Another relatively simple intervention is to restrict dietary sodium. Urinary calcium excretion increases in direct molar proportion to sodium ingestion and subsequent urinary excretion. Increased calcium excretion will lead to increased urinary supersaturation with respect to any of the calcium-containing kidney stones. Sports drinks contain sodium, so they should not be recommended for routine hydration in stone formers.
Other than calcium, the most common component in kidney stones is oxalate. Oxalate is found in food in dramatically varying amounts. Oxalate absorption occurs in the large bowel and is enhanced in several GI maladies, including inflammatory bowel disease, as well as post gastric bypass surgery. A simple approach to reducing oxalate activity is to decrease dietary intake.
In the past, physicians often placed hypercalciuric kidney stone formers on calcium-restricted diets, with the goal of minimizing urinary calcium excretion and thus reducing patients’ propensity to form stones. This approach is almost certainly incorrect. It is now clear that stone formers should consume an age- and gender-appropriate amount of dietary calcium. Borghi et al conducted a randomized controlled trial in which they compared the relapse rate of hypercalciuric stone formers under different dietary conditions (N Engl J Med. 2002;346:77-84, 124-125).
The investigators found that those individuals who consumed a diet that was low in sodium and animal protein but normal in calcium content formed fewer stones than those on a calcium-restricted diet. It appears that a diet with adequate calcium binds more oxalate in the intestine, preventing its absorption and subsequent excretion. This binding of intestinal oxalate reduces the urinary oxalate content while having only a modest effect on urinary calcium content.
Citrate and dietary protein
Urinary citrate is a natural inhibitor of calcium stone formation, as it chelates urinary calcium, forming a soluble complex. Citrate excretion is pH-dependent and reduced in acidic urine. Disease states that result in enhanced urine acidification include chronic diarrhea, metabolic syndrome, and type 2 diabetes. Increased animal protein intake will also increase the acid load delivered to the kidneys, enhancing urine acidification and reducing citrate excretion.
Acidogenic animal protein also will result in enhanced urinary calcium excretion due to a direct tubular effect of acidosis. If urine studies reflect low citrate levels and/or reduced pH, urinary citrate can be increased by dietary changes, e.g., by eating less meat and more vegetables and choosing foods with high citrate content, such as lemons and limes.
Alternatively, urine citrate content can be enhanced by taking supplemental base. Urocit-K is a well-tolerated formulation of potassium citrate that usually is taken two or three times daily and titrated to achieve adequate urinary pH and citrate levels. Sodium citrate should be avoided, though, as it will increase urinary calcium excretion. Careful titration of the urinary pH is required because an alkaline urine promotes calcium phosphate crystallization. In CKD patients, care must be taken in the use of potas-sium citrate, as each equivalent of citrate contains three equivalents of potassium.
Patients with idiopathic hypercalciuria frequently are treated with a thiazide diuretic, such as chlorthalidone. Thiazides have been shown to significantly reduce recurrent stone formation almost certainly due to inducing a decrease in urine calcium excretion resulting in decreased supersaturation with respect to calcium solid phases. Significant volume depletion must be avoided, as this leads to enhanced release of anti-diuretic hormone, thus increasing water retention and decreasing urine volume. Thiazides also have the potential to reduce serum potassium and increase lipids and calcium.
The authors are affiliated with the nephrology division in the department of medicine at the University of Rochester School of Medicine and Dentistry in New York. Dr. Wing is senior instructor in medicine and Dr. Bushinsky is professor of medicine and pharmacology and physiology.