Pediatric renal stones
Safaa. M Abdel Rahman
MD
Lecturer of pediatric nephrology
Cairo university
Pediatric renal stones
Definitions
Epidemiology
Types
Aetiology
Genetic basis
Clinical presentations
Diagnosis
Management
Definitions
 Urolithiasis, kidney stones, renal stones, and renal
calculi are interchangeably used to refer to the accretion of
hard, solid, nonmetallic minerals in the urinary tract
 Nephrocalcinosis is a term that refers to increased
calcium content in the parenchyma of the kidney
Epidemiology
 Children can present with stones at any age (eg, premature
newborn to teenager). In children, calcium stones are most
common. The approximate frequency of kidney stone types
in the pediatric age group is calcium with phosphate or
oxalate (57%), struvite (24%), uric acid (8%), cystine (6%),
endemic (2%), mixed (2%), and other types (1%). With
children, particularly younger children, the primary cause of
stone formation (eg, hypercalciuria, hyperuricosuria) can
usually be identified with a through evaluation.
Type
 Calcium with phosphate or oxalate
 Purine derivatives
 Magnesium ammonium phosphate (struvite)
 Cysteine
 Combinations of the preceding items
 Drugs or their metabolites (eg, phenytoin, triamterene)
 Melamine-contaminated milk powder consumption
Aetiology
 Renal stones occur as a result of the following 3 factors:
 Supersaturation of stone-forming compounds in urine
 Presence of chemical or physical stimuli in urine that
promote stone formation
 Inadequate amount of compounds in urine that inhibit stone
formation (eg, magnesium, citrate)
Aetiology
Risk factors
 Habitually low urine volume
 High urine excretion of calcium
 High urine excretion of uric acid
 High urine excretion of oxalate
 Low urine pH: Uric acid and cysteine are less soluble in acid
urine.
 High urine pH: Struvite and calcium phosphate are less
soluble in alkaline urine.
Drugs and stone formation
Mechanism of Stone Formation
Drug
Primary Stone Composition
Crystallization of highly excreted, poorly
soluble drug or metabolite causes stone
formation.
Phenytoin, triamterene, sulfonamides,
felbamate, ceftriaxone, indinavir,
ciprofloxacin, guaifenesin/ephedrine
Drug or its metabolites
Drug may increase the concentration of
stone-forming minerals.
1. Anti-cancer drugs
1. Uric acid
2. Glucocorticoid
2. Calcium
3. Allopurinol (if used in tumor lysis)
3. Xanthine
4. Loop diuretics
4. Calcium oxalate
5. Calcium and vitamin D
5. Calcium
Drug inhibits activity of carbonic
Topiramate, zonisamide, acetazolamide
anhydrase enzymes in the kidney, causing
metabolic acidosis, hypocitraturia, and
elevated urine pH.
Calcium phosphate
Clinical presentation
 The size of the stone (larger stones tend to be more




symptomatic, although some large stones produce few
symptoms)
The location of the stone
The production of urinary outflow obstruction
The movement of the stone (eg, from the renal pelvis to
bladder)
The presence of infection
Clinical presentation
 The following are 5 fairly typical presentations of stone disease
in children:
1. Intense pain that suddenly occurs in the back and radiates
downward and centrally toward the lower abdomen or groin
2. Hematuria, usually gross, occurring with or without pain:
Hematuria may or may not be present.
3. Infection leading to radiologic imaging in which a stone is
identified
Clinical presentation
4. Asymptomatic stones, which are sometimes identified when
abdominal imaging is performed for another reason
5. Persistent microscopic hematuria, which consists of 5 or
more RBCs per high-power field in 3 of 3 consecutive
centrifuged urine specimens obtained at least 1 week apart
Diagnosis
History






