
- allopurinol is effective
 In patients with cystine stones:
- Alkalinization of urine with sodium
bicarbonate or sodium citrate is effective.
 D- penicillamine, which is a chelating
agent that binds to cysteine or
homocysteine, increasing the solubility of
the product

95. Treatment (cont.)
 Treatment of type 1 RTA
- Involves:
*Correcting the metabolic acidosis
*Replacing lost potassium and sodium
 Treatment of primary hyperoxaluria
- Involves:
* Liver transplantation
* Kidney transplantation

96. Question #1
 What are the 5 most important chemical
abnormalities in stone formers?
Low urinary volume
Hyperoxaluria
Hyperuricosuria
Hypocitraturia
Hypercalciuria

97. Question #2
 What is the strongest chemical promoter of
stone production?
Oxalate

98. Question #3
 What are the three types of hypercalciuria?
Resorptive
Renal
Absorptive

99. Question #4
 What is the medication of choice for renal
hypercalciuria?
Thiazide diuretics augment calcium reabsorption in the
distal and proximal tubules

100. Question #5
The stones least suitable for ESWL are:
1. Calcium oxalate dehydrate
2. Uric Acid
3. Struvite
4. Calcium oxalate monohydrate
5. Cystine

101. Question #6
The ideal treatment for large staghorn calculi
>2.5 cm is:
1. ESWL
2. Multi Access PCNL
3. ESWL followed by PCNL
4. PCNL followed by ESWL
5. Anatrophic pyelolithotomy

102. Question #7
The factors predicting stone clearance after ESWL
for lower pole stones include all except:
1. Infundibulopelvic angle
2. Laterality
3. Renal function
4. Infundibular length
5. Infundibular width

103. Question #8
The best treatment for a 2 cm renal stone with a
UPJO
1. Open pyelolithotomy
2. URS
3. ESWL
4. PCNL with endopyelotomy
5. Retrograde endopyelotomy with laser litho

104. Question #7
The mechanism of stone fragmentation during
ESWL include all the following except
1. Compression fracture
2. Spallation
3. Cavitation
4. Passive Expansion
5. Dynamic fatigue

105. Question #8
What is the most common renal structural
abnormality identified in patients with calcium
containing stones?
1. UPJ obstruction
2. Infundibular obstruction
3. Calyceal obstruction
4. Medullary sponge kidney
5. Proximal tubule obstruction

106. Question #9
Adverse reactions to D-penicllamine include
1. Constipation
2. Diarrhea
3. Melena
4. Visual disturbances
5. Liver toxicity

107. Question #10
Urease-producing bacteria hydrolyze urea
to which of the following?
1. Uric acid
2. Carbon monoxide
3. Carbon dioxide
4. Ammonium and carbon dioxide

108. THANK YOU