Version May 2024
INTRODUCTION — Kidney stones are increasingly recognized in children. The epidemiology and etiology of kidney stones in children will be reviewed here. The clinical manifestations, diagnosis, acute management, and prevention of recurrence are discussed separately. (See "Kidney stones in children: Clinical features and diagnosis" and "Kidney stones in children: Acute management" and "Kidney stones in children: Prevention of recurrent stones".)
EPIDEMIOLOGY
Incidence — The diagnosis of pediatric kidney stones has increased as illustrated by the following:
●A study using data from a commercial health claims database reported the annual rate of pediatric cases for urinary stone disease in the United States rose from 2005 to a peak of 65.2 cases per 100,000 person years in 2011 [1]. Similarly, in a study of a database that included all emergency visits, surgical procedures, and hospital admissions in the state of South Carolina, the incidence of such encounters for nephrolithiasis among individuals aged 15 to 19 years old increased by 25 percent every 5 years between 1997 and 2012 [2].
●An Israeli study based on reported histories during compulsory medical evaluations of 17-year-old military enlistees found the average prevalence rate increased from 69 to 120 cases per 100,000 individuals between the two time periods of 1980 to 1995 and 2010 to 2012 [3]. During the same time period, the authors also noted an increase in body mass index and hypothesized whether a possible association existed.
Data from the United States Pediatric Health Information System (PHIS) have shown a proportional increase in hospitalizations due to pediatric kidney stones with a diagnosis of kidney stones made in 1 case for every 685 pediatric hospitalizations [4,5].
Demographic features — Demographic factors that may affect the incidence of kidney stones include:
●Age – The incidence of kidney stones is lower in children than in adults, and the incidence increases with age, with adolescents having the highest risk of kidney stones [1,6-8]. In a population-based United States study of patients over 10 years of age, adolescents between 10 and 19 years of age accounted for only 4 percent of the total episodes of kidney stones [9]. For the total population, the incidence of kidney stones was 109 per 100,000 men per year and 36 per 100,000 women per year. The explanation for the lower pediatric incidence is unknown, but may be due in part to the higher concentrations of crystal formation inhibitors such as citrate and magnesium in the urine of children compared with adults [10,11].
●Sex – Children do not have the strong male predominance seen in adults with kidney stones. Some studies do show a slightly higher incidence in boys [5,12-17], whereas other studies, including some from Taiwan and the United States, have reported a higher incidence in girls compared with boys [1,2,18].
In the United States, sex distribution varied with age in children who were hospitalized for kidney stones [19]. Boys were more commonly affected in the first decade of life and girls in the second decade. This sex variation may reflect that boys are more likely to have obstructive urinary malformations resulting in kidney stones that typically present early, whereas there is an increase in the rate of urinary tract infections, another risk factor for kidney stones, in postpubertal sexually active girls [20].
●Geography – Similar to adults, the incidence of kidney stones in children varies worldwide, with the highest incidence occurring in endemic areas, such as in Turkey and Thailand. Data from the National Health Insurance Research Database reported that the risk of kidney stones was greater in children who lived in urban areas and in those with urinary tract infection [18].
Overview of risk factors — In children with kidney stones, an underlying risk factor is identified in as high as 75 to 85 percent of affected children [12-17]. In most children, kidney stones are associated with a urinary metabolic abnormality, urinary tract infection, and/or a structural kidney or urinary tract abnormality [12-17,21,22].
METABOLIC RISK FACTORS
Pathogenesis — The two mechanisms by which metabolic factors enhance stone formation include:
●Excessive solute concentration – High urinary concentrations of calcium, oxalate, uric acid, and cystine due to increased renal excretion and/or low urine volume cause solute excess. This leads to solute supersaturation and precipitation, and results in the formation of crystals, which may aggregate into stones.
