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For further information, see CMDT Part 23-05: 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

eTable 23–1.Laboratory findings suggestive ...

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