Dietary and Holistic Treatment of Recurrent Calcium Oxalate Kidney Stones

Laura R. Flagg, MSN, RN, CNP

Disclosures

Urol Nurs. 2007;27(2):113-122, 143. 

In This Article

Dietary Vitamin C in Beverages

Whether dietary alterations of citrate can affect the rate of stone formation is unclear, as various studies contradict each other, and may vary by source of vitamin C. While most vitamin C is excreted as citrate, it can also be metabolized and excreted as oxalate (Mayne Pharma Ltd., 2004).

Curhan, Willett, Speizer, and Stampfer (1998) found that grapefruit juice was directly associated with kidney stone formation in women, echoing similar findings in men (Curhan, Willett, Rimm, Spiegelman, & Stampfer, 1996). Grapefruit juice is a well-known inhibitor of the metabolism of numerous drugs via cytochrome P450 and its use is discouraged with many medications. However, it is not known if grapefruit's effect on stone formation may be due to some unknown metabolic alteration of metabolic processes with food breakdown similar to those associated with drug metabolism.

Orange juice ingestion is associated with no change in risk relative to water in the Nurses' Health Study (Curhan et al., 1998). However, other studies have shown orange juice to reduce stone risk. Wabner and Pak (1993) found that orange juice was equally as effective in reducing the lithogenic qualities of urine as was potassium citrate supplementation among 11 men in a prospective crossover study. Coe, Parks, and Webb (1992) found a favorable change in urinary citrate among six female participants who consumed calcium-fortified orange juice in an 11-week, crossover study. No change was appreciated in the six male participants. It is not known what part the calcium fortification may have played in the reduction of risk in this small study.

As another source of citrate, lemonade is often recommended to patients with stones. Seltzer et al. (1996) found that the intake of lemonade in 12 calcium stone formers could aid in reducing risk factors for stone formation. In this study, lemonade increased urinary citrate in 11 of 12 subjects with hypocitraturia (daily urinary citrate less than 320 mg) by a mean value of 204 mg per day. Lemonade was well tolerated and was believed to provide an inexpensive alternative to potassium citrate supplementation. The study did not seek, though, to determine the actual rates of stone formation. The Nurses' Health Study of 81,000 women showed no significant relationship between lemonade intake and stone risk, although lemonade and fruit punch use were studied together as one category (Curhan et al., 1998).

McHarg, Rodgers, and Charlton (2003) studied the effects of cranberry juice on the urinary qualities expected to impact the risk of stone formation. In a randomized crossover study, 20 South African men were given two different diets with and without cranberry juice, and urinary measurements were analyzed. Use of cranberry juice, which was high in both vitamin C and oxalate, resulted in improvements in urinary properties expected to reduce the risk of calcium oxalate stone formation, specifically increased urinary citrate, and reduced urinary oxalate and phosphate. Urinary calcium oxalate also decreased more with cranberry juice than without. McHarg et al. (2003) reported that while high in oxalate, cranberries' oxalate is not largely bioavailable, and thus, not readily absorbed. This may explain the reduction in urinary oxalate despite higher oxalate content.

Siener et al. (2003) studied dietary patterns in 186 stone-forming individuals with hyperoxaluria vs. normooxaluria. The sample was equally divided with 93 subjects with hyperoxaluria and 93 subjects with normooxaluria. Dietary contents were measured scientifically and recorded. Among those stone formers with hyperoxaluria, they noted higher dietary intake of ascorbic acid through fruits and vegetables. Larger ascorbic acid intake was believed to result in conversion to oxalate and hyperabsorption from the gut, when in the presence of reduced calcium intake. Researchers thought this was at least partly responsible for the presence of hyperoxaluria in this group of 93 stone formers.

Taylor, Stampfer, and Curhan (2004) found a greater incidence of stones among men with larger total vitamin C intake, regardless of origin. Among the 45,600 men studied over 14 years, men with the largest total vitamin C intake (over 1,000 mg daily) had a 41% greater risk of stone relative to those with the smallest intake of total vitamin C (less than 90 mg daily).

Supplemental sources of vitamin C have been implicated in stone risk. Terris, Issa, and Tacker (2001) studied cranberry concentrate supplement use in a very small study of healthy adults. Five men and women provided urine studies before and after use of cranberry supplements for 7 days. Urinary oxalate levels increased in all subjects by an average of 43% after concentrate use. Other factors such as increases in urinary magnesium and potassium were noted which may reduce the risk of stone formation, mitigating the added risk of increased urinary oxalate.

Massey, Liebman, and Kynast-Gales (2005) found that ascorbic acid in supplement form caused increases in urinary oxalate among stone formers and non-stone formers alike, in their randomized crossover controlled study of 48 adults. Forty percent of the subjects had increases in urinary oxalate when given 1,000 mg ascorbic acid twice daily, compared to those without the supplementation. Oxalate stone-forming men and women had higher rates of oxalate absorption and endogenous oxalate synthesis than did non-stone formers when subjected to the same diet. In addition, these stone formers increased their own urinary oxalate levels when given ascorbic acid supplements, implying that vitamin C supplementation may be risky among known stone formers.

Opposing evidence has been presented. Taylor et al. (2004) noted no significant increased risk of stone formation with vitamin C supplementation in their study of men with kidney stones.

