Kidney stones come from minerals and salts that are naturally present in your urine. When those substances become too concentrated, they can crystallize and clump together into solid masses. About 1 in 100 adults under 65 will deal with a kidney stone in any given year, and that number climbs to roughly 4 in 100 for people over 65. Understanding where stones actually come from helps explain why some people get them repeatedly and others never do.
How Minerals Turn Into Stones
Your kidneys filter your blood and pull out waste products like calcium, oxalate, phosphate, and uric acid. In your blood, these substances stay dissolved easily. But your kidneys also extract most of the water from that filtrate, sending it back into your body while directing the waste toward your bladder. That water extraction concentrates the stone-forming salts dramatically.
When the concentration of those salts exceeds what the remaining water can hold in solution, the urine becomes “supersaturated.” Think of stirring sugar into a glass of water: at some point, no more sugar dissolves, and crystals start forming at the bottom. Your urine works the same way. Supersaturation is the driving force behind every kidney stone, regardless of type. At the same time, urine normally contains substances (like citrate) that prevent crystals from sticking together. When those protective factors are low or the mineral load is high, stones get their chance.
Calcium Oxalate: The Most Common Type
The majority of kidney stones are calcium stones, and most of those are made of calcium oxalate. Oxalate is a compound your liver produces daily as a normal byproduct of metabolism. You also absorb it from food. Spinach, beets, nuts, chocolate, and certain other fruits and vegetables are particularly high in oxalate.
Anything that raises the concentration of calcium or oxalate in your urine increases your risk. That includes high doses of vitamin D (which boosts calcium absorption), intestinal bypass surgery (which changes how your gut handles oxalate), and various metabolic conditions. High-dose vitamin C supplements are another overlooked trigger: your body converts excess vitamin C into oxalate. The average person only needs 75 to 90 milligrams of vitamin C per day, but supplements often deliver ten times that amount or more. If you have a history of calcium oxalate stones, those supplements are worth reconsidering.
A rare inherited condition called primary hyperoxaluria causes the body to overproduce oxalate, leading to recurrent calcium oxalate stones starting in childhood or early adulthood.
Uric Acid Stones and Low Urine pH
Uric acid stones form when urine is too acidic. Uric acid dissolves well in slightly alkaline or neutral urine, but once the pH drops below about 5.5, the molecule loses its ability to stay in solution and begins to crystallize. Raising urine pH to around 6 is often enough to stop the process entirely.
The conditions most commonly linked to persistently acidic urine are obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease. These conditions share a common thread of insulin resistance, which appears to impair the kidney’s ability to produce ammonia, a natural urine alkalizer. Gout is another well-known association. Many people with gout have both reduced kidney clearance of uric acid and low urine pH, so uric acid stones and gout frequently coexist.
Infection Stones From Bacteria
Struvite stones are different from other types because they’re caused directly by bacterial infections in the urinary tract. Certain bacteria produce an enzyme called urease, which breaks down urea (a normal component of urine) into ammonia at an extremely fast rate, roughly 10,000 times faster than urea would break down on its own. That flood of ammonia does two things: it sharply raises the pH of the urine, making it very alkaline, and it creates ammonium ions. Those ammonium ions then crystallize with magnesium and phosphate that are already present in urine, forming struvite.
Struvite stones can grow quickly and become quite large. One practical clue is a strong ammonia smell in your urine, which can signal the presence of urease-producing bacteria. These stones are treated by addressing the underlying infection, not just removing the stone itself.
Cystine Stones: A Genetic Cause
A small percentage of kidney stones are made of cystine, an amino acid. These stones result from an inherited condition called cystinuria, caused by mutations in either of two genes (SLC3A1 or SLC7A9). Normally, your kidneys filter cystine out of blood and then reabsorb most of it back. In cystinuria, the protein complex responsible for that reabsorption is defective, so cystine builds up in the urine and crystallizes. People with cystinuria often start forming stones in their teens or twenties and tend to have recurrent episodes throughout life.
Who Gets Kidney Stones
Men are more likely to develop kidney stones than women, especially after age 65. Between 2012 and 2021, the prevalence among men over 65 in the U.S. rose from 4.3% to 6.4%, while for women in the same age group it went from 2.1% to 3.1%. Among younger working-age adults, the gender gap is much smaller. In some populations, women develop stones at rates comparable to men.
Overall prevalence has been climbing for both sexes and across age groups, which researchers attribute to rising rates of obesity, dietary changes, and possibly climate-related dehydration.
What Drives Recurrence
Once you’ve had one kidney stone, your risk of forming another is significant. Doctors may recommend a 24-hour urine collection, where you save all your urine for a full day so a lab can measure the levels of calcium, oxalate, uric acid, citrate, sodium, and other key substances. This test reveals which specific imbalances are pushing your urine toward supersaturation, and it varies widely from person to person. Two collections on your normal diet are preferred over one, since day-to-day variation can mask the real picture.
The single most consistently recommended preventive measure is drinking enough fluid throughout the day to produce at least 2 liters of urine. That’s roughly half a gallon. Spreading your intake across the day matters more than gulping large amounts at once, because the goal is to keep your urine dilute continuously, preventing those minerals from ever reaching the supersaturation point where crystals form. For most people, this means drinking noticeably more water than feels natural, especially in hot weather or after exercise.
Dietary Factors That Raise Risk
Several dietary patterns increase stone risk beyond just oxalate-rich foods. High sodium intake forces your kidneys to excrete more calcium, raising the calcium concentration in your urine. High animal protein intake (red meat, poultry, fish) makes urine more acidic and increases uric acid excretion, creating conditions favorable for both uric acid and calcium stones. Surprisingly, restricting dietary calcium tends to backfire. Calcium in food binds oxalate in the gut before it reaches the kidneys, so eating moderate amounts of calcium-rich foods actually lowers oxalate levels in urine.
The interplay of these factors explains why kidney stones aren’t caused by any single food or habit. They emerge from the overall chemistry of your urine, which reflects your hydration, diet, genetics, body weight, and underlying health conditions all at once.