Kidney stones form when certain minerals in your urine become so concentrated that they crystallize and stick together. About 1 in 10 people will develop a kidney stone at some point, and the causes range from everyday habits like not drinking enough water to underlying medical conditions you might not know you have. Most stones are made of calcium oxalate, but the type of stone you form depends on what’s driving the problem.
How Stones Actually Form
Your kidneys filter waste products out of your blood and dissolve them in urine. When the concentration of certain minerals, particularly calcium, oxalate, and uric acid, gets too high relative to the amount of liquid in your urine, the solution becomes “supersaturated.” At that point, crystals can start to form.
Stone formation is a multi-step process. First, tiny crystals form in the kidney’s drainage tubes. Then those crystals grow, clump together, and eventually anchor themselves to the kidney lining. If they keep growing, they become large enough to block urine flow and cause pain. The speed and likelihood of this happening depend on how concentrated your urine stays over time, which is shaped by what you eat, how much you drink, your genetics, and your overall health.
Not Drinking Enough Water
Low fluid intake is the single most consistent risk factor for kidney stones. When you don’t drink enough, your urine volume drops, and the minerals dissolved in it become more concentrated. The American Urological Association recommends that anyone who has formed a stone aim for a daily urine output of at least 2.5 liters, which typically means drinking around 3 liters of fluid per day. For people with cystine stones (a less common type), the target is even higher, often requiring 4 liters of daily fluid intake.
Both observational studies and randomized controlled trials confirm that higher fluid intake reduces stone risk. This is one of the few causes you can address immediately and for free. If your urine is consistently dark yellow, you’re likely not drinking enough.
Too Much Sodium
Sodium has a direct effect on how much calcium ends up in your urine. When you eat a lot of salt, your kidneys excrete more calcium to compensate. That extra calcium raises the concentration of stone-forming minerals, increasing your risk. Current guidelines suggest limiting sodium to no more than 2,300 milligrams per day, roughly one teaspoon of table salt. Most people consume well above this, largely from processed foods, restaurant meals, and packaged snacks rather than the salt shaker at home.
Diet: Oxalate, Protein, and the Calcium Paradox
Calcium oxalate stones are the most common type, so it’s natural to assume you should avoid calcium. The opposite is true. A randomized controlled trial found that people who ate adequate calcium had fewer stones than those on a low-calcium diet. The reason: calcium in food binds to oxalate in your digestive tract, preventing oxalate from being absorbed into your bloodstream and filtered through your kidneys. Cutting calcium from your diet actually increases the amount of oxalate that reaches your urine.
Calcium supplements, however, tell a different story. Unlike calcium from food, supplements don’t always arrive in your gut at the same time as oxalate-rich foods. They may be linked to an increased risk of stones, so it’s worth discussing supplement use with your doctor if you’re stone-prone.
Oxalate-rich foods like spinach, rhubarb, beets, and nuts get a lot of attention, but limiting them only makes sense if your urine oxalate levels are actually elevated. Not everyone who forms calcium oxalate stones has high urinary oxalate, so blanket restrictions aren’t necessary for all stone formers.
Animal Protein and Uric Acid Stones
Eating large amounts of animal protein, particularly red meat, organ meats, poultry, eggs, and fish, raises uric acid levels and makes your urine more acidic. Both of these changes promote uric acid stone formation. Purines, compounds found at especially high levels in organ meats like liver and kidneys, break down into uric acid. When uric acid builds up and urine stays consistently acidic, the uric acid can crystallize on its own or combine with calcium to form stones.
Obesity and Metabolic Conditions
Carrying excess weight changes your urine chemistry in ways that favor stone formation. Obesity is associated with lower urine pH (more acidic urine), higher calcium excretion, and higher uric acid levels. People with type 2 diabetes face a similar pattern because insulin resistance affects how the kidneys handle acid, keeping urine pH persistently low.
Primary hyperparathyroidism is another important metabolic cause. The parathyroid glands, four tiny glands in your neck, regulate calcium levels. When one of these glands becomes overactive, it pumps too much calcium into your bloodstream. Your kidneys then filter that excess calcium into your urine, sometimes pushing daily calcium excretion to 350 to 450 milligrams, well above normal levels. That flood of calcium creates extremely high supersaturation in the urine, and stones form as a direct result. This condition is detected through a routine blood test showing elevated calcium, and surgical removal of the overactive gland typically resolves the problem.
Urinary Tract Infections
Some kidney stones aren’t caused by diet or metabolism at all. They’re caused by specific bacteria that infect the urinary tract. Certain species, particularly Proteus bacteria, produce an enzyme called urease that breaks down urea (a normal waste product in urine) into ammonia. This reaction happens roughly 10,000 times faster than urea would break down on its own. The ammonia makes urine dramatically more alkaline, and in that environment, magnesium and phosphate combine with the ammonium to form struvite crystals.
Struvite stones can grow rapidly and sometimes fill an entire branch of the kidney’s collecting system, forming what’s called a staghorn stone. These stones are more common in women (who are more prone to urinary tract infections) and in people who use catheters. Treatment involves both removing the stone and eliminating the underlying infection, because the stone will keep growing as long as the bacteria persist.
Medications That Raise Risk
Several common medications can contribute to stone formation. Certain diuretics (water pills) increase the amount of calcium in your urine. Topiramate, used for seizures and migraines, lowers citrate levels in urine and raises pH, creating conditions favorable for calcium phosphate stones. Some protease inhibitors used in HIV treatment can themselves crystallize in the kidneys. Certain antibiotics, including some sulfonamides and fluoroquinolones, can also form crystals in concentrated urine. If you’ve had a kidney stone and take any of these medications, your prescriber may be able to adjust your treatment or add preventive measures.
Family History and Genetics
Your risk of forming kidney stones roughly doubles if a close family member has had them. Some of this is genetic: inherited conditions like cystinuria cause the kidneys to leak excessive amounts of the amino acid cystine into the urine, leading to cystine stones that can start forming in childhood. Other genetic factors are subtler, influencing how efficiently your kidneys reabsorb calcium or how much oxalate your liver produces. Even without a clear genetic diagnosis, a strong family history of stones suggests your baseline urine chemistry may lean toward supersaturation, making lifestyle factors like hydration and diet even more important.
Climate and Seasonal Patterns
Stone rates are higher in hotter climates and peak during summer months. The mechanism is straightforward: heat causes sweating, sweating reduces urine volume, and lower urine volume raises mineral concentration. People who work outdoors, exercise heavily, or live in consistently warm regions face higher baseline risk simply because they lose more fluid through their skin. This is one reason the southeastern United States has long been called the “kidney stone belt.”