A patient who has osteopenia, hypercalcemia, and nephrolithiasis most probably has an excess of

The following are recommendations in the dietary treatment of hypercalciuria:

• Limit daily calcium intake to 600-800 mg/day unless otherwise instructed

• Limit dietary oxalate, especially when calcium intake is reduced; high oxalate levels are found in strong teas; nuts; chocolate; coffee; colas; green, leafy vegetables (eg, spinach); and other plant and vegetable products

• Avoid excessive purines and animal protein (< 1.7 g/kg of body weight)

• Reduce sodium (salt) and refined sugar to the minimum possible

• Increase dietary fiber (12-24 g/day)

• Limit alcohol and caffeine intake

• Increase fluid intake, especially water (sufficient to produce at least 2 L of urine per day)

Dietary modifications involving reasonable restrictions of dietary calcium, oxalate, meat (purines) and sodium, have been useful in reducing the urinary supersaturation of calcium oxalate. This effect is more pronounced in calcium oxalate ̶ stone formers with hypercalciuria than in calcium nephrolithiasis patients who are normocalciuric.

Some have suggested that the following 3 criteria need to be fulfilled for any dietary factor to be implicated in kidney stone disease:

• Intake of the dietary constituent should be increased in patients with stones compared with controls

• Restriction of the dietary factor should decrease stone formation rates

• The reason the dietary factor causes stones needs to be understood

The main dietary contributions of calcium, sodium, potassium, animal protein, fiber, alcohol, caffeine, water, oxalate, and carbohydrates are reviewed individually below. No relationship between dietary fat and hypercalciuria has been found.

Calcium intake

Avoidance of an excessively high-calcium diet is an obvious recommendation for calcium-stone formers. (See the image below for a list of calcium-rich foods.) Stone formers as a group are much more sensitive to dietary calcium than non–stone formers. For any given change in dietary calcium, urinary calcium has been shown to increase an average of only 6% in healthy controls, but it can increase 20% in calcium-stone formers. Ingestion of more than 2000 mg of calcium per day generally results in hypercalciuria and/or hypercalcemia in calcium-stone formers.

The recommended dietary calcium intake for most calcium-stone formers is about 600-800 mg/day. Avoiding a diet that is too severely limited in calcium is important, however, because otherwise a negative calcium balance may occur, with subsequent osteopenia or actual osteoporosis.

Moreover, when calcium is removed from the diet without also restricting oxalate intake, the lack of intestinal oxalate-binding sites may too much intestinal oxalate unbound and available for easy absorption. When this occurs, urinary oxalate levels rise. Proportionately, oxalate is 15 times stronger than calcium in promoting nephrolithiasis, so the net stone formation rate may actually increase if dietary oxalate intake and hyperoxaluria are not controlled. In 2 large population studies involving men and women, patients with the highest daily calcium intake were demonstrated to have significantly fewer stones (within reasonable limits) than did patients with the lowest dietary calcium levels.

Calcium citrate is recommended if calcium supplements are needed. This combination has been shown to be the most effective in limiting the new stone formation rate for those who require calcium supplements.

Any patient with kidney stones who is placed on a long-term, reduced calcium diet for any reason should have his/her bone density measured periodically, preferably in the spine. Urinary oxalate levels should also be checked regularly.

Pediatric patients

Children with hypercalciuria should be referred to a dietitian to accurately assess daily calcium, animal protein, and sodium intake. A trial low-calcium diet can be administered transiently to determine if exogenous calcium intake is contributing to the high urinary calcium. However, great caution should be used when trying to restrict calcium intake for long periods.

Because of concerns regarding poor bone matrix calcification and subsequent osteoporosis, no child should receive less than the daily recommended intake (DRI) of calcium for long periods without careful monitoring. If the dietary calcium is restricted to less than the DRI, bone density measurements and growth parameters should be taken at regular intervals to monitor the development of osteoporosis and growth retardation.

Reducing sodium and animal protein to the DRI may facilitate lowering of urinary calcium. However, the authors recommend that great caution be used when placing any child on a diet with less than the DRI of calcium and that a dietitian be consulted for assistance. If dietary changes do not provide the desired results of symptom relief, prevention of nephrolithiasis, and normalization of calcium excretion (< 4 mg/kg/day), pharmacotherapy should be initiated.

