- 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 calculus (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%)
- Absorptive hypercalciuria: increased jejunal calcium absorption
- Renal leak: increased calcium excretion from renal proximal tubule
- Resorptive hypercalciuria: mild hyperparathyroidism
- Paget disease
- 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
- Enteric hyperoxaluria
- Seen in 10% of calcium stone formers
- Caused by increased dietary purine intake, systemic acidosis, myeloproliferative diseases, gout, chemotherapy, Lesch-Nyhan syndrome
- Thiazides, probenecid
- 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
- White > Asian > African American
- 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.
- Surgically/medically induced malabsorption (Crohn disease, gastric bypass, celiac, primary hyperparathyroidism)
- Horseshoe kidney (incidence of 21–60%) (1)
- Medications that can increase risk of forming calcium, uric acid stones
- Recent literature suggesting possible association between microbiome (gut and urinary) and urolithiasis (2)
- Hydration (3)
- Decrease salt and meat intake.
- Avoid oxalate-rich foods.
- Increasing in prevalence due to obesity, diabetes, 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 workup to evaluate for metabolic abnormality or hereditary etiology.
- Children with uncomplicated ureteral stones of ≤10 mm can be offered observation with or without medical expulsive therapy (MET) using α-blockers.
- 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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