The most common types of kidney stones are composed predominantly of calcium oxalate.  A smaller proportion are composed mainly of calcium phosphate.  Many stones can be mixtures of calcium oxalate and phosphate, but usually oxalate will predominate.  

Many factors contribute to the development of calcium oxalate stones.  Physicians perform urinary studies to analyze calcium, oxalate, uric acid, and citrate levels and for dietary levels of sodium and protein.  There can be derangements in the concentrations of one or more of these urine components.  These tests are necessary to guide treatment and dietary changes. 

Calcium is absorbed from the gut and stored in bone.  Body levels are in part regulated by the kidney.  High urine concentrations of calcium can lead to stone formation.  Causes of high urine calcium include a genetic disorder known as familial HYPERCALCIURIA, and also hyperparathyroidism, which is less common in young people.

The cause of hypercalciuria appears to be multifactorial.  Typically there is increased absorbtion of calcium from the diet and/or bones with subsequent increased calcium excretion into the urine.  Treatment is NOT directed at lowering calcium in the diet, or absorption from the gut.  Instead, therapy is designed to decrease calcium concentrations in the urine.  

High levels of OXALATE in the urine (called HYPEROXALURIA)can result from genetic defects and also from diet.  Certain oxalate containing foods such as chocolates (dark or milk) and berries contain large amounts of oxalate.  People with moderate hyperoxaluria and without genetic defects are encouraged to avoid high oxalate containing foods and to eat foods containing calcium, such as dairy products.  These people usually have what is called Dietary Hyperoxaluria. It may be particularly beneficial to eat these calcium containing foods with meals.  Since calcium binds oxalates contained in the food, it prevents the absorption of oxalate in the gut.  The calcium-oxalate complex in the gut is non-absorbable and will be passed in the stool.  In fact, stone formers on low calcium diets form more stones.

Another form of hyperoxaluria is Enteric Hyperoxaluria.  People with this condition usually have digestive disorders such as Crohn's disease, ulcerative colitis, chronic pancreatitis, ileal bypass surgery for the treatment of obesity, or celiac sprue.  These conditions are are characterized by an inability to absorb fat (fat malabsorption). which leads to excess oxalate absorption.  Treatment includes avoiding high oxalate foods and calcium with meals to bind oxalate in the gut to prevent its absorption. 

A rare genetic disease is Primary Hyperoxaluria.  This is an inherited disease characterized by kidney stone formation at a young age and very high urine oxalate levels.  It is due to a liver gene defect.  The only effective treatment is liver transplantation, so that affected people will receive a new iver with the normal gene.  Dieatary therapy is also encouraged but likely of little or no benefit.  If liver transplant is delayed, the kidneys can be irreversibly damaged by massive crystal and stone deposition.  If this happens, then a dual kidney and liver transplantion may be needed.  Another rare cause of hyperoxaluria that must be considered is excessive ingestion of vitamin c. 

HYPOCITRATURIA refers to low amounts of citrate in the urine. High citrate levels help prevent stones from forming.  Some causes include severe potassium deficiency, high levels of protein in the diet, diarrhea, and metabolic acidosis (including renal tubular acidosis).  Treatment is usually with potassium citrate.  Monitoring the blood to detect excess potassium levels may be necessary.  Sodium citrate is avoided.  Increased sodium intake can cause increased calcium excretion in the urine and contribute to hypertension in some patients.  

HYPERURICOSURIA refers to high urinary uric acid concentrations.  Although this can cause uric acid stones, it also can lead to calcium stones.  It is not fully understood how calcium stones occur.  The uric acid crystal may serve as a "seed" crystal on which calcium crystals  will grow, or uric acid may somehow cause calcium crystals to precipitate.  Dietary and pharmacologic treatments are available.