Sodium intake

A high sodium intake promotes various effects that enhance urinary calcium excretion and increase overall kidney stone formation rates. These effects include a rise in urinary pH, as well as in urinary calcium and cystine levels, and a decrease in urinary citrate excretion. Sodium and calcium share common sites for reabsorption in the renal tubules.

Urinary calcium levels

In healthy adults, high sodium intake has been associated with increased fractional intestinal calcium absorption and a rise in PTH and vitamin D3 levels. Each 100-mEq increase in daily dietary sodium raises the urinary calcium level by about 50 mg.

Enhanced renal calcium excretion from high dietary sodium consumption is thought result from an increase in extracellular fluid volume, which ultimately results in inhibition of renal tubular calcium reabsorption.

Sodium intake among stone formers has been found to be equal to or higher than the intake in control groups of non–stone formers. Moreover, patients with recurrent nephrolithiasis and hypercalciuria have been found to be particularly sensitive to the hypercalciuric actions of a high-sodium diet.

Urinary pH levels

The rise in urinary pH is caused by an increase in serum and urinary bicarbonate levels. High serum bicarbonate lowers urinary citrate excretion by a direct effect on citrate metabolism in proximal renal tubular cells.

Dietary sodium reduction

Dietary sodium reduction has been shown to decrease urinary calcium excretion in stone formers with hypercalciuria, whereas high dietary sodium is associated with increased urinary calcium excretion and low bone density. (In postmenopausal women, high sodium intake has been directly associated with low bone density in calcium-stone formers.)

Patients should be aware that most restaurant meals and fast food items, such as pizza, contain a considerable amount of sodium. In addition, ketchup, mustard, teriyaki sauce, Worcestershire sauce, soy sauce, canned soups, cold cuts, prepared vegetables, and TV dinners have large amounts of sodium. However, many prepared foods have low-sodium varieties available.

Daily dietary salt intake should be restricted to levels sufficient to keep the urinary sodium excretion below 150-200 mEq/day. Most experts recommend limiting dietary sodium (salt) in calcium-stone formers to about 100 mEq/day, but this is difficult because many people find that salt enhances the taste of food. In children, a good target range for dietary sodium intake is 2-3 mEq/kg/day.

Recommendations to reduce sodium (salt) intake include the following:

• Remove the saltshaker from the dining table; other spices, such as pepper, salt substitutes, or Mrs. Dash, can be used instead

• Use little or no salt in food preparation or cooking

• Avoid eating foods with high salt content whenever possible; most fast food is high in sodium.

• Do not add any additional salt to foods that already contain it; this would apply to most prepared or canned foods, such as soups, gravies, TV dinners, and canned vegetables

• Use fresh or frozen vegetables whenever possible; to reduce the salt content of canned vegetables, they should be drained and then rinsed with water before cooking

• Use one half or less of the specified amount of salt when following cooking recipes

• Everyone in the family should participate in the low-sodium diet so that the patient does not feel singled out

Dietary sodium needs to be controlled during any calcium testing, such as a calcium-loading test, to avoid affecting the results.

Potassium intake

Some evidence suggests that low potassium intake may be a risk factor for stones, but this has not been confirmed in all studies. [36, 37, 38] The potential influence of a low-potassium diet may be due to its relationship to sodium intake in stone formers, who generally have a higher sodium/potassium ratio than do non–stone formers.

Potassium decreases urinary calcium excretion by inducing transient sodium diuresis, which results in a temporary contraction of the extracellular fluid volume and an increase in renal tubular calcium reabsorption. Potassium also increases renal phosphate absorption, raising serum phosphate levels, which reduces serum vitamin D3, resulting in decreased intestinal calcium absorption.

Animal protein intake

High protein intake has been judged second only to vitamin D ingestion in its ability to increase intestinal calcium absorption. Other effects of a high animal protein diet include an increase in urinary oxalate and uric acid, as well as a reduction in urinary citrate.

Urinary sulfate levels can be used as a general marker of oral animal protein intake. Generally, up to 40 mg of sulfate per day is considered normal, whereas in calcium-stone formers, optimal levels would be below 25-30 mg daily.

