approach to a child with renal stone

1. EVALUATION OF RENAL
STONE IN CHILDREN
Presented By-
DR. AZMERY SAIMA
DR. RAKHI MAITRAYEE BHOWMIC
PHASE A ( NEONATOLOGY)
Bangabandhu Sheikh Mujib Medical
University (BSMMU), Dhaka.

2. Case scenario
• A 15 year old boy admitted in hospital with the
complaints of severe left flank pain ,
haematuria for 10 days. But patient has no
fever, gave history of inadequate fluid intake.
Family history of nephrolithiasis positive.

3. INTRODUCTION
 Kidney Stones, also known as renal
calculus or nephrolith, are small, hard deposits of
mineral and acid, salts on the inner surfaces of the
kidneys.
 If stones grow to sufficient size they can cause
blockage of the ureter.

4. • Urolithiasis- stone in urinary tract.
• Nephrolithiasis- stone in renal tissue.
• Nephrocalcinosis- deposition of calcium in
the substance of the kidney.

5. EPIDEMIOLOGY
• Urinary lithiasis in children is related to
genetic, climatic, dietary & socioeconomic
factors.
• The incidence is increasing : in 1996 the rate of
symptomatic nephrolithiasis was 7.9 in 10000,
whereas in 2007 it was 18.5 in 10000 .
• Approximately 7% of urinary calculi occur in
children younger than 16 year of age.

6. EPIDEMIOLOGY
• The prevalence of pediatric urolithiasis in
developed countries had fallen following
improved socioeconomic condition, but
currently is increasing. This may be explained
by an increase in diagnosis secondary to
improved diagnostic technique.

7. INCIDENCE
 Urinary calculi are more common in men than in women.
(3:1)
 Incidence of urinary calculi peaks between the 3rd and 5th
decades of life.
 80% of stones under 2mm in size
 90% of stones pass through the urinary system
spontaneously
 There is seasonal variation with stone occurring more often
in the summer months.

8. STONE FORMATION
 Highly concentrated urine constituents crystallize and
harden to form calculi.
 Kidney stones form when urine contains more crystal-
forming substances - such as calcium, oxalate and uric
acid.
 At the same time, urine may lack substances that prevent
crystals from sticking together, creating an ideal
environment for kidney stones to form.
 The crystals get deposited on the nucleus and continue to
grow. These can some times adhere to the renal papillae.

9. Inhibitors and promotors of stone
formation
INHIBITORS
Inhibits crystal Growth -
 Citrate
 Magnesium
 Pyrophosphate
 Zinc
Inhibits crystal Aggregation
 Glycosaminoglycans
 Tamm- Horsfall Protein

10. PROMOTERS
 Bacterial Infection
 Anatomic Abnormalities – PUJ obst.
 Altered Ca and oxalate transport in renal
epithelium.
 Prolonged immobilisation.
 Increased uric acid levels - taking increased
purine subs– promotes crystalisation of Ca
and oxalate

11. Stone formation
• Stone formation depends on four factors:
1. Matrix
2. Precipitation-crystallization
3. Epitaxy
4. Absence of inhibitors of stone
formation in the urine

13. TYPES OF KIDNEY STONES
 Calcium oxalate
 Calcium phosphate
 Struvite
 Uric acid
 Cystine

15. Fig: staghorn calculi

16. Calcium stones: Most kidney stones are calcium
stones, usually in the form of calcium oxalate and
calcium phosphate. Oxalate is a naturally
occurring substance found in food. Some fruits
and vegetables, as well as nuts and chocolate,
have high oxalate levels.

17. Uric Acid: This type of kidney stone is more
common in men than in women. They can occur
in people with gout or those going through
chemotherapy.
Struvite: This type of stone is found mostly in
women with urinary tract infection. These stones
can be quite large and cause urinary obstruction.
Cystine: Cystine stones are rare. They occur in
both men and women who have the genetic
disorder cystinuria.
Other: Other, rarer types of kidney stones also
can occur. Such as xanthine, dihydroadenine
stone, indinavir etc.

18. RISK FACTORS
HIGH MINERAL CONTENT IN
DRINKING WATER
DEHYDRATION
FAMILY OR PERSONAL
HISTORY
DIETARY INTAKE
BEING OBESE

19. PATHOPHYSIOLOGY
• Slow urine flow, resulting in super saturation of the urine.
• Damage to the lining of the urinary tract
• Decreased inhibitor substances in the urine that would otherwise
prevent super saturation and crystalline aggregation.

20. Approach to diagnosis of renal stone

21. Approach to renal stone
1. Detailed history
2. Clinical examination
3. Relevant Investigations

22. HISTORY
• Age – uncommon in children.
• Sex- more common in male (3:1)
• Geography -More in southeast Asia.
• Climatic & geographic factors
• Occupation – sedentary lifestyle.

