Nephrolithiasis

Epidemiology

• 10% lifetime prevalence in men, 5% in women

Pathophysiology

• Low urine output/poor oral intake
• Increased uric acid, which precipitates in low pH
• Low pH, which precipitates animal protein
• Hypercalciuria
  • Genetic (familial)
  • Hypercalcemia: hyperparathyroidism, vitamin D
• Increased oxalate
  • Genetic
  • Diet: nuts, greens, chocolate, etc.
  • IBD: fatty acids bind to calcium in gut, allowing oxalate absorbtion
  • Malabsorption
  • Vitamin C
• Decreased citrate (i.e. 3 bicarbs), e.g. from RTA
• Increased phosphate, e.g. from carbonated beverages, which precipitates in high pH
• Urinary tract infection caused by urease-positive bacteria, leading to struvite stones
• Urinary stasis, e.g. in polycystic kidney disease, medullary sponge kidney
• Medications, especially HIV medications

Investigations

• Dietary assessment
• Electrolytes (especially for K and HCO3), calcium profile, PTH, urinalysis, urine microscopy
• 24h urine collection, sent for
  • volume
  • creatinine, CrCl
  • Na, K, urea
  • calcium
  • oxalate
  • uric acid
  • phosphate
  • spot test for cystine
  • citrate and magnesium in a separate collection

Management

• Imaging
• Stone diet
  • Maintain urine output 2L/d
  • Low salt
  • Normal calcium
  • Increased fruit and vegetables
  • Moderate meat and alcohol
• Potassium citrate 20mEq BID, to increased citrate and pH of the urine
• Hydrochlorothiazide, to decrease urine calcium
• Allopurinol, to decrease urine urate