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Safaa. M Abdel Rahman MD Lecturer of pediatric nephrology Cairo university Pediatric renal stones

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Definitions Epidemiology Types Aetiology Genetic basis Clinical presentations Diagnosis Management

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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

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Uric acid /Glomerular >yrs