Kidney stones form when certain minerals in your urine become so concentrated that they crystallize and clump together into solid masses. About 10% of U.S. adults will develop a kidney stone at some point, and the causes range from not drinking enough water to underlying medical conditions and genetic factors. The specific cause depends largely on what type of stone you develop.
How Stones Actually Form
Your kidneys filter waste products from your blood and flush them out in urine. When the concentration of certain minerals rises too high, those dissolved substances start forming tiny crystals in a process called nucleation. Think of it like sugar crystallizing at the bottom of an oversaturated glass of iced tea.
Once those microscopic crystals exist, they attract more mineral ions from the surrounding urine and grow. But the real problem comes from aggregation: individual crystals stick together into larger and larger clumps, layering on top of each other. This is how a stone goes from invisible to large enough to block a ureter and cause pain. The entire process is driven by one core issue: too much of a stone-forming substance, too little fluid to keep it dissolved, or a shortage of the natural inhibitors in urine that normally prevent crystals from clumping.
Calcium Oxalate Stones
Calcium oxalate is the most common type, responsible for roughly 70% to 80% of all kidney stones. Despite the name, eating too much calcium is not the main culprit. In fact, getting adequate calcium from food actually helps prevent these stones because calcium binds to oxalate in your digestive tract and keeps it from reaching your kidneys.
The real drivers are high oxalate levels and excess calcium in the urine (which is different from calcium in your diet). Oxalate is a natural compound found in many plant foods. Spinach, rhubarb, wheat bran, nuts, and peanuts are especially high in oxalate. When you eat large amounts of these foods without enough dietary calcium to offset them, more oxalate ends up in your urine, raising your risk.
Two dietary habits reliably push calcium oxalate stone risk higher. First, eating a lot of sodium. In the kidneys, sodium and calcium share a transport pathway, so when your body dumps excess sodium into urine, it drags calcium along with it. Second, eating large amounts of animal protein. A meat-heavy meal can trigger a temporary acid shift in your blood, which causes calcium and phosphate to leach from your bones and eventually pass through your kidneys.
Uric Acid Stones
Uric acid stones account for about 5% to 10% of kidney stones and form when urine is persistently acidic (a pH below roughly 5.5). At that acidity level, uric acid stops dissolving properly and crystallizes instead. Alkaline urine keeps uric acid in solution; acidic urine does not.
Several things push urine toward the acidic end. A diet rich in purines, found in red meat, organ meats, and shellfish, increases the amount of uric acid your body produces. Metabolic syndrome, the cluster of conditions that includes obesity, insulin resistance, and high blood pressure, also plays a significant role. People with metabolic syndrome excrete less ammonium in their urine, which is one of the body’s main tools for buffering acid. The result is chronically acidic urine and a higher incidence of uric acid stones.
Infection-Related Struvite Stones
Struvite stones are caused by urinary tract infections with specific types of bacteria. These bacteria produce an enzyme called urease, which splits urea in your urine into ammonia and carbon dioxide. The ammonia makes urine extremely alkaline, reaching a pH above 7.2, which is far more alkaline than normal physiology allows. At that pH, magnesium, ammonium, and phosphate crystallize together into struvite.
The alkaline environment also damages the protective lining of the urinary tract, letting bacteria embed themselves in biofilms along the kidney’s inner surfaces. The stone then grows layer by layer, molding itself to the shape of the kidney’s internal chambers. These “staghorn” stones can become very large. Nearly all Proteus species produce urease, making them a frequent cause, along with Klebsiella, Staphylococcus, and Pseudomonas. Notably, E. coli, the most common cause of urinary tract infections overall, almost never produces urease, so routine UTIs caused by E. coli rarely lead to struvite stones.
Cystine Stones and Genetics
Cystine stones are the least common type and are entirely genetic. They’re caused by cystinuria, an inherited condition where mutations in the SLC3A1 or SLC7A9 gene prevent the kidneys from properly reabsorbing the amino acid cystine from urine. Normally, a protein complex in the kidneys pulls cystine back into the bloodstream before it reaches the bladder. When that protein complex doesn’t work, cystine builds up in the urine and crystallizes.
Cystinuria tends to cause recurrent stones starting in childhood or early adulthood. If both of your parents carry a copy of the mutated gene, you’ll develop the condition. There’s no way to prevent it entirely, but high fluid intake and medications that make urine less acidic can reduce how often stones form.
Medical Conditions That Raise Risk
Primary hyperparathyroidism is one of the most well-established medical causes. The parathyroid glands, four tiny glands behind your thyroid, regulate calcium levels. When one of them becomes overactive, it pulls too much calcium from your bones and boosts calcium absorption from food. The excess calcium floods your kidneys, creating ideal conditions for calcium-based stones. Surgical removal of the overactive gland typically resolves the problem.
Chronic kidney disease, inflammatory bowel disease, and a history of gastric bypass surgery also increase risk. Bowel conditions are particularly relevant because they can cause your body to absorb more oxalate from food than it normally would, a condition called enteric hyperoxaluria. Type 2 diabetes and obesity raise uric acid stone risk through the metabolic syndrome pathway described above.
Medications That Can Trigger Stones
Certain medications increase stone risk either by changing your urine chemistry or by crystallizing in the urine themselves. Anti-seizure medications like topiramate and zonisamide are notable offenders. They cause a type of metabolic acidosis that lowers citrate in the urine. Citrate is one of the body’s natural stone inhibitors, so when levels drop, calcium phosphate stones become more likely.
Loop diuretics, often prescribed for heart failure and high blood pressure, increase calcium excretion into urine. The potassium-sparing diuretic triamterene can actually form stones made of the drug itself. Some antibiotics, including certain sulfa drugs and ciprofloxacin, can crystallize in urine at high doses or when fluid intake is low. If you take any of these medications long-term, staying well-hydrated becomes especially important.
Dehydration: The Universal Risk Factor
Regardless of stone type, low fluid intake is the single most consistent risk factor. When you don’t drink enough, your urine becomes concentrated, and every stone-forming substance in it gets closer to the point of crystallization. The American Urological Association recommends producing at least 2.5 liters of urine per day to keep concentrations low enough to prevent stones. For most people, that means drinking roughly 3 liters of fluid daily, though the exact amount varies with climate, activity level, and body size.
If you’ve already had a stone, the recurrence rate is high. Maintaining that urine volume target is the single most effective thing you can do to lower your odds of forming another one. Water is the best choice, though citrus-based drinks add citrate, which helps block calcium crystal formation.