Frequent urinary tract infections
frequent bouts of abdominal pain, hematuria (gross or
microscopic), passage of previous calculus
dietary intake (eg, oxalate, purine, calcium, phosphate,
fructose, animal protein)
drug intake (eg, anticancer drugs, glucocorticoids,
allopurinol, loop diuretics), vitamin intake (A, D), fluid
intake
habitual fluid type (eg, water, milk, tea, sports drinks),
The history should also include questions on chronic disease
(eg, renal tubular acidosis, inflammatory bowel disease,
short-gut syndrome, intractable seizures, cystic fibrosis),
prior urologic surgery (eg, kidney transplant), or recent
immobilization.
Diagnosis
Examinations
 Wt
 Ht
 Examination for 2ry cause
- Distal renal tubular acidosis
-Oxalosis
-IBD
-Cystic fibrosis
-Short-gut syndrome
Diagnosis
laboratory studies:
 Complete blood count (CBC)
 Electrolyte, blood urea nitrogen (BUN), creatinine, calcium,
phosphorus, alkaline phosphatase, uric acid, total protein,
albumin, parathyroid hormone (PTH), and vitamin D
metabolite levels
Diagnosis
laboratory studies:
 Spot urine analysis and culture, including ratio of calcium,
uric acid, oxalate, cystine, citrate, and magnesium to
creatinine
 Urine tests, including a 24-hour urine collection for calcium,
phosphorus, magnesium, oxalate, uric acid citrate, cystine,
protein, and creatinine clearance
 Uric acid /Glomerular >yrs <0.5mguric acid /dl of
glomerular filtrate
Calculated as uric acid x serum creatinine
urine creatinine
Diagnosis
Imaging
 Renal ultrasonography is very effective for identifying stones in
the urinary tract. Generally, ultrasonography should be used as a
first study. If no stone is found but symptoms persist,
 helical (spiral) computed tomography (CT) scanning is indicated.
Noncontrast spiral CT scanning is the most sensitive test for
identifying stones in the urinary system. It is safe, rapid, and has
been shown to have 97% sensitivity and 96% specificity.
 Plain abdominal x.ray .
 Intravenous pyelography is rarely used in children.
Diagnosis
Diagnosis
Evaluation of Stones
Attempting to obtain a stone for histologic and crystallographic
evaluation is essential
B.Hoppe, and Milliner , 2009
Treatment
Managements
Aim
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.
Managements
A. Conservative therapy
B. Surgical management of urolithiasis
C. Medical treatment
D. Monitoring
Managements
A. Conservative therapy
Obstructed renal stone
Non obstructed renal stone
Managements
A. Conservative therapy
 High fluid intake
 Diet
 A restriction of minerals after stone analysis
 Calcium stone: sodium and animal protein restriction
Excessive intake D is to be avoided
 hyperuricosuria may benefit from avoiding purine-rich
foods
Managements
B. Surgical management of urolithiasis
The specific aims of surgical care
 drainage of the urinary tract
 removal of stones present in the urinary tract
 surgical correction of anatomic abnormalities
Managements
C. Medical

1.
2.
Idiopathic hypercalciuria
Renal tubular calcium leak thiazid therapy
gastrointestinal (GI) absorptive and a low-calcium
diet does not return urinary calcium levels to the
reference range, neutral sodium phosphate
Hypocitraturia oral potassium citrate.
Managements
Medical
 Struvite stones
appropriate antibiotic.
Surgical intervention or ESWL may be necessary
 Uric acid stone
1. Alkalinization of urine with sodium bicarbonate or
potassium citrate in 4 divided doses (5-15 mL diluted in up
C.
to 6 oz water/juice PO PC & HS PRN
2. Xanthine oxidase inhibitors (Allopurinol)
10 mg/kg/day PO divided q12hr
Managements
Monitoring
 Effects of treatment should be monitored by
measurement of urinary and plasma chemistries 1 month
after initiating treatment and then every 2 months until a
steady state is established.
 Children on calcium restriction should have serum
calcium, parathyroid hormone (PTH), and urine calcium
excretion determined at onset, in 2 months, and then at
6-month intervals.
Managements
Monitoring
 Children receiving thiazides should have serum
electrolytes, cholesterol, uric acid, and urinary calcium
excretion measured at onset, at 2 months, and then at 6month intervals.
 Children receiving allopurinol should have a complete
blood count (CBC), liver function tests, and urinary uric
acid excretion tests performed every 2 months.
Managements
Monitoring
 Patients should undergo annual imaging with renal
ultrasonography to look for new or growing stones.
 Because of increased incidence of low bone density in
children with hypercalciuria and nephrolithiasis, (DEXA)
scanning should be performed at onset and then yearly in
children aged 5 years and older.
(Schwaderer et al 2008)