The main cause of kidney stones is urine becoming too concentrated with dissolved minerals, a condition called urinary supersaturation. When levels of calcium, oxalate, uric acid, or phosphate rise high enough in the urine, these substances crystallize and gradually build into solid stones. About 10% of U.S. adults will develop a kidney stone in their lifetime, and without preventive changes, the five-year recurrence rate reaches as high as 40%.
Several factors push urine toward that tipping point: not drinking enough fluid, eating too much salt or animal protein, certain medical conditions, and genetics. Understanding which factors apply to you is the key to prevention.
How Kidney Stones Actually Form
Your kidneys filter waste from the blood and dissolve it in urine. Normally, that waste stays dissolved. But when the concentration of stone-forming substances climbs too high, or when the volume of urine drops too low, crystals begin to form. This process follows a predictable sequence: supersaturation, then tiny crystal seeds (nucleation), then growth and clumping of those crystals into a visible stone.
Healthy urine contains natural inhibitors that work to prevent crystals from sticking together or latching onto the walls of kidney tissue. Citrate is one of the most important. It binds to calcium in the urine, reducing the amount available to form crystals, and it directly blocks crystal growth and clumping. Whether you develop a stone depends on the balance between these protective inhibitors and the concentration of stone-forming minerals. When the scale tips toward supersaturation, stones start to grow.
Calcium Oxalate: The Most Common Type
Most kidney stones are calcium stones, and the vast majority of those are calcium oxalate. Oxalate is a natural compound your liver produces daily, and you also absorb it from food. When oxalate levels in the urine get too high, it pairs with calcium and crystallizes.
Foods especially high in oxalate include spinach, rhubarb, nuts and nut products, peanuts, and wheat bran. That said, the goal isn’t to eliminate calcium from your diet. In fact, eating calcium-rich foods with meals helps bind oxalate in the digestive tract before it ever reaches the kidneys. The problem isn’t dietary calcium itself; it’s the oxalate-to-calcium ratio in the urine.
A less common subtype, calcium phosphate stones, tends to form in people with specific metabolic conditions that make urine more alkaline.
Low Fluid Intake Is the Biggest Modifiable Risk
If there’s one factor within your control that matters most, it’s how much water you drink. The core prevention guideline from urologists is to drink enough fluid to produce more than 2.5 liters (about 10.5 cups) of urine per day. Most people fall well short of that.
When urine volume is low, every stone-forming substance becomes more concentrated. Drinking more water is the simplest way to dilute those minerals below the threshold where crystals form. This applies regardless of the type of stone you’re prone to. For many people, chronic mild dehydration over years is the single biggest contributor to their first stone.
How Salt Drives Calcium Into the Urine
High sodium intake is one of the most underappreciated causes of calcium stones. The kidneys handle sodium and calcium through related pathways. When you eat a lot of salt, your kidneys excrete more sodium, and calcium gets pulled along with it. Research shows that for every 2,300 mg of sodium you consume (roughly one teaspoon of table salt), your body excretes an additional 40 to 44 mg of calcium in the urine.
That extra urinary calcium raises your supersaturation level and makes crystal formation more likely. Reducing sodium intake to below 2,300 mg per day is one of the most effective dietary changes for people with calcium stones, often more impactful than restricting dietary calcium.
Uric Acid Stones and Urinary pH
Uric acid stones account for a smaller but significant share of kidney stones. They form through a different mechanism than calcium stones. The critical factor is the acidity of your urine, not just how much uric acid is present. When urinary pH drops below 5.5, uric acid becomes much less soluble and starts to crystallize. Someone with normal uric acid levels but persistently acidic urine can still develop these stones.
Conditions that increase the risk include insulin resistance, type 2 diabetes, obesity, gout, and chronic diarrhea (which causes the body to lose bicarbonate and makes urine more acidic). Because uric acid solubility is so pH-dependent, treatment often focuses on raising urinary pH rather than just reducing uric acid production.
Infection-Related Stones
Struvite stones form when certain bacteria colonize the urinary tract and produce an enzyme that breaks down urea into ammonia. This chemical reaction raises the pH of the urine dramatically and creates conditions where magnesium, ammonium, and phosphate crystallize together. The bacteria responsible include species commonly found in urinary tract infections. These stones can grow rapidly and become quite large, sometimes filling the entire interior of the kidney. They’re more common in people with recurrent UTIs or structural abnormalities that make infections hard to clear.
Medical Conditions That Raise Risk
Several medical conditions can shift your body’s chemistry toward stone formation. One of the most well-known is overactivity of the parathyroid glands, which sit behind the thyroid in the neck. These glands regulate calcium balance. When they overproduce parathyroid hormone, the body pulls more calcium from bones and absorbs more from food, flooding the bloodstream and eventually the urine with excess calcium. The resulting spike in urinary calcium is a direct driver of stone formation.
Inflammatory bowel conditions and intestinal bypass surgery can also increase stone risk by changing how the gut absorbs oxalate and other minerals. Metabolic syndrome, which includes high blood pressure, elevated blood sugar, and excess abdominal fat, raises the likelihood of both calcium and uric acid stones.
Genetic Causes
Some people form stones because of inherited conditions. Cystinuria is the clearest example. It’s caused by mutations in genes that control how the kidneys reabsorb certain amino acids from urine. Normally, cystine (an amino acid) is filtered and then pulled back into the blood. In people with cystinuria, that reabsorption system doesn’t work, so cystine builds up in the urine and forms crystals. This condition typically causes stones starting in childhood or adolescence and requires lifelong management.
Even for common calcium oxalate stones, genetics plays a role. Family history is one of the strongest predictors of stone risk, likely because traits like how efficiently your kidneys handle calcium, oxalate, and citrate are partly inherited.
The Role of Citrate in Prevention
Citrate is your urine’s built-in defense against calcium stones. It works in three ways: it binds to calcium so less is available to pair with oxalate, it directly inhibits crystal growth and clumping, and it can reduce overall calcium excretion by forming complexes with calcium in the gut. People with low urinary citrate levels, a condition called hypocitraturia, face a significantly higher risk of stone formation.
Citrus fruits and their juices are natural sources of citrate. Lemon juice in particular is often recommended as a simple dietary addition. For people with very low citrate levels, supplemental citrate salts can help restore that protective balance.