A comprehensive look at kidney stones
A right kidney stone as seen on abdominal CT
At a glance
- The time-honored recommendation for lowering the risk of stone formation is to increase oral fluid intake to two or more liters per day.
- Most patients with kidney stones complain of intermittent pain that can be correlated with stone migration. Nonobstructive stones produce no symptoms.
- NSAIDs are usually recommended for analgesia, but these agents can further progression of renal failure through vasoconstrictive mechanisms.
Approximately 12% of males and 5% of females will develop at least one episode of symptomatic nephrolithiasis by the seventh decade of life. Moreover, 7-10 of every 1,000 hospital admissions have been attributed to kidney stones.
How do stones form?
Stone formation usually begins when normally soluble materials, such as calcium and oxalate,
supersaturate the urine and form crystals. Over time, the crystals aggregate and these aggregations grow into stones. This process usually occurs at the distal portions of the tubule, specifically at the collecting ducts.
Calcium phosphate crystals, thought to originate in the medullary interstitium, make their way to the renal papillae. The result is “Randall's plaques,” which serve as a nidus for further deposition of crystals.1
Other stones are composed of magnesium ammonium phosphate (struvite), calcium carbonate apatite, or a combination of the two. Known collectively as struvite stones, they are usually associated with UTIs due to such urease-producing organisms as Proteus or Klebsiella. The urease causes the formation of ammonia and an alkaline urine.
Uric acid stones require increased uric acid concentration and an acid urine. Low urine volume also predisposes to uric acid stone formation.
What puts patients at risk?
Several irreversible risk factors are known to influence the rate of stone formation, including age, gender, race, and family history. For example, the rate of stone formation increases with age, and the incidence of stones is higher in whites than it is in blacks.
Interestingly, there is significant regional variation in the prevalence of stones in the United States. The highest prevalence has been demonstrated in residents of the southeastern states, as compared with those in the mid-Atlantic and northwestern states.2 These geographical differences may provide clues to potentially reversible risk factors, such as fluid consumption and diet.3 A list of risk factors, both reversible and irreversible, appears in Table 1.
The time-honored recommendation for lowering the risk of stone formation is to increase oral fluid intake to two or more liters daily. The goal of this approach is to increase urine flow rate and decrease urine solute concentration; both mechanisms prevent stones. In warmer climates, dehydration secondary to inadequate fluid intake increases the acidity and concentration of urine, thereby promoting stone formation.3
The high consumption of certain fluids, such as colas (soft drinks) and tea, in southeastern states has been linked to increased incidence of stones.3 On the other hand, alcohol and coffee consumption (lower in southeastern states) was negatively associated with stones. Other studies have found the association between kidney stones and coffee, tea, and alcohol variable and inconsistent. Although the exact mechanism remains unknown, grapefruit juice consumption has been linked to increased risk of stones. But vitamin C supplementation had a negative association with kidney stones.3
Certain dietary indiscretions promote stone growth. Consumption of large amounts of animal protein predisposes patients to increased urinary levels of calcium and uric acid. Metabolism of sulfur-containing amino acids generates sulfuric acid, thereby increasing the daily acid load and predisposing the patient to stone formation.
A high-salt diet increases urinary calcium. Re-absorption of sodium and water creates a favorable concentration gradient that allows for passive reabsorption of calcium in the proximal tubule. However, a high-salt diet also creates a volume-expanded state, which decreases sodium reabsorption in the proximal tubule. This leads to a parallel decrease in calcium transport, hence increased urinary calcium excretion.
Interestingly, restriction of dietary calcium promotes calcium oxalate stone formation because the decreased availability of calcium in the intestine leads to increased absorption and subsequent excretion of oxalate that would otherwise bind with the calcium.4 Sunlight, by virtue of its role in vitamin D metabolism in the kidneys, indirectly enhances intestinal absorption of calcium.3
Diets rich in potassium, e.g., those high in fruits and vegetables, result in reduced urinary calcium and increased urinary citrate excretion. Both these conditions prevent stone formation. Some vegetables, such as spinach and rhubarb, as well as nuts, such as peanuts, cashews, and almonds, have a high oxalate content and should be avoided.
Citrate inhibits stones. It forms a poorly dissociable but soluble complex with calcium, thereby reducing the amount of calcium binding to oxalate and/or phosphate. Potassium citrate (Urocit-K) or potassium bicarbonate can be prescribed to increase urinary citrate, thereby preventing stone formation. In contrast, cranberry juice, which has a high citrate content, has not been shown to significantly increase urinary citrate levels. Foods with a high phytate content, such as cereals and whole grains, have been recommended to lower the risk of stone formation.5
Some medications predispose to formation of crystals (indinavir) and stones (triamterene). And vitamin C in high doses (>1,000 mg/day) increases urinary levels of oxalate and hence calcium oxalate stone formation.
On the other hand, some medications aid in the management of stones by addressing the predisposing metabolic abnormality. For instance, thiazide diuretics increase re-absorption of calcium in the distal tubules, thereby decreasing urinary calcium excretion; allopurinol, a xanthine oxidase inhibitor, prevents formation of uric acid; and potassium citrate is an additional source of urinary citrate, a known inhibitor of stone formation.
Certain comorbid systemic illnesses can predispose patients to stone formation. These include gout, nephropathy, obesity in diabetic patients, recurrent UTI, and inflammatory bowel diseases. Effective treatment of these conditions may lower risk.