●Decreased levels of inhibitors of stone formation – Natural inhibitors of urinary stone formation include citrate, magnesium, and pyrophosphate. Low levels of these inhibitors, particularly hypocitraturia, are associated with kidney stones in both adults and children.
In two case series of children with kidney stones, approximately 90 percent of patients had at least one metabolic risk factor [23,24]. Common risk factors include low urine flow rate, hypercalciuria and hypocitraturia.
Stone composition — In general, stone composition varies based on age and sex in both adults and children (figure 1). Based upon case series, the frequency of different stone composition in children is as follows [21,25,26]:
●Calcium oxalate – 45 to 65 percent
●Calcium phosphate – 6 to 30 percent
●Struvite – 4 to 13 percent
●Cystine – 2 to 5 percent
●Uric acid – 0 to 4 percent
●Mixed or miscellaneous – 4 to 32 percent
Hypercalciuria
Overview — Hypercalciuria is the most common metabolic abnormality associated with pediatric stone disease [27,28]. It is identified as the major contributing factor in at least half of the children with a metabolic cause for kidney stones [12,21].
Hypercalciuria may also cause nephrocalcinosis, a condition in which calcium salts precipitate out of solution within the kidney parenchyma. Hematuria, dysuria, and urinary frequency can be seen in children with hypercalciuria [29-31]. (See "Evaluation of gross hematuria in children" and "Evaluation of microscopic hematuria in children".)
Children with hypercalciuria and isolated microscopic hematuria are at risk for kidney stones. An observational study of children with hematuria found 58 children with hypercalciuria. Of those with hematuria and hypercalciuria, 17 percent (10/58) had developed a kidney stone within a mean interval of 13 months [31]. In another observational study of children with unexplained isolated hematuria, 13 percent (8/60) of patients with hypercalciuria had developed kidney stones within a one to four year follow-up period [29].
Definition — Hypercalciuria is defined as urinary calcium excretion rate that is greater than 4 mg/kg per 24 hours in a child greater than two years of age who is ingesting a routine diet (table 1) [32,33]. The diagnosis of hypercalciuria is discussed in detail separately. (See "Kidney stones in children: Prevention of recurrent stones", section on 'Definitions of specific urine metabolic abnormalities'.)
Pathogenesis — Three mechanisms contribute to higher urinary calcium excretion [34-38]:
●Increased intestinal absorption ("absorptive hypercalciuria") in which there is an increase in intestinal calcium absorption resulting in excess serum calcium and high urinary calcium excretion.
●Increased renal losses ("renal hypercalciuria") in which there is a defect in renal tubular calcium reabsorption resulting in an increase in urinary calcium excretion.
●Increased bone resorption ("resorptive hypercalciuria") in which the source of the excess calcium is bone.
Both genetic and environmental factors can affect these mechanisms, thereby increasing urinary calcium excretion and the risk for kidney stones. As an example, high dietary sodium intake increases urinary calcium excretion. (See "Kidney stones in adults: Epidemiology and risk factors", section on 'Sodium'.)
Genetic factors — There is evidence that many cases (and likely a majority of cases) of idiopathic hypercalciuria represent a complex interaction among many genes and environmental factors [39,40]. Proposed specific involvement includes genes that affect the calcium sensing receptor, calcium channels in the intestine and kidney, vitamin D receptor, enzymes related to vitamin D metabolism (eg, CYP24A1 deficiency), intestinal oxalate exchangers, renal and bone resorption, and renal excretion of calcium, oxalate, and citrate. (See "Kidney stones in adults: Epidemiology and risk factors", section on 'Family history'.)
Less commonly, a monogenic defect can cause hypercalciuria via any of the three physiologic mechanisms that results in kidney stones or nephrocalcinosis [38-40].
