There are four main types of kidney stones, classified by their chemical composition: calcium stones, uric acid stones, struvite (infection) stones, and cystine stones. Calcium-based stones are by far the most common, making up 65 to 70% of all cases. Knowing which type you have matters because each one forms for different reasons and responds to different prevention strategies.
Calcium Stones
Most kidney stones contain calcium, and they come in two main varieties. Calcium oxalate stones are the most frequent, accounting for 35 to 70% of all kidney stones. Calcium phosphate stones are less common, making up 5 to 20% of cases. Another 10 to 30% of stones are a mixture of both.
Calcium oxalate stones form when there’s too much calcium or oxalate in the urine. Many people who develop them have a condition where their body puts excess calcium into the urine. This can happen because the intestines absorb too much calcium from food, the bones release too much calcium, or the kidneys simply don’t regulate calcium output properly. High-oxalate foods like spinach, rhubarb, nuts, and chocolate also contribute, since oxalate binds with calcium in the urine to form crystals.
Here’s a detail that surprises many people: eating enough calcium actually helps prevent calcium oxalate stones rather than causing them. When you consume calcium with meals, it binds to oxalate in your intestines before either substance reaches your kidneys. If there’s not enough calcium in your gut, the oxalate gets absorbed into your bloodstream instead and ends up concentrated in your urine, raising your stone risk.
Calcium phosphate stones tend to form in people with a condition called renal tubular acidosis, where the kidneys don’t properly regulate acid levels in the blood. These stones develop in more alkaline (less acidic) urine, which distinguishes them from calcium oxalate stones.
A molecule called citrate plays a protective role against both types. Citrate binds to calcium in the urine, preventing it from linking up with oxalate or phosphate to form crystals. People with low urinary citrate levels are at higher risk for calcium stones.
Uric Acid Stones
Pure uric acid stones account for about 10% of all kidney stones. They form under two conditions: when uric acid levels in the urine are too high, and when urine is persistently too acidic.
Diet is a major driver. Animal proteins, including beef, poultry, pork, eggs, and fish, contain compounds called purines that break down into uric acid. Organ meats like liver and kidneys have the highest purine concentrations. Eating large amounts of these foods causes uric acid to build up in the urine.
But diet isn’t the only factor. Uric acid stones are closely tied to metabolic health. People with a BMI over 25, type 2 diabetes, or insulin resistance are at elevated risk. High salt and sugar intake, a sedentary lifestyle, certain medications (including some diuretics), and a family history of kidney stones all increase the chances. Patients who’ve undergone bariatric surgery also face higher risk because of changes in how their bodies process nutrients.
Unlike calcium stones, uric acid stones are invisible on standard X-rays, which can make them trickier to detect. They can sometimes be dissolved by making the urine less acidic, a treatment approach that doesn’t work for other stone types.
Struvite (Infection) Stones
Struvite stones make up about 15% of kidney stones and form through a completely different mechanism than the others. They’re caused by urinary tract infections involving bacteria that produce an enzyme called urease. This enzyme breaks down urea, a normal waste product in urine, at a rate roughly 10,000 times faster than it would break down on its own.
When urease-producing bacteria split urea apart, the chemical reaction releases ammonium ions and alkaline compounds that dramatically raise the urine’s pH. In this newly alkaline environment, ammonium crystallizes with magnesium and phosphate (minerals normally dissolved harmlessly in urine) to form struvite crystals. The combination of high ammonium levels and high pH creates ideal conditions for rapid stone growth.
Struvite stones are particularly concerning because they can grow quickly and fill the entire interior drainage system of the kidney, forming what’s known as a staghorn stone, named for its branching, antler-like shape. These large stones can cause serious kidney damage if left untreated. Treatment typically requires both removing the stone and clearing the underlying infection, since the stone itself harbors bacteria that antibiotics alone can’t reach.
Cystine Stones
Cystine stones are rare, accounting for about 2% of all kidney stones, but they tend to affect people at a younger age and recur frequently. They’re caused by an inherited genetic disorder called cystinuria.
Normally, the kidneys filter cystine (an amino acid) out of the blood and then reabsorb most of it back before it leaves the body in urine. In people with cystinuria, mutations in one of two specific genes disrupt the protein complex responsible for this reabsorption. The result is that cystine builds up in the urine to concentrations high enough to form crystals and eventually stones.
Because cystinuria is genetic, people who form cystine stones will deal with the condition for life. Both parents must carry a copy of the affected gene for the condition to develop, though the inheritance pattern varies depending on which gene is involved. Management focuses on keeping cystine dissolved in the urine through high fluid intake and sometimes medications that make cystine more soluble.
How Stone Type Is Identified
If you pass a kidney stone or have one removed, your doctor will send it to a lab for chemical analysis. The American Urological Association recommends that every stone former have at least one stone analyzed, with repeat analysis for anyone whose stones keep coming back despite treatment. Knowing the composition changes the entire prevention plan.
Beyond the stone itself, a 24-hour urine collection helps identify the metabolic imbalances driving stone formation. This test measures urine volume, pH, and levels of calcium, oxalate, uric acid, citrate, sodium, and other substances. Two separate collections are preferred for accuracy, and follow-up collections are recommended within six months of starting any prevention plan to see if it’s working.
Prevention by Stone Type
One recommendation applies to every stone type: drink enough fluid to produce at least 2.5 liters of urine per day. Beyond that, prevention depends on what kind of stone you form.
For calcium oxalate stones, the focus is on limiting high-oxalate foods, getting adequate calcium from meals (not supplements taken on an empty stomach), and keeping sodium under 2,300 mg per day. Excess sodium causes the kidneys to excrete more calcium, raising stone risk. This sodium limit applies to calcium phosphate stone formers as well.
For uric acid stones, reducing animal protein intake is the primary dietary change. Cutting back on purines lowers the amount of uric acid the body needs to excrete. Maintaining a healthy weight and managing blood sugar also help, since insulin resistance contributes to overly acidic urine.
For struvite stones, prevention centers on treating and preventing urinary tract infections. Without an active infection, these stones don’t form.
For cystine stones, very high fluid intake (often 3 liters or more per day) is essential to keep cystine diluted below the concentration at which it crystallizes. Some people also need medications that chemically bind to cystine, making it more soluble in urine.