Urinary Stone Disease

Key Features

Essentials of Diagnosis

• Severe flank pain

• Nausea and vomiting

• Identification on noncontrast CT scan or ultrasonography

General Considerations

• Affects 240,000–720,000 Americans per year

• The prevalence of kidney stones has increased to 8.8%, or 1 in 11 Americans, representing a 70% increase over the last 15 years

• Males > females (1.5:1)

• Initial presentation usually occurs in the third through fifth decades; more than 50% of patients will have recurrent stones

• Incidence is greatest during hot summer months

• Contributing factors to urinary stone formation

  • Geographic factors

    • High humidity

    • Elevated temperatures

  • Genetic factors

    • Cystinuria

    • Distal renal tubular acidosis

  • High protein and high salt intake

  • Persons in sedentary occupations have a higher incidence than manual laborers

• Increasing evidence is revealing that urinary stone disease may be a precursor to subsequent cardiovascular disease

• Five major types of urinary stones

  • Calcium oxalate

  • Calcium phosphate

  • Struvite (magnesium ammonium phosphate)

  • Uric acid

  • Cystine

• Most urinary stones contain calcium (85%) and are radiopaque

• Pure uric acid stones are radiolucent; some may be composed of a combination of uric acid and calcium oxalate and thus may be partially radiopaque

• Cystine stones frequently have a smooth-edged ground-glass appearance and are faintly radiolucent, similar to struvite stones

• Hypercalciuric calcium nephrolithiasis (> 250 mg/24 h) can be caused by absorptive, resorptive, and renal disorders (eTable 23–1)

  • Absorptive hypercalciuria

    • Secondary to increased absorption of calcium at the level of the small bowel, predominantly in the jejunum

    • Can be further subdivided into types I, II, and III

    • Type I: Independent of calcium intake. There is increased urinary calcium on a regular or even a calcium-restricted diet

    • Type II: Diet dependent

    • Type III: Secondary to a renal phosphate leak, which results in increased vitamin D synthesis and secondarily increased small bowel absorption of calcium

  • Resorptive hypercalciuria

    • Secondary to hyperparathyroidism

    • Hypercalcemia, hypophosphatemia, hypercalciuria, and an elevated serum parathyroid hormone level are found

  • Renal hypercalciuria

    • Occurs when the renal tubules are unable to efficiently reabsorb filtered calcium

    • Hypercalciuria and secondary hyperparathyroidism result

• Hyperuricosuric calcium nephrolithiasis is secondary to dietary excesses or uric acid metabolic defects

• Hyperoxaluric calcium nephrolithiasis is usually due to primary intestinal disorders, including chronic diarrhea, inflammatory bowel disease, or steatorrhea

• Hypocitraturic calcium nephrolithiasis is secondary to disorders associated with metabolic acidosis including chronic diarrhea, type I (distal) renal tubular acidosis, and long-term hydrochlorothiazide treatment

• Uric acid calculi: Contributing factors include

  • Low urinary pH

  • Myeloproliferative disorders

  • Malignancy with increased uric acid production

  • Abrupt and dramatic weight loss

  • Uricosuric medications

• Struvite calculi (magnesium-ammonium-phosphate, "staghorn" calculi)

  • Occur with recurrent urinary tract infections with urease-producing organisms, including Proteus, Pseudomonas, Providencia and, less commonly, Klebsiella, Staphylococcus, and Mycoplasma (but not Escherichia coli)

  • Urine pH ≥ 7.2

• Cystine calculi: Inherited disorder with recurrent stone disease