●Monogenic disorders that increase intestinal absorption of calcium include hypophosphatemia and absorptive hypercalciuria, enzymes related to vitamin D metabolism, congenital malabsorption disorders (ie, congenital lactase deficiency, congenital sucrase-isomaltase deficiency, and glucose/galactose malabsorption), and Blue diaper syndrome. (See "Hereditary hypophosphatemic rickets and tumor-induced osteomalacia" and "Etiology of hypercalcemia", section on 'Congenital lactase deficiency'.)
●Monogenic disorders that impair renal tubular calcium reabsorption include the following:
•Dent disease, also referred to as X-linked recessive kidney stones (see "Dent disease (X-linked recessive nephrolithiasis)")
•Bartter syndrome (see "Inherited hypokalemic salt-losing tubulopathies: Pathophysiology and overview of clinical manifestations")
•Wilson disease (see "Wilson disease: Clinical manifestations, diagnosis, and natural history", section on 'Other organs')
•Glycogen storage disease type 1a (see "Glucose-6-phosphatase deficiency (glycogen storage disease I, von Gierke disease)", section on 'Clinical features')
•Hereditary distal renal tubular acidosis (RTA) with identified mutations in either the basolateral chloride-bicarbonate cotransporter or in the apical hydrogen-ATPase (see "Etiology and diagnosis of distal (type 1) and proximal (type 2) renal tubular acidosis", section on 'Distal (type 1) RTA' and "Nephrolithiasis in renal tubular acidosis" and "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance")
•Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (see "Hypomagnesemia: Causes of hypomagnesemia", section on 'Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC)' and "Hypomagnesemia: Causes of hypomagnesemia")
●Monogenic disorders that increase bone absorption include multiple endocrine neoplasia type 1 syndrome with hyperparathyroidism [41], and McCune-Albright syndrome. (See "Multiple endocrine neoplasia type 1: Clinical manifestations and diagnosis".)
Environmental factors — The following environmental factors can increase urinary calcium excretion [22,34-37]:
●Immobilization with increased bone resorption [17,42].
●Medications such as loop diuretics, which increase calcium renal excretion (especially in neonates), and glucocorticoids, which increase bone resorption. (See "Nephrocalcinosis in neonates".)
●Excessive amounts of vitamin D.
●High sodium intake (ie, a high salt diet). (See "Kidney stones in adults: Epidemiology and risk factors", section on 'Sodium'.)
The role of calcium, routine dietary vitamin D supplementation, and other solutes as risk factors in kidney stone formation is unclear and is discussed separately. (See "Kidney stones in adults: Epidemiology and risk factors", section on 'Dietary factors'.)
Other factors — Secondary forms of hypercalciuria include hyperparathyroidism [41], chronic metabolic acidosis in association with hypocitraturia, hypercalcemia from any cause, and hypophosphatemia. (See "Primary hyperparathyroidism: Clinical manifestations" and 'Hypocitraturia' below and "Etiology of hypercalcemia" and "Hypophosphatemia: Causes of hypophosphatemia".)
Hyperoxaluria — In case series of pediatric kidney stone disease, hyperoxaluria was detected in 10 to 20 percent of children [12,21].
●Definition – Hyperoxaluria is defined as a urinary oxalate excretion rate that is greater than 0.7 mmol (62 mg)/1.73 m2 per 24 hours or random urine oxalate to creatinine ratio greater than normal for age (table 1) [32]. The diagnosis of hyperoxaluria is discussed in detail elsewhere. (See "Kidney stones in children: Prevention of recurrent stones", section on 'Definitions of specific urine metabolic abnormalities'.)
●Etiology – Any patient with elevated urinary oxalate requires evaluation for hyperoxaluria. Causes of hyperoxaluria include the following:
•Primary hyperoxaluria – The three types of primary hyperoxaluria (types I, II, and III) are rare autosomal disorders affecting genes that encode enzymes involved in glyoxylate metabolism. These disorders are characterized by enhanced conversion of glyoxalate to poorly soluble oxalate, resulting in increased serum oxalate and hyperoxaluria, which can lead to kidney stones, nephrocalcinosis, chronic kidney disease, and end stage kidney disease. These disorders are discussed in greater detail separately. (See "Primary hyperoxaluria".)
