Kidney Stones


The incidence of nephrolithiasis in children is lower in children than in adults. Hospitalizations for nephrolithiasis are on the rise, secondary to dietary changes with increased protein and sodium in our diets, as well as an increase in childhood obesity.

Boys: More common in 1st decade of life (secondary to obstructive urinary malformations)

Girls: More common on 2nd decade of life (secondary to increased UTIs)

Risk factors 

These three RFs are identified in 75-85% of pediatric nephrolithiasis:

  1. Urinary Metabolic abnormality
  2. Urinary tract infections
  3. Structural renal abnormality


Solute excess or deficiency of inhibitors of stone formation, which occur through genetic and/or environmental factors

  1. Hypercalciuria- most common metabolic abnormality in pediatric nephrolithiasis
    1. Increased intestinal absorption absorptive
    2. Increased renal losses (decreased renal reabsorption) renal
    3. Increased bone resorption resorptive
  2. Hyperoxaluria – 10-20% pediatric nephrolithiasis
    1. Idiopathic- most common cause, often in conjunction with hypercalciuria
      1. Calcium oxalate crystals and stones.
      2. Cause thought to be increased oxalate production or increased GI absorption
    2. Primary hyperoxaluria
      1. Type I and II, Rare autosomal disorders.
    3. Fat malabsorption
      1. Leads to enhanced enteric absorption of oxalate.
        1. The excess fatty acid binds to calcium, resulting in less available calcium to combine with oxalate.
      2. IBD, CF, pancreatitis, extensive bowel resection are risk factors
    4. Excessive oxalate ingestion
      1. Ethylene glycol, ascorbic acid are metabolized to oxalate
  3. Hyperuricosuria – 2-8 % of pediatric nephrolithiasis
    1. Uric acid excretion higher in children than adults
      1. Highest in infants, remains elevated children until adolescence.
    2. Enhanced renal excretion vs. increased production of uric acid.
    3. Idiopathic hyperuricosuria
      1. Thought to be defect in renal tubular uric acid excretion
    4. Pure uric acid stones in kids
      1. Uncommon, most likely due to tumor lysis syndrome, lymphoproliferative/myeloproliferative disorders, Lesch-Nyhan, or glycogen storage diseases            
    5. Precipitation of uric acid in renal tubules can cause acute renal failure
  4. Cystinuria- 5 percent
    1. Cystinuria
      1. Autosomal recessive disorder of renal tubular transport
        1. Excessive excretion of cystine, arginine, lysine, and ornithine
      2. Diagnosis
        1. Colorless, flat hexagonal cystine crystals in urine diagnostic
          1. Only found in 25%  (Specific but not sensitive)
  5. Hypocitraturia- reported in ~10% kids with renal calculi
    1. Citrate combines with Ca resulting in less free calcium to bind to oxalate.
    2. Citrate also inhibits crystal agglomeration.
    3. Risk factors: kids with chronic metabolic acidosis
      1. Chronic diarrhea (CF), topiramate use, ifosfamide, recreational drugs (glue sniffing)
  6. Miscellaneous other metabolic causes of nephrolithiasis
    1. High animal protein diet, ketogenic diet, CF, Drugs (furosemide, acetazolamide, allopurinol)Adenine phophoribosyl transferase deficiency, xanthine oxidize deficiency, erotic aciduria, alkaptonuria


Detected in 20-25% of children with nephrolithiasis. Can be primary cause or associated with underlying metabolic or structural abnormalities

  1. Bacteria that produce urease are strongly associated with nephrolithiasis
    1. Proteus, Providenxia, Klebsiella, Pseudomonas, enterococci
      1. Predispose to struvite stones
      2. staghorn caliculi
  2. Structural abnormalities & UTI found more often in boys than girls.


Reported in 10-25% of pediatric nephrolithiasis cases.

  1. These congenital or structural abnormalities are associated with urinary stasis to form stones
  2. Possible abnormalities:
    1. Medullary sponge disease, ADPKD, Ureteropelvic junction obstruction, horseshoe kidney, bladder exstrophy, augmentation of the bladder, neurogenic bladder.

Management of Nephrolithiasis

Management is divided into acute management of the pain and prevention of subsequent episodes.

In the acute setting, initial medical management should include pain control (NSAIDs for outpatient up to three days before a procedure, Toradol and opiods in inpatient for severe pain), urine culture, and imaging of the stone. While less sensitive than CT for detecting nephrolithiasis, an ultrasound and a KUB radiography (if the stone is radioopaque) is used first line in children, as it is less expensive and less radiation exposure.  Parents should be instructed to strain the child's urine with a strainer for three days for stone retrieval. However, urologic intervention should be initiated for unremitting severe pain and urinary obstruction.  Observation and adequate pain control should be done as much as possible if the stone is less than 5mm in diameter, both because of the high rate of spontaneous stone passage as well as the risks of a urologic procedure.

Possible procedures include lithotripsy, percutaneous nephrostolithotomy, and ureteroscopy.

Long-term prevention depends on determining the etiology of the kidney stone and working on those risk factors.



  1. Lendvay, TS; Smith, J; Stapleton, FD. Acute management of nephrolithiasis in children.
  2. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2011.
  3. Milliner DS, Murphy ME. Urolithiasis in pediatric patients. Mayo Clin Proc 1993; 68:241.
  4. Smith, J; Stapleton, FB. Epidemiology of risk factors for nephrolithiasis in children. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2011.
  5. Stapleton FB. Nephrolithiasis in children. Pediatr Rev 1989; 11:21.