Christopher P. Coppola, Alfred P. Kennedy, Jr. and Ronald J. Scorpio (eds.)Pediatric Surgery2014Diagnosis and Treatment10.1007/978-3-319-04340-1_68
© Springer International Publishing Switzerland 2014
Pediatric Urolithiasis
(1)
Department of Urology, Geisinger Medical Center, 100 N. Academy Av. MC 13-16, Danville, PA 17822, USA
(2)
Department of Pediatric Urology, Janet Weis Children’s Hospital, 100 N. Academy Av. MC 13-16, Danville, PA 17822, USA
Abstract
The incidence of urolithiasis in all age groups has been increasing in the USA. Generally males are affected more than females. Almost equal distribution of kidney and ureteral calculi; low incidence of bladder calculi in pediatric population unless in children with bladder augmentations. Children can develop urolithiasis in the first decade of life but peak age affected is 20–50-years-old. Signs and symptoms of stone disease include irritability, abdominal pain, vomiting, diarrhea, and hematuria; symptoms become the more classic unilateral flank colicky pain and hematuria as the child ages.
The incidence of urolithiasis in all age groups has been increasing in the USA. Generally males are affected more than females. Almost equal distribution of kidney and ureteral calculi; low incidence of bladder calculi in pediatric population unless in children with bladder augmentations. Children can develop urolithiasis in the first decade of life but peak age affected is 20–50-years-old. Signs and symptoms of stone disease include irritability, abdominal pain, vomiting, diarrhea, and hematuria; symptoms become the more classic unilateral flank colicky pain and hematuria as the child ages.
1.
Pathophysiology:
(a)
Genetics: 20–40 % of patients have 1st or 2nd degree relative with history of stones.
(i)
Cystinuria: autosomal recessive defect in transport of cysteine, arginine, lysine, and ornithine in renal tubular and intestinal epithelium leading to recurrent stone disease from supersaturation; newborn screening checks for the 2 genes responsible (SLC3A1 and SLC7A9); accounts for 5–10 % pediatric stones
(ii)
Distal renal tubular acidosis (RTA type 1): urinary acidification defect; causes alkaline urine, hypokalemia, hypercalciuria, hypocitraturia leading to stone formation; can be autosomal dominant defect presenting in adulthood or autosomal recessive presenting in infancy with deafness, bone defects, and poor growth
(iii)
Other genetic disorders associated with urolithiasis: Lesch-Nyan syndrome, primary hyperoxaluria, and xanthine dehydrogenase deficiency.
(b)
Environmental: western diet high in sodium, animal protein, and carbonated beverages with phosphoric acid increase risk of urolithiasis.
(c)
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Metabolic:
(i)
Hypercalciuria: idiopathic, secondary to medications, hyperparathyroidism, RTA, hypermetabolic states from neoplasms.
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