The possible link between high animal protein intake and kidney stones has been known since at least 1973. This link was found in epidemiologic studies first in India and then in England, Germany, Austria, Japan, Italy, and, finally, the United States. [39] Known stone formers appear to be more sensitive to the stone-enhancing effects of high–animal protein diets than do non–stone forming control populations.

Animal protein affects urinary calcium mainly through its acid-loading ability. Animal protein is high in purines, which are metabolized to uric acid, contributing to the acid load. Animal protein also increases the body's acid load directly. Methionine and cystine, which contain relatively high levels of sulfur, are more common in animal protein than plant protein. When the sulfur is oxidized to sulfate, additional acid is generated. (Sulfate also can form a soluble complex with calcium in the renal tubules, reducing calcium reabsorption and contributing to hypercalciuria.)

Excess acid needs to be neutralized. This often occurs in the bone, where the extra acid is buffered, releasing calcium from the bony stores. The released calcium eventually contributes to increased urinary calcium. Moreover, acid loading directly inhibits calcium reabsorption in the distal renal tubule, which further exacerbates any hypercalciuria. The extra acid also reduces urinary citrate excretion, by enhancing citrate reabsorption in the proximal renal tubule.

Dietary animal protein reduction

Each 75 g of additional dietary animal protein raises the urinary calcium level by 100 mg/day. In one study, increasing methionine ingestion by just 6 g/day was found to raise the daily urinary calcium excretion by 80 mg. Dietary animal protein intake should be less than 1.7 g/kg of body weight per day.

An intriguing randomized study that compared the stone production rates in about 100 known calcium oxalate stone formers who differed in their dietary protein and fiber intakes found significantly fewer stones in the group with the high-fiber, low–animal protein diet. [40] Of course, the possibility exists that the fiber or just the combination of the high fiber and animal protein restriction was effective.

The first group in the study was instructed just to increase fluid intake, whereas the second group was told to increase fluid intake and consume a high-fiber, low–animal protein diet; both groups were observed for 4.5 years. [40] Additional studies are needed to determine exactly which dietary modifications are most efficacious and to eliminate variables, such as uncontrolled sodium and calcium intake, that might influence the outcome.

Oxalate excretion

An association may also exist between high animal protein ingestion and increased oxalate excretion. [41] For example, the production of glycolate, an oxalate precursor, is strongly linked to animal protein intake. However, although some investigators have found a link between high animal protein intake and increased urinary oxalate, others have not. Further studies are needed to determine the presence and significance of any such correlation.

Fiber intake

Calcium-stone formers as a group have a lower intake of dietary fiber than do healthy control populations. Dietary fiber, including oat, wheat, and rice bran, can reduce hypercalciuria and lower intestinal calcium absorption by 20-33%. As much as 24 g of dietary fiber per day may be necessary. Wheat bran, for example, is rich in oxalate, which accounts in part for its ability to bind and absorb free intestinal calcium.

However, although no significant adverse effects from increased dietary fiber have been reported, some potential risks exist. For example, dietary fiber may reduce intestinal magnesium, resulting in a deficit. Patients on a very high-fiber diet should be checked periodically for magnesium deficiency. A magnesium supplement, such as magnesium oxide, can be added if necessary.

Another potential problem is reactive enteric hyperoxaluria. Whenever intestinal calcium is reduced, fewer intestinal oxalate-binding sites are available. This leads to more free intestinal oxalate, which is absorbed more easily than oxalate bound to calcium or other agents. The increased free intestinal oxalate is absorbed and is eventually excreted in the urine, increasing urinary oxalate levels.

Because oxalate is proportionately about 15 times stronger than calcium with regard to stone promotion, limiting oxalate absorption in known stone formers makes sense. The easiest way to accomplish this is to limit dietary oxalate any time that intestinal oxalate-binding sites are reduced (such as when dietary calcium intake is reduced). Dietary oxalate can be lowered by limiting such foods as iced tea, coffee, colas, collard greens, spinach, chocolate, nuts, rhubarb, and green, leafy vegetables. Another approach is to use an alternate oxalate-binding agent, such as an iron supplement.