23. HISTORY…
Presentation is variable.
• Children may present initially with-
loin pain (50%),abdominal pain
haematuria
features of UTI, N, V
dysuria, urgency, frequency
may be asymptomatic

25. • Birth history- PT (12-64%), LBW, diuretics, duration
of oxygen therapy.
• Family history of nephrolithiasis, consanguinity
• Past illness – similar type illness, IBD, Cystic fibrosis,
malignancy.
• Dietary history-Fluid intake, vitamin & mineral
suplementation, tea, coffee, dairy products, spinach,
beet, peanuts.
• Personal history- immobility, bowel habit (cr.
Diarrhoea).
• Drug history-Loop diuretics, corticosteroid, is
geeting chemotherapy.

26. • An underlying metabolic abnormality –
symptoms of thirst
polyuria, anorexia, muscle cramps,
abdominal & bone pain
• Evaluation of growth & development,
bone structure, blood pressure.

27. Presentation
• Factors
–Size of stone
–Location of stone
–Degree of obstruction
–Presence of infection
–Presence/absence of normal contralateral
kidney

28. Clinical feature:

29. Renal stone:
• 1.Recurrent flank pain or renal colic
occurs in 40-75% of children or
Abdominal pain
• 2.Gross or Microscopic hematuria in 33-
90% of children
• 3.Repeated attack of UTI
• 4.Occasionally the stone may be silent &
leads to obstructive uropathy .

30. Ureteric
Calculus
1. Always of Renal Origin
2. Commonly of elongated shape
3. Can get impacted at 3
constrictions of ureter
4. Can cause:
Obstruction
Hydronephrosis
Infection
Ureteral Stricture
5. C/F:
Colicky Pain (from loin to tip
genitalia)
Hematuria, dysuria, frequency,
strangury
Tenderness in iliac fossa

31. Bladder Calculus
1. Primary vesical calculus:
• occurs in sterile urine
• Comes down from kidney through
ureter and gets enlarged in
bladder (usually oxalate stone).
• Can irritate bladder mucosa
causing hematuria
2. Secondary vesical calculus:
• Occurs in presence of infection
(commonest bladder stone)
• Usually phosphate stone, occurs in
bladder only

32. Urethal stone:
• Dysuria
• Inability to void/difficulty voiding.
• Present with terminal hematuria
• It is uncommon to pass urethral calculus
without symptoms

33. Investigations for Urolithiasis:
• 1.Imaging
Plain X-ray
Ultrasonography
IVU
CT abdomen

34. • URINE for
Routine analysis(including & specific gravity)
Culture
Spot specimen: Ca, protein, uric acid, oxalate, citrate ,Mg,
creatinine.
24hr urine:
Volume, protein, creatinine, Na, Ca, Mg, oxalate,
phosphorus, uric acid, citrate, cystine.
• Stone analysis.
P
H

35. BLOOD for
• Urea
• Creatinine
• Electrolytes
• PH
• HCO3
• Ca
• Phosphorus
• Uric acid
• Citrate
• Cystine
• CBC

36. Imaging: Plain X-ray KUB
• Not useful
– Radioluscent stone
– Stone <4mm
– Lies over sacrum/bony structures
• Bowel gas can obscure its efficacy
• Cannot differentiate
– Stones
– Calcified LN
• Sensitivity: 50-70%

37. X-ray findings:
75% radiopaque

38. Imaging: KUB Ultrasound
• Sensitivity to detect renal calculi ~95% (complement KUBXR)
• Very sensitive to detect obstruction and radioluscent
stone,Hydronephrosis
• Non-invasive
• May miss small stone (<5mm) and ureteral stone

39. Imaging: IVU
• Provide anatomical and functional informations
• Size and location of the stone
• Presence and severity of obstructions
• Renal and ureteral abnormalities

40. IVU:

41. CT Scan Renal Stone
On CT almost all stones are opaque(has
96% sensitivity& specificity), but vary
considerably in density.
1. calcium oxalate +/- calcium
phosphate: 400-600HU
2. struvite (triple phosphate): usually
opaque but variable
3. uric acid: 100 - 200HU
4. cysteine: opaque
5. HIV medication related stones
(indinavir) difficult to visualize

42. Urine analysis:

43. Normal urinary excretion of important
constituents:
Constit
uent
24hrs excretion
Ca Less than 4mg/Kg
Protein Less than 100mg/m2
Oxalate Less than 2mg/Kg
Mg More than 0.8mg/Kg
Uric
acid
Less than 35mg/kg
Cystine Below 10yrs :less than 13
mg/1.73m2
Above 10yrs :30-50
mg/1.73m2
Citrate More than 320 mg/1.73m2
Creatini
ne
Newborn: 8-10mg/Kg
Child: 15-20mg/Kg

