Kidney stones are more common in men than in women. They are formed when the concentration of components in the urine reaches a levels at which crystallization is possible. Kidney stones are generally composed of calcium salts, uric acid, cystine or struvite. The cause of the different types of kidney stones and their treatment differ. Several long-term follow-up studies suggest that stones will reoccur in most patients who pass a single stone. For this reason, it is advisable that there be a stone analysis and metabolic evaluation after the first or second stone. Analysis of the kidney stone is not as important as identifying and treating the underlying condition.

Regardless of the type of stone or its cause, it is important to drink between 1.5 – 3 litres of fluid every day in order to produce 2 litres of urine daily. This is essential for treating and preventing further kidney stone formation. The goal of this rigorous hydration is to keep the urine dilute, preventing the crystallization of stone-forming minerals.

One study showed that fluid in the form of tea, decaffeinated coffee, regular coffee or wine reduced the risk of stone formation. Milk, sodas and fruit juice had no effect on the risk of stone formation. Grapefruit juice however, increased the risk of stone formation and should therefore be limited.

Calcium Oxalate and Calcium Phosphate Stones

About 80% of stones are composed of calcium oxalate (alone or with a core of calcium phosphate) and are most common in middle aged men. Their causes are multiple and include hyperparathyroidism, hyperuricosuria (excessive amounts of uric acid in the urine), idiopathic hypercalciuria (excessive amounts of calcium in the urine), low urine citrate level, distal renal tubular acidosis (accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine), hyperoxaluria (excessive urinary excretion of oxalate) and possibly infection with nanobacteria.

The primary treatment of calcium oxalate and calcium phosphate stones involves correction of the specific defect. For hyperparathyroidism this includes the removal of parathyroid adenoma; for hyperuricosuria, dietary protein reduction and medication with allopurinol is required; hypercalciuria requires protein restriction or diuretic use and for RTA, medication with bicarbonate and potassium will be needed.

Overproduction of oxalate, or primary hyperoxaluria, is a rare inherited, metabolic disorder. It leads to recurrent calcium oxalate stones and eventually deposition of calcium oxalate in the kidney, progressive kidney insufficiency and usually death before the third decade of life. A long-term study found that optimal treatment seems to include early diagnosis and treatment with large doses of pyridoxine.

Another form of hyperoxaluria, enteric hyperoxaluria, results from the gut over absorbing oxalate. This is commonly seen in diseases of the small intestine such as Crohn’s disease, celiac sprue, intestinal bypass surgery or pancreatic insufficiency. It is also possible that excessive intakes of Vitamin C over 1000mg per day may increase urinary oxalate. Treatment of this disorder requires 800 – 1200mg/day of oral calcium (which binds oxalate) as well as a low-oxalate intake. Even though foods can have high levels of oxalate, to date only eight foods have been shown to actually raise urinary oxalate excretion: rhubarb, spinach, strawberries, chocolate, wheat bran, nuts, beets and tea. Eliminating these foods from the diet will result in a low oxalate intake. Another factor to consider is the wide variation in an individual’s abilities to degrade dietary oxalate in the gut. Oxalate is degraded by oxalobacter formigenes, anaerobic microflora in the human intestine. The presence of these microbes and the amount of degradation of dietary oxalate in the gut could influence the amount of oxalate absorbed, and thus the level in the urine. This may be the reason for enteric hyperoxaluria – an alteration in the presence of oxalate-degrading microbes.

Hypercalciuria (more than 200mg of calcium in a 24hour urine collection) may be the single most important condition underlying calcium stone formation. This condition can either be absorptive (increased intestinal absorption of calcium), renal (impaired absorption of calcium by the kidney: a renal ‘leaker’), or resorptive (excessive resorption of calcium from bone due to primary hyperparathyroidism, which is treated with surgery). The absorptive and renal forms are referred to as idiopathic hypercalciuria, which is by far the most common type of hypercalciuria. The only situation in which a low calcium diet (400 – 600mg daily) would be appropriate is the patient who is a renal ‘leaker’ and even then it poses a threat to bone loss. No studies show that reduced calcium intake, which can reduce urinary calcium, makes a difference in stone recurrence. In most other cases, it may be appropriate to increase dietary calcium intake in order to increase the binding of oxalate by calcium in the gastrointestinal tract, thus reducing the body’s supply of urinary oxalate.