Alcohol intake

Acute alcohol ingestion causes hypoparathyroidism with hypercalciuria and hypocalcemia. PTH levels can drop by 70% after acute alcohol intoxication. Prolonged, moderate alcohol intake, however, eventually raises PTH levels. People with chronic alcoholism develop low serum vitamin D levels, which cause impaired intestinal calcium absorption and hypocalciuria.

A direct inhibitory effect on osteoblast activity by alcohol ingestion also appears to exist. This effect is enhanced in smokers. Urinary calcium excretion during periods of alcohol consumption can increase by more than 200% over control subjects. Osteopenia has also been linked to alcohol consumption.

Caffeine intake

Caffeine has been shown to increase urinary calcium excretion, but the clinical importance is relatively small unless very large amounts of caffeine are ingested. Ingestion of 34 ounces of caffeine is necessary to cause the loss of 1.6 mmol of total calcium. This caffeine-induced hypercalciuria seems to parallel changes in urinary prostaglandin F2-alpha (PGF2-alpha), which suggests that prostaglandins may play a role in hypercalciuria.

Fluid intake

Several studies have shown that on average, stone formers have a lower overall fluid intake than do non–stone formers. Not surprisingly, the highest incidence of kidney stone formation was in the group with the lowest overall fluid intake.

The need for a high fluid intake to increase urinary fluid volume seems obvious, because extra water decreases urinary concentration and reduces the likelihood of stones, even if the total calcium excretion is unchanged. The amount of extra water to be consumed is variable. In general, the author suggests an amount of water that produces a 24-hour urinary volume of 2000 mL or more. This amount may need to be increased in selected cases.

Citrus intake

Potassium-rich citrus fruits and juices, such as oranges, grapefruit, and cranberries, are recommended. Orange juice, for example, has natural potassium citrate. Lemon juice also has a very high citrate content, so lemonade made from real lemon juice is recommended. In contrast, lime juice contains mostly citric acid and does not increase urinary citrate substantially.

Oxalate intake

Oxalate is an organic acid found primarily in the leaves, bark, and fruit of plants. Its only known function in plants is to bind tightly with calcium. This is useful because it allows the plant to extract unwanted calcium from the internal circulation. The leaves containing the calcium-oxalate complex then can be discarded or shed by the plant. Humans absorb oxalate when oxalate-containing leaves and other vegetable products are eaten. Oxalate has no known useful function in human nutrition.

A relatively mild restriction of foods that contain high amounts of oxalate enables the body to avoid a reactive hyperoxaluria when intestinal oxalate-binding sites are reduced from a drop in oral calcium intake. Common foods with relatively high oxalate content include nuts, chocolate, colas, vegetables, rhubarb, spinach, collard greens, tea, and green, leafy vegetables.

Refined carbohydrate intake

Several large population studies have investigated the issue of the potential contribution of a high-carbohydrate diet to stone production. For example, Curhan found that carbohydrates were not a significant risk factor for stone formation in men but that they were associated with increased stone production in women. Some investigators found that stone formers tend to have a higher carbohydrate intake than non ̶ stone formers, but other researchers have failed to confirm this association.

Good evidence indicates that a high-carbohydrate diet causes an increase in urinary calcium excretion because of decreased distal renal tubular calcium reabsorption and an increase in intestinal calcium absorption. There is also evidence to indicate that excessive carbohydrate loading can increase endogenous oxalate production. This seems reasonable, because glucose is involved in oxalate metabolism through a series of chemical interactions with glyoxylate. (Glyoxylate is involved not only in the metabolism of endogenous oxalate but also in the gluconeogenesis pathway and urea metabolism.)

Ketogenic diet

The ketogenic diet is sometimes used to treat intractable seizure disorders in children. It involves an initial period of fluid restriction and starvation until ketone bodies appear in the urine. This is followed by a low-protein, low-carbohydrate, fluid-restricted diet, which tends to cause chronic metabolic acidosis with hypocitraturia and relatively low urinary volumes, which, in turn, induce kidney stone formation. Elevated uric acid levels have also been reported.

The average time from initiation of the diet until stone presentation is about 18 months, so patients who are started on this diet should be checked for stone formation at about 12 months after diet application. Fluid liberalization and citrate supplements can be used to prevent kidney stone formation in these patients.

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