44. Method of stone analysis

45. Test Procedure Observation
1- pH
Sample + 1 drop of universal
indicator
Yellow- red:
Acidic
Green: Neutral
Blue: Alkaline
2-Carbonate Sample + 2 drops of 2N HCL Effervescence
3-Oxalate Sample mixed with equal
portion of resorcinol +1 drop
of conc. Sulphuric acid
Dark blue green
color
4-Phosphate Sample + mixture of [2 drops
of cobalt chloride + 2 drops
of Na CN ]+ 1 drop of 10N
NaOH
Blue color
5-Calcium Sample + 2 drops of H2O + 2
drops of 2N HCL + 5 drops
Gelatinous PPt.

46. 6- Cystine
Sample + 2 drops of NaOH
10% + 1 drop of amm.
Hydroxide 25% + 2 drops
of Na CN allow to stand for
5 min. + few crystals of
sodium nitroprusside
Red color
7-
Ammonium
salts
Sample+ 2 drops NaOH
10% + 5 drops of cobalt
chloride
Blue color
8-Uric acid Sample + 2 drops of NaOH
mix. + 3 drops of
phosphotungestic acid
Blue color
9-
Magnesium
Sample + 2 drops of
NH4OH 25% + 2 drops
Gelatinous
white PPt.

47. How to Investigate Urolithiasis??Urine
- RME
- 24 hour
urine
collectio
n
- Urine
C+S
Blood
- CBC
- Renal
Profile
Imaging
- KUB X-
ray
- KUB
Ultrasoun
d
- IVU
Plan for
Intervention
- DTPA
If IVU
contraindicate
d
- CTU

48. Algorithm for the investigation of renal calculi:
Stone
Hypercalciuria
Hyperoxaluria(primary/enteri
c)
Hypocitraturia
Increased urinary
cystine(cystinuria)
Hyperuricaemia(IEM,Diuretic
)
Hyperuicosuria(IEM,TLS,Chr.
diarrhea)
Infection
Passed
In
urina
ry
tract
Mg
NH4
PO4
Paedia
tric
urologi
Hypercalcemia
Metabolic
acidosis(DRTA,PRTA)
Hypokalaemia(RTA,Bartter’s
)
Hypochloremia
Hypomegnesaemia
Captu
red
Ca
phosphat
e
Ca
OxalateCysti
ne
Uric
acid
Not
captur
ed
Metabolic evaluation
Not captured

49. Hypercalciuria:
Hypercalcaem
ia
Hypophosphatasia
vit D excess
Immobilization
malignancy
hyperparathyroidis
m
Yes
N
o
N
o
Metabolic
acidosis
Metabolic
alkalosis
N
o
Yes
Yes
Rickets,GF
,
aminoacid
uria,
glycosuria
,
acidosis
Hyperchlor
aemia,urina
ry p
H
6
Proximal
RTA,Fanconi’s
Syndrome,Tubulo-
interstitial disorder
Distal RTA
Bartter’s syndrome,loop
diuretics
Idiopathic hypercalciuria,
immobilization ,
Juvenile chronic arthritis
Dent’s disease
Medullary sponge
kidney
Haematuria,UTI,dilated
tubules on IVP
Low mol.
Wt.
proteinuria,f
am his
Electroly
tes,
urinalysi
s NAD

50. Case:Siam,6months old boy
presented with passage of sand like
substance during micturition and not
growing well since his 2months of
age.

51. Nephrocalcinosis
• Refers to renal parenchymal calcification. The
calcification may be dystrophic or metastatic.
1.With dystrophic calcification, there is deposition of
calcium in necrotic tissue. This type of parenchymal
calcification occurs in tumors, abscesses, and
hematomas.
2.Metastatic nephrocalcinosis occurs most often with
hypercalcemic states caused by hyperparathyroidism,
renal tubular acidosis, and renal failure.
Metastatic nephrocalcinosis can be
• further categorized by the location of calcium
deposition as cortical or medullary.

52. Causes of Nephrocalcinosis
• Causes of cortical nephrocalcinosis include
1. Acute cortical necrosis
2. Chronic glomerulonephritis
3. Chronic hypercalcemic states
ethylene glycol poisoning, sickle cell disease, and
rejected renal transplants
• Causes of medullary nephrocalcinosis include
1. Hyperparathyroidism (40%)
2. Renal tubular acidosis (20%)
3. Medullary sponge kidney
bone metastases, chronic pyelonephritis, cushing’s
syndrome, hyperthyroidism, malignancy, renal papillary
necrosis, vitamin D excess, and Wilson’s disease.