Kidney stone secondary prevention
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]
Overview
Effective measures for the secondary prevention of nephrolithiasis include measures to prevent recurrence of the stones and prevent complications. It includes measures like correcting hydration and dietary habits. Drugs like allopurinol to prevent hyperuricemia, potassium citrate to alkalinize the urine and avoidance or judicious use of diuretics.
Secondary Prevention
Effective measures for the secondary prevention of nephrolithiasis include measures to prevent recurrence of the stones and prevent complications:[1]
- Drinking enough water to make 2 to 2.5 liters of urine per day.
- A diet low in protein, nitrogen and sodium intake.
- Restriction of oxalate-rich foods and maintenance of an adequate intake of dietary calcium.
- Taking drugs such as thiazides, potassium citrate, magnesium citrate and allopurinol, depending on the cause of stone formation.
- Avoidance of cola beverages [2]
- For those patients interested in optimizing their kidney stone prevention options, it's essential to have a 24 hour urine test performed. This should be done with the patient on his or her regular diet and activities. The results can then be analyzed for abnormalities and appropriate treatment given.
Diuretics
- Although it has been claimed that the diuretic effects of alcohol can result in dehydration, which is important for kidney stone sufferers to avoid, there are no conclusive data demonstrating any cause and effect regarding kidney stones.
- However, some have theorized that frequent and binge drinkers create situations that set up dehydration, (alcohol consumption, hangovers, and poor sleep and stress habits).
- In this view, it is not the alcohol that creates a kidney stone but it is the alcohol drinker's associated behavior that sets it up.[3]
- One of the recognized medical therapies for prevention of stones is thiazides, a class of drugs usually thought of as diuretics. These drugs prevent stones through an effect independent of their diuretic properties: they reduce urinary calcium excretion. Nonetheless, their diuretic property does not preclude their efficacy as stone preventive.
- Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Though some have said that the effect probably fades after two years or so of therapy (tachyphylaxis), in fact it is only randomized controlled trials lasting 2 years or more that show the effect; there is really no good evidence from studies of calcium metabolism that the thiazide effect does not last indefinitely. Thiazides are the medical therapy of choice for most cases of hypercalciuria (excessive urinary calcium) but may not be suitable for all calcium stone formers; just those with high urinary calcium levels.
Allopurinol
- Hyperuricosuria, too much uric acid in the urine, is a risk factor for calcium stones.
- Allopurinol (Zyloprim) is another drug with proven benefits in some calcium kidney stone formers. Allopurinol interferes with the liver's production of uric acid.
- Allopurinol reduces calcium stone formation in such patients. The drug is also used in patients with gout or hyperuricemia, but hyperuricosuria is not the critical feature of uric acid stones.
- Uric acid stones are more often caused by low urine pH. Even relatively high uric acid excretion will not be associated with uric acid stone formation if the urine pH is alkaline. Therefore prevention of uric acid stones relies on alkalinization of the urine with citrate.
- Allopurinol is reserved for patients in whom alkalinization is difficult.
- For patients with increased uric acid levels and calcium stones, alloprinol is one of the few treatments that has been shown in double-blinded placebo controlled studies to actually reduce kidney stone recurrences. Dosage is adjusted to maintain a reduced urinary excretion of uric acid.
- Serum uric acid level at or below 6 mg/dL is often the goal of the drug's use in patients with gout or hyperuricemia.
Decreased Protein Diet
- A high protein diet might be partially to blame. Protein from meat and other animal products is broken down into acids, including uric acid. The most available alkaline base to balance the acid from protein is calcium phosphate (hydroxyapatite) from the bones (buffering).
- The kidney filters the liberated calcium which may then form insoluble crystals (i.e., stones) in urine with available oxalate (partly from metabolic processes, partly from diet) or phosphate ions, depending on conditions. High protein intake is therefore associated with decreased bone density as well as stones.
- The acid load is associated with decreased urinary citrate excretion; citrate competes with oxalate for calcium and can thereby prevent stones. In addition to increased fluid intake, one of the simplest fixes is to moderate animal protein consumption.
- However, despite epidemiologic data showing that greater protein intake is associated with more stones, randomized controlled trials of protein restriction have not shown reduced stone prevalence. In this regard, it is not just dietary calcium per se that may cause stone formation, but rather the leaching of bone calcium.
- Some diseases (e.g., distal renal tubular acidosis) which cause a chronically acidic state also decrease urinary citrate levels; since citrates are normally present as potent inhibitors of stone formation, these patients are prone to frequent stone formation.
Other Modifications
Potassium Citrate
- This is available as both a tablet and liquid preparation. The medication increases urinary pH (makes it more alkaline), as well as increases the urinary citrate level, which helps reduce calcium oxalate crystal aggregation.
- Optimal 24 hour urine levels of citrate are thought to be over 320 mg/liter of urine or over 600 mg per day. There are urinary dipsticks available that allow patients to monitor and measure urinary pH so patients can optimize their urinary citrate level.
- Though caffeine does acutely increase urinary calcium excretion, several independent epidemiologic studies have shown that coffee intake overall is protective for stones.[4]
- Measurements of food oxalate content have been difficult and issues remain about the proportion of oxalate that is bio-available, versus a proportion that is not absorbed by the intestine.
- Oxalate-rich foods are usually restricted to some degree, particularly in patients with high urinary oxalate levels, but no randomized controlled trial of oxalate restriction has been performed to test that hypothesis.
Calgranulin
- Crystallization of calcium oxalate (CaOx) appears to be reduced by molecules in the urine that retard the formation, growth, aggregation, and renal cell adherence of calcium oxalate. By purifying urine using salt precipitation, preparative isoelectric focusing, and sizing chromatography, some researchers have found that the molecule calgranulin is able to inhibit calcium oxalate crystal growth.[5] Calgranulin is a protein formed in the kidney.
- Given the large amounts of calcium oxalate in the urine, and considering its potency, calgranulin could become an important contribution to the normal urinary inhibition of crystal growth and aggregation. If so, it will be an important tool in the renal defense against kidney stones.
References
- ↑ Goldfarb DS, Coe FL (1999, November 15). "Prevention of recurrent nephrolithiasis". Am Fam Physician. 60 (8): 2269–76. PMID 10593318. Check date values in:
|date=(help) - ↑ "nytimes.com: The Claim: Too Much Cola Can Cause Kidney Problems". Retrieved 2008-01-25.
- ↑ Rodman, John, S (May, 1997). "No More Kidney Stones". Prevention. Check date values in:
|date=(help) - ↑ Curhan GC, Willett WC, Rimm EB, Spiegelman D, Stampfer MJ (1996, February 1). "Prospective Study of Beverage Use and the Risk of Kidney Stones". Am Jour Epidemiology. 143 (3): 240–247. PMID 8561157. Check date values in:
|date=(help) - ↑ http://ajprenal.physiology.org/cgi/content/abstract/275/2/F255 Calcim Oxalate crystallization experiment