• 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


  • The worldwide epidemiology differs according to both geographic area (higher prevalence in hot, arid, or dry climates) and socioeconomic conditions (dietary intake and lifestyle). Radiolucent stones and stones secondary to infection are less influenced by environmental conditions.
  • Vesical calculosis (bladder stones) due to malnutrition during early life is frequent in Middle East and Asian countries.
  • Incidence in industrialized countries seems to be increasing, probably due to improved diagnostics as well as to increasingly rich diets.
  • Increased incidence in patients with surgically induced absorption issues, such as Crohn disease and gastric bypass surgery (1)


  • 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
    • Prevalence in women increasing

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 disease, 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 in regions with both populations
  • Male sex
  • Family history (increases risk by up to 2.5 times)
  • Previous history of nephrolithiasis
  • 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)
  • Medications that can increase risk of forming calcium, uric acid stones (1)

General Prevention

  • Hydration (2)
  • Decrease salt and meat intake.
  • Avoid oxalate-rich foods.

Pediatric Considerations

  • Increasing in prevalence due to obesity, diabetes, hypertensions
  • Additional risk factor considerations include renal disease or immaturity, preterm birth, low birth weight.
  • Ultrasound should be considered in children before CT imaging to reduce radiation exposure.
  • Consider additional workup to evaluate for metabolic abnormality or hereditary etiology.

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.

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