•Fat malabsorption (ie, enteric hyperoxaluria) – Children with fat malabsorption may have an enhanced enteric absorption of oxalate known as enteric hyperoxaluria. Excess fatty acid binds calcium, leaving less available calcium to combine with oxalate, and thus more free oxalate is absorbed. Children with inflammatory bowel disease [43], extensive bowel resection, pancreatitis, and cystic fibrosis are at risk for hyperoxaluria and kidney stones. (See "Kidney stones in adults: Epidemiology and risk factors", section on 'High urine oxalate' and "Clinical manifestations, diagnosis, and prognosis of Crohn disease in adults", section on 'Malabsorption' and "Chronic complications of short bowel syndrome in children", section on 'Hyperoxaluria and kidney stones'.)
In these patients, the degree of hyperoxaluria is dependent on the dietary intake of oxalate. Urinary oxalate excretion can be reduced by decreasing dietary oxalate, eating a low-fat diet, and increasing fluid intake. In addition, taking dietary calcium supplements when eating high oxalate foods facilitates calcium binding to the oxalate in the diet.
•Idiopathic hyperoxaluria often occurs in conjunction with hypercalciuria resulting in calcium oxalate crystals and stones (picture 1A-B). The underlying pathogenesis of idiopathic hyperoxaluria is unknown. It has been proposed that affected patients have increased urinary oxalate excretion because of increased oxalate production or enhanced gastrointestinal oxalate absorption.
•Excessive oxalate ingestion – Ethylene glycol, ascorbic acid, and methoxyflurane are metabolized to form oxalate. Excessive ingestions of these products result in increased serum oxalate and hyperoxaluria. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)
Hyperuricosuria — While uric acid stones are rare in children, hyperuricosuria is detected in 2 to 8 percent of children with kidney stones. Determining whether uric acid excretion is abnormally elevated in children can be challenging. Uric acid excretion is highest in infants and remains high in children until adolescence when values decrease to adult values. In infants, the normal urinary uric acid excretion is so high that crystals may precipitate in the diaper and be misidentified as blood (picture 2A-B and picture 3).
●Definition – The definition of hyperuricosuria is discussed elsewhere. (See "Kidney stones in children: Prevention of recurrent stones", section on 'Definitions of specific urine metabolic abnormalities'.)
●Etiology – Increased urinary excretion of uric acid can result from either enhanced renal excretion or increased production of uric acid.
Idiopathic hyperuricosuria is thought to be due to a defect in renal tubular uric acid excretion and is often seen in conjunction with hypercalciuria. It is also frequently present in families and is generally asymptomatic. However, in some families, formation of uric acid stones occurs, usually in individuals with constantly acidic urine.
In childhood, pure urate stones are uncommon and are generally due to overproduction of uric acid. Causes include:
•Tumor lysis syndrome (see "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology and risk factors")
•Lymphoproliferative and myeloproliferative disorders (see "Treatment of acute lymphoblastic leukemia/lymphoma in children and adolescents")
•Rare genetic disorders, including:
-Lesch-Nyhan (hypoxanthine-guanine phosphoribosyl transferase deficiency) (see "Hyperkinetic movement disorders in children", section on 'Lesch-Nyhan syndrome')
-Uric acid transporter mutations (see "Kidney stones in adults: Uric acid nephrolithiasis")
-Autosomal dominant tubulointerstitial kidney disease (see "Autosomal dominant tubulointerstitial kidney disease")
-Glycogen storage diseases (see "Glucose-6-phosphatase deficiency (glycogen storage disease I, von Gierke disease)" and "Phosphofructokinase deficiency (glycogen storage disease VII, Tarui disease)")
In addition, a high dietary intake of purines or hemolysis has been associated with uric acid kidney stones.
