Nephrolithiasis

FIGURE 17.1 Cumulative recurrence rate for stone disease (Uribarri, 1989) (from UpToDate, with permission.)

Medical Conditions Associated with Calcium Stones

■ Hypercalcemia (especially primary hyperparathyroidism and granulomatous disorders such as sarcoidosis)

■ Hypercalciuria

■ Idiopathic (primary)

■ Secondary

• Hyperparathyroidism (also have hypercalcemia)

• Granulomatous disorders (especially sarcoidosis) due to increased conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D by activated macrophages (may not have hypercalcemia)

• RTA, classic distal type—Failure of H+ excretion results in acidemia, leading to calcium release from bone and hypercalciuria; alkaline urine leads to calcium phosphate stones

TABLE	Risk of Calcium Stone Formation Relative to Urinary Calcium Excretion
17.1

24-h Calcium (mg/d)	Relative Stone Risk

<100	1.0
100–199	1.5
200–299	2
>300	2.5

■ Hyperoxaluria

■ Increased dietary oxalate

■ High-dose vitamin C (metabolized to oxalate)

■ Enteric hyperoxaluria (malabsorption syndromes such as inflammatory bowel disease, leading to decreased calcium-oxalate binding in the gut coupled with bile salt-induced increase in oxalate absorption) (Chadwick et al., 1973; Smith et al., 1972); bariatric surgery (Roux-en-Y gastric bypass) can cause hyperoxaluria, nephrolithiasis and occasionally irreversible renal failure (Nasr et al.,2008))

■ Hyperuricosuria (gout, high animal protein intake; uric acid can serve as nidus for calcium stone formation leading to calcium and mixed calcium/urate stones as well as lead to pure uric acid stones) (Coe et al., 1975)

Inhibitors of Stone Formation

■ Citrate (impairs calcium oxalate lattice formation) (Ettinger et al., 1997; Nicar et al., 1993)

■ Filtered and reabsorbed by proximal tubule

■ Amount reabsorbed dependent on tubular and intracellular pH

■ Decreased tubular and intracellular pH will increase citrate reabsorption and decrease urinary citrate excretion; treatment with alkali will have opposite effect. Hypokalemia will decrease intracellular pH and urinary citrate excretion

■ Glycoprotein inhibitors

■ Tamm-Horsfall protein (uromodulin)

■ Nephrocalcin

■ Uropontin

Treatment of Calcium Stones

■ Increase fluid intake (Pak et al., 1980)

■ Dietary interventions (decrease protein and sodium intake) (Muldowney et al., 1982)

■ Thiazide diuretics (if at high risk for recurrence, coexistent medical conditions, or recurrent/multiple stones) (Laerum & Larsen, 1984)

■ Potassium citrate (if urinary citrate low) (Ettinger et al., 1997)

■ Allopurinol (if coexistent hyperuricosuria unreponsive to dietary restriction) (Ettinger et al., 1986)

URIC ACID STONES

Risk Factors for Uric Acid Stones