There are five main types of kidney stones, and knowing which kind you have changes everything about how it’s treated and prevented. Roughly 80% of all kidney stones contain calcium, making calcium-based stones by far the most common. The remaining 20% are split among uric acid, struvite, and cystine stones, each with distinct causes and risk factors.
Calcium Oxalate Stones
Calcium oxalate stones account for the majority of all kidney stones. They form when calcium and oxalate, both naturally present in urine, reach concentrations high enough that they can no longer stay dissolved. At that point, tiny crystals begin to form. These crystals can grow layer by layer as more calcium and oxalate ions attach, and individual crystals can clump together into larger particles that eventually become a stone.
One well-studied pathway involves something called Randall’s plaque: small deposits of calcium phosphate form in the tissue of the kidney, and when this plaque becomes exposed to urine, it acts as a seed for calcium oxalate crystals to latch onto and grow. Your body also produces proteins and other molecules that can act like glue between crystals, accelerating the process.
Foods high in oxalate (spinach, rhubarb, beets, nuts, chocolate) can raise oxalate levels in urine, but dietary calcium actually helps. Calcium binds oxalate in the gut before it reaches the kidneys, so cutting calcium from your diet tends to make things worse, not better. Dehydration is the single biggest modifiable risk factor: when urine is concentrated, calcium and oxalate are more likely to exceed their solubility threshold.
Calcium Phosphate Stones
Calcium phosphate stones make up a smaller share of calcium-based stones and tend to form under different conditions than their oxalate counterparts. They’re strongly associated with urine that is more alkaline (higher pH) and with specific medical conditions. People with renal tubular acidosis, a condition where the kidneys can’t properly acidify urine, are especially prone to these stones. Overactive parathyroid glands (primary hyperparathyroidism) also raise calcium levels enough to promote calcium phosphate crystallization.
These stones can form on mineral plugs that fill and damage the tiny tubules at the tip of the kidney, which distinguishes them from the plaque-seeded process more typical of calcium oxalate stones. Treatment focuses on managing the underlying condition. If hyperparathyroidism is the cause, for example, correcting it often stops new stones from forming.
Uric Acid Stones
Uric acid stones make up roughly 5% to 10% of kidney stones and are unique because they can often be dissolved without surgery. The key factor isn’t how much uric acid you produce. It’s how acidic your urine is. When urine pH drops below about 5.5, uric acid becomes nearly insoluble and crystals form readily. Most uric acid stone formers have an average urine pH around 5.3 to 5.4, well within that danger zone.
Raising urine pH above 6.0, typically with a potassium citrate supplement, prevents new uric acid stones and can dissolve existing ones. This makes uric acid the most medically treatable stone type. Contrary to popular advice, restricting purine-rich foods like red meat and organ meats has not been shown to make a meaningful difference on its own. pH and urine volume are what matter.
People with type 2 diabetes, obesity, or metabolic syndrome are at higher risk because these conditions tend to produce persistently acidic urine. Chronic diarrhea can also lower urine pH by depleting the body’s bicarbonate stores.
Struvite Stones
Struvite stones are fundamentally different from other types because they’re caused by bacterial infection, not metabolism. Certain bacteria, most commonly Proteus species, produce an enzyme that breaks down urea in urine into ammonia. This raises the urine pH above 7.2, creating an alkaline environment where magnesium, ammonium, and phosphate crystallize together.
These stones grow quickly and can fill the entire interior of the kidney, forming a branching shape called a staghorn calculus. Because they expand to fill the space rather than blocking a narrow passage, they often don’t cause the sharp, sudden pain people associate with kidney stones. Many are discovered during imaging for other reasons or when a persistent urinary tract infection won’t clear up.
Struvite stones contain a higher proportion of organic material (proteins from the bacterial infection) than other stone types, which can shield the bacteria from antibiotics. This is why treatment almost always requires complete surgical removal. Leaving fragments behind risks re-infection and rapid regrowth. Women and people who use urinary catheters are at higher risk because of their greater susceptibility to urinary tract infections with urease-producing bacteria.
Cystine Stones
Cystine stones are the rarest type, caused by an inherited genetic condition called cystinuria. Mutations in one of two genes (SLC3A1 or SLC7A9) disable a protein complex in the kidneys that normally reabsorbs the amino acid cystine back into the bloodstream. Without this reabsorption, cystine builds up in the urine until it crystallizes.
Because the cause is genetic, cystine stones typically appear early in life, often in childhood or adolescence, and recur throughout a person’s lifetime. They tend to be harder than other stone types and more resistant to the shock wave treatments used to break up calcium stones. Management revolves around keeping urine very dilute (targeting at least 3 liters of urine output per day) and alkalinizing the urine to a pH of 7.0 or higher with potassium citrate, since cystine dissolves more readily in alkaline conditions.
How Stone Type Is Identified
When you show up with flank pain and a suspected stone, a non-contrast CT scan is the standard diagnostic tool, with sensitivity as high as 97% for detecting stones of all sizes. Ultrasound is less reliable overall (24% to 57% sensitivity on grayscale), though adding color Doppler imaging improves detection significantly, especially for small stones. Plain X-rays miss most stones under 5 mm, catching only about 8% of them.
Imaging tells your doctor where the stone is and how big it is, but not what it’s made of. That requires either lab analysis of a passed or surgically removed stone, or clues from blood and urine tests. A 24-hour urine collection measures calcium, oxalate, uric acid, citrate, and pH levels, helping identify which metabolic imbalances are driving stone formation. This is especially important for people who’ve had more than one stone, since targeted prevention depends entirely on knowing the type.
Prevention Across All Types
Regardless of stone type, producing enough urine to keep minerals diluted is the single most effective preventive measure. The target is at least 2.5 liters of urine per day, which for most people means drinking about 3 liters of fluid daily. Men, people with higher body weight, and those who eat more salt and animal protein tend to reach this target more easily, while others may need to make a conscious effort.
Beyond hydration, prevention becomes type-specific. For calcium stones that keep recurring, options include medications that reduce how much calcium the kidneys release into urine, potassium citrate to raise citrate levels (citrate inhibits crystal formation), or medications that lower uric acid production. These are typically started after a second stone episode, even when urine tests don’t show an obvious abnormality. For uric acid stones, alkalinizing the urine is the primary strategy. For cystine stones, high fluid intake and urine alkalinization are the foundation, sometimes combined with medications that make cystine more soluble.
For stones between 5 and 10 mm stuck in the lower ureter, medications that relax the smooth muscle of the urinary tract can improve the chances of passing the stone naturally, reduce pain, and help avoid surgery.