●Clinical significance – Many of the conditions with hyperuricosuria can also lead to acute kidney failure due to precipitation of uric acid within the renal tubules. (See "Uric acid kidney diseases", section on 'Acute uric acid nephropathy'.)
Cystinuria — Cystine stones account for 5 percent of pediatric kidney stone disease and are caused by cystinuria, an autosomal recessive disorder of renal tubular transport. Cystinuria is characterized by excessive urinary excretion of the dibasic amino acids cystine, ornithine, lysine, and arginine. Cystinuria appears to be caused by mutations and/or genomic rearrangements in two genes, SLC3A1 and SLC7A9. Recurrent kidney stones appear to be the only manifestation of cystinuria; 20 to 25 percent of individuals with cystinuria have pathognomonic colorless, flat, hexagonal cystine crystals in the urinary sediment (picture 4). (See "Cystinuria and cystine stones".)
Evaluation and diagnosis of cystinuria in children with kidney stones are discussed in detail elsewhere. (See "Kidney stones in children: Prevention of recurrent stones", section on 'Definitions of specific urine metabolic abnormalities'.)
Hypocitraturia — Citrate is an inhibitor of calcium oxalate and calcium phosphate crystallization. In adult patients with idiopathic kidney stones, hypocitraturia is a frequent finding. Hypocitraturia has also been reported in up to 68 percent of children with kidney stones [23,44,45]. In one study, citrate excretion was lower in 78 children with calcium stones compared with a control group of 24 healthy non stone-forming children [46].
Citrate excretion is greater in children than adults. In children, hypocitraturia is defined as a urinary citrate excretion rate that is less than 400 mg/g of creatinine in a 24 hour urine collection (table 1) [47]. Diagnosis of hypocitraturia is discussed in detail elsewhere. (See "Kidney stones in children: Prevention of recurrent stones", section on 'Definitions of specific urine metabolic abnormalities'.)
Citrate combines with calcium in the tubular lumen to form a nondissociable but soluble complex resulting in less free calcium available to combine with oxalate. Citrate also appears to inhibit crystal agglomeration, in which individual calcium oxalate crystals combine to form a stone. Citrate also alkalinizes the urine.
Children with chronic metabolic acidosis have an increased risk of kidney stones. In these patients, because of enhanced proximal renal tubular citrate reabsorption, citrate excretion is decreased, leading to stone formation. Conditions associated with chronic metabolic acidosis and kidney stones include:
●Conditions causing chronic diarrhea (ie, cystic fibrosis, inflammatory bowel disease, short bowel syndrome)
●Use of carbonic anhydrase inhibitors (eg, topiramate, zonisamide and diamox)
●Ketogenic diet
●Glycogen storage disease
●RTA, including acquired forms due to medications (ie, ifosfamide) or recreational drugs (eg, toluene exposure from glue sniffing) stones [48]
Although the cause of idiopathic hypocitraturia is unknown, proposed etiologies include ingestion of a high protein diet and polygenetic factors. (See "Kidney stones in adults: Epidemiology and risk factors", section on 'Low urine citrate'.)
Melamine exposure — Melamine is a synthetic product used to form resins with formaldehyde and is found in a variety of products in which resin-based coatings are used. The stones are not radiopaque and therefore not seen on plain films; however, they are easily visualized by abdominal ultrasonography or computed tomography.
Increased melamine exposure has been linked to urolithiasis in both children and adults. This risk was highlighted by the 2008 melamine-tainted baby formula in China that resulted in over 50,000 affected infants, including 13,000 who were hospitalized for acute kidney failure due to urinary obstruction, and six deaths [49-53].
Other metabolic causes — There are a wide range of disorders that result in urine solute excretion abnormalities that increase the risk of kidney stones. They include the following:
●High animal protein diet – Diets with a high content of animal protein can result in high urinary excretion rates of uric acid, calcium, and oxalate, and low urinary excretion rate of citrate. These changes in urinary solute excretion may predispose the child to the formation of calcium oxalate crystals and stones. We generally do not restrict children’s protein intake because protein is required for appropriate growth, but we do obtain a dietary history which includes protein intake and source (ie, animal, plant).
