There are four main types of kidney stones, each formed by different chemicals and driven by different underlying causes: calcium oxalate, calcium phosphate, uric acid, struvite, and cystine. A fifth category, drug-induced stones, is rare but worth knowing about. The type you have determines how it’s treated and what you can do to prevent another one.
Calcium Oxalate Stones
Most kidney stones are made of calcium and oxalate, making this the most common type by a wide margin. They form when calcium and oxalate concentrations in urine get high enough to crystallize together. The underlying cause varies from person to person. Some people absorb too much calcium from food, others release too much calcium from their bones, and some simply have kidneys that let excess calcium pass into urine.
High oxalate levels in urine can also drive these stones. Inflammatory bowel diseases like Crohn’s or ulcerative colitis increase oxalate absorption, as does prior intestinal surgery. Urinary oxalate levels above 25 milligrams per day raise stone risk, and levels above 40 milligrams per day suggest a more serious underlying problem with oxalate metabolism.
One counterintuitive point: eating enough calcium actually helps prevent calcium oxalate stones. Under normal conditions, calcium binds to oxalate in the intestine and both are eliminated from the body. If you cut calcium from your diet, oxalate has nothing to bind with, gets reabsorbed, and ends up in your urine where it can form stones. Aiming for 300 to 400 milligrams of calcium with each meal is a practical target. At the same time, limiting high-oxalate foods like spinach, chard, rhubarb, star fruit, and beets reduces the raw material available for stone formation. Potatoes, chocolate, nuts, and bran are moderate-oxalate foods worth eating in smaller portions.
Your body also has a natural defense: citrate, a molecule in urine that binds to calcium and prevents it from latching onto oxalate or phosphate. Low citrate levels leave calcium free to crystallize, which is why citrate-boosting strategies (like drinking lemon water) are a common prevention recommendation.
Calcium Phosphate Stones
Calcium phosphate stones are the less common sibling of calcium oxalate stones. They form through a similar mechanism, with excess calcium in urine, but the calcium pairs with phosphate instead of oxalate. Alkaline urine (higher pH) favors their formation, which is the opposite of what triggers uric acid stones.
One specific condition linked to calcium phosphate stones is renal tubular acidosis, a disorder where the kidneys fail to properly acidify urine. This creates the persistently alkaline environment that promotes phosphate crystallization. If you’ve been told you have calcium phosphate stones, your doctor will likely check for this condition, since treating it can prevent recurrence.
Uric Acid Stones
Uric acid stones form in acidic urine and account for a meaningful minority of all kidney stones. Unlike calcium-based stones, which show up clearly on standard X-rays, uric acid stones are radiolucent, meaning they’re invisible on plain imaging. Detecting them typically requires a CT scan.
The chemistry is straightforward: uric acid dissolves in alkaline urine but crystallizes when urine pH drops too low. People with metabolic syndrome, which includes insulin resistance, obesity, and type 2 diabetes, are especially prone to uric acid stones. Insulin resistance reduces the kidneys’ ability to excrete ammonium, a buffer that normally keeps urine from becoming too acidic. Without enough ammonium, urine stays acidic and uric acid precipitates into crystals.
This also means uric acid stones are uniquely treatable without surgery. Because the stones dissolve in alkaline conditions, raising urine pH through medication or dietary changes can shrink or eliminate existing stones and prevent new ones. High fluid intake and reducing purine-rich foods (red meat, organ meats, shellfish) also help by lowering the amount of uric acid the kidneys need to process.
Struvite Stones
Struvite stones are fundamentally different from other types because they’re caused by urinary tract infections, not metabolic imbalances. Certain bacteria produce an enzyme called urease that splits urea in urine into ammonia and carbon dioxide. This reaction makes urine extremely alkaline, pushing the pH above 7.2, a level the body can’t reach on its own. At that pH, magnesium ammonium phosphate and calcium phosphate crystallize rapidly.
The bacteria responsible include Proteus (100% of Proteus species produce urease), along with Klebsiella, Staphylococcus, and Pseudomonas, among others. Notably, E. coli, the most common cause of urinary tract infections, almost never produces urease, so not every UTI leads to struvite stones.
What makes struvite stones dangerous is how they grow. The highly alkaline urine damages the protective lining of the urinary tract, allowing bacteria to form biofilms on the tissue surface. Crystals precipitate within these biofilms, and as bacteria keep secreting material, the stone grows outward, often filling the entire interior of the kidney. These large, branching stones are sometimes called “staghorn” stones because of their shape. They can cause serious kidney damage if untreated and almost always require surgical removal along with antibiotics to clear the underlying infection.
Cystine Stones
Cystine stones are rare, accounting for only 1% to 2% of all kidney stones in adults, though they make up 6% to 8% of kidney stones in children. They’re caused by cystinuria, an inherited genetic condition passed down in an autosomal recessive pattern, meaning a child must receive the defective gene from both parents.
The defect prevents the kidneys from properly reabsorbing an amino acid called cystine. Normally, the kidneys filter cystine out of blood and then pull most of it back in. In cystinuria, too much cystine stays in the urine, where it’s poorly soluble and forms hexagonal crystals. The same genetic defect also affects reabsorption of three other amino acids (ornithine, lysine, and arginine), but only cystine is insoluble enough to form stones.
Because cystinuria is a lifelong genetic condition, people with cystine stones tend to form them repeatedly starting at a young age. Management focuses on keeping urine diluted through very high fluid intake and raising urine pH to increase cystine solubility. Like uric acid stones, cystine stones are radiolucent and don’t show up on standard X-rays.
Drug-Induced and Rare Stones
A small percentage of kidney stones are caused by medications or extremely rare metabolic conditions. Certain drugs, including some HIV medications, a diuretic called triamterene, and sulfonamide antibiotics, can crystallize in urine and form stones directly. These stones are also radiolucent, making them harder to detect on routine imaging.
Hereditary xanthinuria is one of the rarest stone-forming conditions. People with this genetic disorder can’t properly break down a compound called xanthine, which accumulates in the kidneys, forms tiny crystals, and occasionally builds into stones large enough to block urine flow or impair kidney function.
Radiolucent stones of all types, including uric acid, cystine, and drug-induced varieties, make up roughly 10% of all kidney stones. When standard imaging comes back clean but symptoms persist, a low-dose CT scan can reveal what a plain X-ray misses.
How Stone Type Affects Treatment
Identifying your stone type matters because it changes both the immediate treatment and the long-term prevention strategy. For stones 10 millimeters or smaller stuck in the lower ureter, the initial approach is often a medication that relaxes the ureter walls, giving the stone about 30 days to pass on its own. Stones that don’t pass, or that are larger than 10 millimeters, typically need a procedure.
The two most common procedures are ureteroscopy, where a thin scope is threaded up to the stone and breaks it apart, and shockwave lithotripsy, which uses external sound waves to fragment the stone. For larger kidney stones over 2 centimeters, a more involved procedure through a small incision in the back is the recommended first-line approach. Uric acid stones are the notable exception to the surgical track, since they can often be dissolved by making urine more alkaline.
If you’ve passed a stone, saving it for analysis is one of the most useful things you can do. Knowing whether your stone is calcium oxalate, uric acid, struvite, or cystine gives you a specific prevention plan rather than generic advice. A 24-hour urine collection can further pinpoint the metabolic imbalance driving stone formation, whether that’s excess calcium, low citrate, acidic urine, or high oxalate.