• Stone formation within the urinary tract: Urinary crystals bind to form a nidus, which grows to form a calculus (stone).
  • Range of symptoms: asymptomatic to obstructive; febrile morbidity if result of infection


  • Vesical calculosis (bladder stones) due to malnutrition during early life is frequent in the Middle East and in Asian countries.
  • Incidence in industrialized countries seems to be increasing, probably due to improved diagnostics and increasingly rich diets.
  • Increased incidence in patients with surgically induced absorption issues (IBD, gastric bypass)


  • In industrialized countries: 100 to 200/100,000 per year
  • Predominant age: Mean age is 40 to 60 years.
  • Predominant sex: male > female (~3:1)


  • 10–15% in the United States
  • Lifetime risk of >14% in men, >6% in women
    • Incidence is increasing in female, pediatric, and adolescent populations.

Etiology and Pathophysiology

  • Supersaturation and dehydration lead to high salt content in urine which congregates.
  • Stasis of urine
    • Renal malformation (e.g., horseshoe kidney, ureteropelvic junction obstruction)
    • Incomplete bladder emptying (e.g., neurogenic bladder, prostate enlargement, multiple sclerosis)
  • Crystals may form in pure solutions (homogeneous) or on existing surfaces, such as other crystals or cellular debris (heterogeneous).
  • Balance of promoters and inhibitors: organic (Tamm-Horsfall protein, glycosaminoglycan, uropontin, nephrocalcin) and inorganic (citrate, pyrophosphate)
  • Calcium oxalate and/or phosphate stones (80%)
    • Hypercalciuria
      • Absorptive hypercalciuria: increased jejunal calcium absorption
      • Renal leak: increased calcium excretion from renal proximal tubule
      • Resorptive hypercalciuria: mild hyperparathyroidism
    • Hypercalcemia
      • Hyperparathyroidism
      • Sarcoidosis
      • Malignancy
      • Immobilization
      • Paget disease
  • Hyperoxaluria
    • Enteric hyperoxaluria
      • Intestinal malabsorptive state associated with irritable bowel syndrome, celiac sprue, or intestinal resection
      • Bile salt malabsorption leads to formation of calcium soaps.
    • Primary hyperoxaluria: autosomal recessive, types I and II
    • Dietary hyperoxaluria: overindulgence in oxalate-rich food
  • Hyperuricosuria
    • Seen in 10% of calcium stone formers
    • Caused by increased dietary purine intake, systemic acidosis, myeloproliferative diseases, gout, chemotherapy, Lesch-Nyhan syndrome
    • Thiazides, probenecid
  • Hypocitraturia
    • Caused by acidosis: renal tubular acidosis, malabsorption, thiazides, enalapril, excessive dietary protein
  • Uric acid stones (10–15%): hyperuricemia causes as discussed earlier
  • Struvite stones (5–10%): infected urine with urease-producing organisms (most commonly Proteus sp.)
  • Cystine stones (<1%): autosomal recessive disorder of renal tubular reabsorption of cystine
  • Bladder stones: seen with chronic bladder catheterization and some medications (indinavir)
  • In children: usually due to malnutrition


  • Up to 20% of patients have a family history. However, spouses of those who form stones have higher calcium excretion rates than controls, suggesting strong dietary–environmental factors.
  • Autosomal dominant: idiopathic hypercalciuria
  • Autosomal recessive
    • Cystinuria, Lesch-Nyhan syndrome, hyperoxaluria types I and II
    • Ehlers-Danlos syndrome, Marfan syndrome, Wilson disease, familial renal tubular acidosis

Risk Factors

  • White > Asian > African American
  • Male
  • Family history (increases risk by up to 2.5 times)
  • Diet rich in protein, refined carbohydrates, and sodium; carbonated drinks; low calcium diet; low fluid intake
  • Occupations associated with a sedentary lifestyle or with a hot, dry workplace
  • Incidence rates peak during summer secondary to dehydration, hot climates.
  • Obesity
  • Surgically/medically induced malabsorption (Crohn disease, gastric bypass, celiac, primary hyperparathyroidism)
  • Horseshoe kidney (incidence of 21–60%)
  • Medications that can increase risk of forming calcium and uric acid stones
  • Recent literature suggesting possible association between microbiome (gut and urinary) and urolithiasis

General Prevention

  • Hydration (1)
  • Decrease salt and meat intake.
  • Avoid oxalate-rich foods.

Pediatric Considerations

  • Increasing in prevalence due to obesity, diabetes, and hypertension
  • Additional risk factor considerations include renal disease or immaturity, preterm birth, and low birth weight.
  • Ultrasound should be considered in children before CT imaging to reduce radiation exposure.
  • Consider additional work-up to evaluate for metabolic abnormality or hereditary etiology.
  • Children with uncomplicated ureteral stones of ≤10 mm can be offered observation with or without medical expulsion therapy (MET) using α-blockers.

Pregnancy Considerations

  • Pregnant women have the same incidence of renal colic as do nonpregnant women.
  • Most symptomatic stones occur during the 2nd and 3rd trimesters, heralded by symptoms of flank pain/hematuria.
  • Most common differential diagnosis is physiologic hydronephrosis of pregnancy. Use ultrasound to avoid irradiation. Noncontrast-enhanced CT scan also is diagnostic.
  • 30% require intervention, such as stent placement.
  • Pregnant women who have ureteral stones with symptoms that are generally well controlled should be offered observation as first-line therapy.

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