●Ketogenic diet – Kidney stones are reported in 3 to 10 percent of children treated with a ketogenic diet for management of their seizures disorders [54-57]. Urinary metabolic abnormalities include hypercalciuria, hyperuricosuria, and hypocitraturia. In patients with kidney stones, the stone composition varies and includes calcium oxalate, uric acid, and ammonium urate, as well as mixed stones of calcium and uric acid. (See "Ketogenic dietary therapies for the treatment of epilepsy".)
●Cystic fibrosis – Patients with cystic fibrosis have an increased risk of kidney stones, most commonly due to calcium oxalate, and nephrocalcinosis [58,59]. Although hyperuricosuria, hypercalciuria, and hypocitraturia can be present, hyperoxaluria due to enhanced enteric oxalate absorption is thought to be the primary contributor to stone formation. In addition, tubular dysfunction from cotrimoxazole and ceftazidime therapy may play a role in kidney stones [59].
●Drugs – Many drugs alter solute excretion such as topiramate, zonisamide, furosemide, acetazolamide, and allopurinol, resulting in stone formation. A rare complication of allopurinol therapy is secondary xanthinuria and hypouricosuria. Some classes of oral antibiotics (oral cephalosporins, fluoroquinolones, sulfas, nitrofurantoin, and broad-spectrum penicillins) have been associated with increased risk of kidney stones [60]. The greatest risk was observed among younger children, those with the most recent use, and those on high doses or with prolonged use.
●Inborn errors of metabolism – Inborn errors of metabolism associated with kidney stones include abnormalities in purine and pyrimidine metabolism, such as the following:
•Adenine phosphoribosyltransferase deficiency, a rare inborn error of purine metabolism, is an autosomal recessive trait that is associated with radiopaque calculi composed of 2,8-dehydoxyadenine [61,62].
•Xanthine oxidase deficiency, an autosomal disorder of purine metabolism, results in xanthine calculi in one-third of affected patients [63]. These patients have a low urinary excretion of uric acid.
•Orotic aciduria is a rare inborn error of pyrimidine metabolism that is recessively inherited. This disorder is characterized by an onset in early infancy, growth failure, developmental delay, hypochromic anemia, and excessive urinary excretion of orotic acid, an intermediary of uridine synthesis [64].
•Another inborn error of metabolism, alkaptonuria, is a disorder of tyrosine metabolism that is usually associated with kidney stones in adulthood, but there are cases of kidney stones reported in childhood [65]. (See "Disorders of tyrosine metabolism", section on 'Alkaptonuria'.)
•Lesch-Nyhan syndrome (hypoxanthine-guanine phosphoribosyl transferase deficiency) results in a marked increase in production of uric acid and hyperuricemia. (See "Hyperkinetic movement disorders in children", section on 'Lesch-Nyhan syndrome'.)
INFECTION — Infection may be the primary cause of a stone or occur concomitantly with a underlying urinary metabolic abnormality or structural abnormality.
Functional or anatomic obstruction of the urinary tract predisposes children to stasis and infection, which promote stone formation. Because boys are more likely to have obstructive uropathy, 80 percent of children with stones associated with infections are male. Infection-associated stones are usually detected before five years of age. All races are equally affected. Improvements in the detection and repair of obstructive uropathy have reduced the incidence of stones due to infections.
Bacteria that produce the enzyme urease are strongly associated with pediatric kidney stones and include Proteus, Providencia, Klebsiella, Pseudomonas, and enterococci. Urease breaks down urea to form ammonium and bicarbonate, which creates a favorable biochemical milieu for the formation of struvite stones (magnesium ammonium phosphate). Struvite stones, which can contain carbonate apatite, tend to branch, enlarge, and often fill the renal calyces, producing a "staghorn" appearance (image 1 and image 2). (See "Kidney stones in adults: Struvite (infection) stones".)