The general policy of calcium restriction for patients with kidney stones containing calcium is not appropriate. Findings provide no support for the belief that a diet low in calcium reduces the risk of kidney stones. In fact, higher dietary calcium intake may decrease the incidence of kidney stones by making more calcium available in the gut to form insoluble calcium oxalate that will not be absorbed. Patients with idiopathic hypercalciurua have been treated effectively with ample fluid intake and thiazide diurectics, which decrease urinary calcium. Maximal effectiveness of thiazides is accomplished by mildly restricting sodium intake to 4 – 5 g/day.

Hyperuricosuria usually leads to the formation of calcium oxalate rather than uric acid stones. Uric acid may form a nidus on which calcium oxalate precipitates. Uric acid also encourages calcium oxalate growth by binding calcium oxalate inhibitors. Dietary intake of protein is directly related to risk of stone formation. Animal protein intake increases the excretion of uric acid and calcium and lowers urinary citrate excretion, all of which are risk factors for stone formation. Hyperuricosuria is treated by limiting protein intake to the level of the recommended dietary allowance (RDA). Potassium supplementation leads to a reduction in calcium excretion in healthy adults and reduces the risk of stone formation. A decreased intake of sodium may also help decrease the risk of calcium stone formation.

Uric acid stones

Uric acid stones are associated with gout and malignant disease as well as some gastrointestinal diseases characterized by diarrhoea. Drugs such as aspirin or probencid can increase uric acid excretion, and thus lead to stone formation. The most important factor involved in forming uric acid stones appears to be the production of acidic urine. For this reason, the cornerstone of management of uric acid stones, in addition to fluid ingestion, is to raise the normally slightly acidic urine pH to within the range of 6.0 – 6.5. This can be accomplished with a high-alkaline ash diet, supplemented with citrate or bicarbonate. Protein may be decreased to the recommended dietary allowance (RDA) if too much uric acid accumulates in the urine.

Potentially Acid or Acidic-Ash Foods should be avoided in excess:           

Meat: Meat, fish, poultry, shellfish, eggs, all types of cheese, peanut butter and peanuts

Fat: Bacon and nuts (Brazil nuts, hazelnuts, walnuts)

Starch: All types of bread (especially whole-wheat), cereal, crackers, macaroni, spaghetti, noodles and rice

Vegetables: Corn and lentils

Fruits: Cranberries, plums and prunes

Desserts: Plain cakes and biscuits

 Potentially Basic or Alkaline-Ash Foods should be included in the diet:

Milk: Milk and milk products, cream, buttermilk

Fat: Nuts (almonds, chestnuts and coconut)

Vegetables: All types (except corn and lentils

Fruits: All types (except cranberries, prunes and plums)

Sweets: Molasses

Neutral Foods can be included in the diet:

Fats: Butter, margarine, cooking fats and oils

Sweets: plain candies, sugar, syrup and honey

Starches: Arrowroot, corn and tapioca

Beverages: Coffee and tea

Cystinine Stones

Cystinine stones, caused by a hereditary disorder of amino acid transport, are a rare and difficult problem to manage. Treatment consists of oral intakes of fluid over 4 litres per day, often requiring getting up during the night to drink and urinate. In addition, an alkaline ash diet and alkaline therapy are needed to raise the urinary pH to 7.5. If these measures alone do not control stone formation, the addition of penicillamine has been beneficial but can have serious effects. Cystinine stones usually cause progressive kidney destruction.

Struvite Stones

Struvite stones constitute 5 – 15% of stones and are usually seen in women. They contain ammonium, magnesium and phosphate and are formed when the urinary tract is infected with organisms, most commonly Proteus or Klebsiella, which produce high concentrations of ammonium. Large stones typically lodge in the renal pelvis, forming staghorn calculi. Recurrent urinary tract infections and progressive kidney failure usually develop with eventual obstruction. Treatment consists of long-term antibiotic therapy as well as surgical or ultrasonic removal of the stones. Dietary management has no significant role in this form of stone disease.

   Article written by Brindy Watson ((RD) SA  - Dieticians at work