Renal calculi
From IDWiki
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
