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
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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.
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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
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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)
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Aetiology
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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.
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Drugs and stone formation Mechanism of Stone
FormationDrugPrimary 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 2. Glucocorticoid 3. Allopurinol (if
used in tumor lysis) 4. Loop diuretics 5. Calcium and vitamin D 1.
Uric acid 2. Calcium 3. Xanthine 4. Calcium oxalate 5. Calcium Drug
inhibits activity of carbonic anhydrase enzymes in the kidney,
causing metabolic acidosis, hypocitraturia, and elevated urine pH.
Topiramate, zonisamide, acetazolamideCalcium phosphate
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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
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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
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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
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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.
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Diagnosis Examinations Wt Ht Examination for 2ry cause - Distal
renal tubular acidosis -Oxalosis -IBD -Cystic fibrosis -Short-gut
syndrome
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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
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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