The reabsorption of sodium and water in the kidney's proximal tubule provides a mechanism for passive reabsorption of calcium to the blood from the kidney's filtrate. Overingestion of sodium provides for less calcium reabsorption to the blood via passive reabsorption, leading to calcium excretion in larger quantities via the urine. A low-sodium diet is expected to conversely increase the reabsorption of sodium and calcium from the proximal tubule into the blood so that less remains in the urine, reducing stone risk. The recommendation for reduced dietary sodium is based on this understanding of the balance of sodium and calcium in the blood and urine. Kok, Iestra, Doorenbos, and Papapoulos (1990) found that a high sodium diet induced increases in urinary calcium and reductions in urinary citrate, which are commonly recognized as risks for stone formation. This effect was more dramatic when diets were high in sodium and protein at the same time.

The role of sodium in actual stone formation, however, is less clear. Borghi et al. (2002) found reduced recurrence of stones in 120 men with a history of hypercalciuric stone formation if they maintained a low-protein, low-sodium diet, compared with a low-calcium diet. Curhan et al. (1993), however, found no relationship between sodium intake and stone formation in their study of 45,000 men. It would appear that recommendations for low-sodium diets are based mostly on the physiologic processes, yet is not yet solidly borne out by epidemiologic evidence.

Magnesium is thought to reduce stone risk by complexing with oxalate in the gut thereby reducing oxalate excretion into the urine. Sources of dietary magnesium include dairy products, meat, seafood, apples, apricots, avocados, bananas, whole grain cereals, nuts, dark green vegetables, and cocoa. Hirvonen, Pietinen, Virtanen, Albanes, and Virtamo (1999) studied 27,000 Finnish smoking men in a prospective epidemiologic study of the risks of stones. This was part of a larger study that looked at smoking men's risk of lung cancer if they supplemented their diets with alpha-tocopherol and beta-carotene. After 5 years of followup, 329 men developed kidney stones. They found that magnesium intake had a protective effect on stone formation. Those men with the highest magnesium intake (563 mg or more) had a relative risk of 0.52 for stone formation, compared to those with the lowest magnesium intake (382 mg or less). It is not known whether these results might be reproducible in other cultural groups, or what effect smoking may have had, if any, on these results.

Taylor et al. (2004) also found a reduced risk for stone formation among men aged 40 to 75 with increased dietary magnesium intake. Men with the highest dietary magnesium intake (over 450 mg/day) had a relative risk of stone formation of 0.71, compared with men who consumed the lowest amount of magnesium (less than 314 mg/day). In a study of the physiology of magnesium intake's effect on oxalate, Liebman and Costa (2000) found that a diet high in magnesium oxide reduced oxalate absorption and oxalate excretion, compared to a diet with low magnesium oxide among 24 healthy men and women. This may at least partially explain the phenomenon of variable stone risk.

High-protein intake has long been proposed as a stone-forming dietary pattern. Those eating a high-protein, low-carbohydrate diet, so popular in recent years, may be at greater risk of stone formation than those with a more balanced nutritional intake.

Kok et al. (1990) studied eight healthy Dutch men who were given sodium and protein dietary modifications for 1 week followed by urine measurements of select elements. Results showed a diet high in protein (more than 2 g per kg body weight per day) produced increases in urinary calcium and uric acid, and decreases in urinary citrate, especially when the high-protein diet was accompanied by a high-sodium intake. The urine showed a significant decrease in the ability to inhibit the formation of calcium oxalate stones. The relative inability was dependent proportional to the degree of decrease in urinary citrate.

Curhan et al. (1993) studied the rate of stone formation in men relative to animal protein intake. They found that animal protein intake was directly associated with stone formation, with the highest protein intake (77 grams daily or more) showing a relative risk of 1.33 compared with the lowest protein intake (50 grams daily or less).

Giannini et al. (1999) took the protein intake question further by studying the effect of protein restriction on a small group of stone-forming adults. Researchers studied 18 men and women, all with histories of calcium stones and hypercalciuria. These 18 subjects restricted their protein intake to 0.8 g per kg of body weight per day for 15 days, after which serum levels and urinary excretion of significant elements were measured. Researchers noted a significant reduction in urinary uric acid, calcium, and oxalate after protein restriction, and increases in urinary citrate. Giannini et al. (1999, p. 270) noted "a reduction of the entire lithogenic potential of these patients" after the short 30 day trial. No measurements were made of the residual effects of a reduced-protein diet, nor of the effects of the reduction if it were undertaken for a longer period.

Hiatt et al. (1996) conducted a randomized controlled trial of 99 persons with histories of one former stone to determine if a low-protein diet might further reduce the risk of stone recurrence. Though not highly controlled over 4.5 years, their low-protein intake intervention group showed a significant increase in rates of recurrent stone formation compared to those who were instructed to only increase fluids (7.1 stones in 100-person years vs. 1.2 stones in 100-person years, respectively). Martini and Wood (2000) performed a meta-analysis of studies related to calcium and protein restrictions. They cautioned against stone-forming individuals undertaking low-protein diets, citing risk of elevation of parathyroid hormone, inducing bone loss. Martini and Wood (2000, p. 116) concluded that diets "restricting dietary protein to below RDA levels of 0.8 grams per kilogram per day are dangerous and should be avoided." As expected, these authors called for further studies to further delineate the connection, if any, between protein intake and stone formation.

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