In addition, infections may also produce a soft radiolucent mucoid substance called "matrix concretion" that may calcify readily and account for the rapid formation of some infection-related calculi.
Xanthogranulomatous pyelonephritis is a rare, severe chronic infection of the kidney that leads to renal parenchymal destruction and chronic inflammation characterized by lipid-laden macrophages [66-68]. In 70 percent of affected children, obstruction is caused by kidney stones, resulting in a nonfunctioning or poorly functioning kidney. Nephrectomy or partial nephrectomy is often required to treat these patients [69]. (See "Xanthogranulomatous pyelonephritis".)
CONGENITAL/STRUCTURAL ABNORMALITIES — In case series of children with kidney stones, structural abnormalities are reported in 10 to 25 percent of patients [21,70,71]. Congenital and structural abnormalities that are accompanied by urinary stasis are associated with kidney stones. Urinary stasis and turbulent urine flow predispose to crystal and stone formation.
Kidney and urinary tract abnormalities associated with urinary stasis and kidney stones include:
●Ureteropelvic junction (UPJ) obstruction – The association remains even after repair of the UPJ obstruction due to urinary stasis (see "Congenital ureteropelvic junction obstruction").
●Autosomal dominant polycystic kidney disease (see "Autosomal dominant polycystic kidney disease (ADPKD): Kidney manifestations", section on 'Nephrolithiasis').
●Medullary sponge disease (see "Medullary sponge kidney", section on 'Kidney stones and nephrocalcinosis').
●Horseshoe kidney (image 3) (see "Renal ectopic and fusion anomalies", section on 'Horseshoe kidney').
●Bladder exstrophy.
●Augmentation of the bladder – Patients who have surgically augmented bladders are at risk for kidney stones, most commonly bladder stones composed of struvite [72].
●Neurogenic bladder.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pediatric nephrolithiasis".)
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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Kidney stones in children (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Pathogenesis – Urinary stones develop when there is precipitation of solutes because of urinary solute supersaturation. This is due to two mechanisms (see 'Pathogenesis' above).
•Excessive solute concentration due to increased urinary concentration of solutes due to increased renal excretion and/or low urine volume.
•Decreased levels of inhibitors of stone formation, including citrate.
●Risk factors – An underlying risk factor is identified in 75 to 85 percent of children with kidney stones. Predisposing conditions include a urinary metabolic abnormality, infection, and/or structural abnormality of the kidney or urinary tract. (See 'Overview of risk factors' above.)
•Metabolic risk factors – A urinary metabolic abnormality is identified in approximately 40 to 50 percent of children with kidney stones. The most common disorder is hypercalciuria, followed by hyperoxaluria, and hypocitraturia. Hyperuricosuria and cystinuria are less commonly seen in children with pediatric kidney stones. (See 'Metabolic risk factors' above.)
Monogenic disorders that increase intestinal absorption of calcium, impair renal tubular calcium reabsorption, or increase bone absorption can lead to hypercalciuria. (See 'Genetic factors' above.)
•Urinary tract infection – In 20 to 25 percent of children with kidney stones, a urinary tract infection (UTI) is detected or there is a history of a UTI. Infection may be the primary cause of pediatric kidney stones or occur concomitantly with underlying urinary metabolic abnormality or structural abnormality. Bacteria that produce the enzyme urease are strongly associated with pediatric kidney stones and include Proteus, Providencia, Klebsiella, Pseudomonas, and enterococci. (See 'Infection' above.)
•Structural abnormalities – Structural abnormalities are reported in 10 to 25 percent of children with kidney stones. In these children, urinary stasis predisposes to crystal formation and stone formation. (See 'Congenital/structural abnormalities' above.)
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