Kidney stones form when minerals in your urine become so concentrated that they crystallize and stick together. The most common culprit is calcium oxalate, but the specific cause depends on the type of stone, your diet, how much water you drink, and whether you have an underlying medical condition. About 11% of American men and 9% of American women will develop a kidney stone in their lifetime, and once you’ve had one, the recurrence rate is as high as 50% within five years.
How Stones Actually Form
Your kidneys filter waste products into urine, and that urine naturally contains dissolved minerals like calcium, oxalate, phosphate, and uric acid. Normally, these substances stay dissolved and pass out of your body without issue. Problems start when the concentration of these minerals rises beyond what the urine can hold in solution, a state called supersaturation.
Once urine is supersaturated, tiny crystals begin to form. These microscopic crystals then clump together through a process called aggregation, which is the primary way stones grow larger. If the crystals get trapped in the kidney tissue, possibly at a site of prior injury, they continue to attract more mineral deposits and grow into a full stone over weeks or months. Your body does have natural defenses against this. Certain compounds in urine, like citrate, normally prevent crystals from forming or sticking together. When those protective factors are low or the mineral load is too high, the balance tips toward stone formation.
The Four Types of Kidney Stones
Not all kidney stones are made of the same material, and knowing the type matters because each one has different causes.
Calcium oxalate stones are by far the most common. They form when calcium and oxalate, a compound your liver produces and that you absorb from food, combine in concentrated urine. A smaller subset are calcium phosphate stones.
Uric acid stones develop when urine is too acidic. They’re linked to high-protein diets (especially organ meats and shellfish), chronic diarrhea, diabetes, and metabolic syndrome. The sulfur-containing amino acids in animal protein create an acid load that drops urine pH, while purines in meat get metabolized into uric acid.
Struvite stones are caused by urinary tract infections. Certain bacteria produce an enzyme called urease that breaks down urea into ammonia, making the urine highly alkaline (pH 7.2 to 8.0). That alkaline environment triggers crystallization of magnesium ammonium phosphate. Proteus, Providencia, and Morganella bacteria always produce urease, but 84% of Klebsiella species and 55% of Staphylococcus species do as well. Struvite stones can grow rapidly and become quite large.
Cystine stones are the rarest type, caused by an inherited condition called cystinuria. People with this disorder have a genetic defect in the kidney’s cystine transporters, causing their kidneys to leak excessive amounts of the amino acid cystine into the urine. Cystine stones tend to appear early in life and recur frequently.
Dehydration Is the Single Biggest Risk Factor
Low urine volume is one of the most consistent risk factors for both first-time stones and recurrences. When you don’t drink enough fluids, the minerals in your urine become more concentrated, pushing you toward that supersaturation threshold. People who have had a kidney stone are generally advised to drink at least 2 liters (8 cups) of water per day, with 3 liters (12 cups) being the ideal target. The goal is to produce enough urine that minerals stay diluted and pass through before they can crystallize.
This is why kidney stones are more common in hot climates and during summer months. Sweating reduces the fluid available for urine production, concentrating minerals even if your overall water intake hasn’t changed.
How Diet Drives Stone Formation
Several dietary patterns increase your risk, and some of them are counterintuitive.
Oxalate and Calcium Work Together
High-oxalate foods (spinach, rhubarb, beets, nuts, chocolate) contribute to calcium oxalate stones, but the relationship with calcium is surprising. When you eat calcium alongside oxalate, the two bind together in your gut and get eliminated in your stool rather than being absorbed into your bloodstream and filtered by your kidneys. Reducing dietary calcium from 1,000 mg to 400 mg per day on a moderate-oxalate diet increased urinary oxalate excretion by 20% to 50% in study participants. In other words, eating too little calcium can actually raise your stone risk. The practical strategy is to maintain normal calcium intake while limiting high-oxalate foods.
Salt Pulls Calcium Into Your Urine
A high-sodium diet forces your kidneys to excrete more calcium. Research on men consuming different sodium levels showed that urinary calcium excretion rose significantly as salt intake increased, driven primarily by changes in how much calcium gets filtered through the kidneys. If you’re prone to calcium stones, reducing sodium intake is one of the more effective dietary changes you can make.
Animal Protein Creates Multiple Problems
Diets heavy in red meat, poultry, and seafood contribute to both uric acid and calcium stones through several mechanisms at once. The sulfur-containing amino acids in animal protein generate acid that lowers urine pH and reduces citrate, your body’s natural crystal inhibitor. The purines in meat get broken down into uric acid, raising levels in the blood and urine. High protein intake also increases calcium excretion. These effects compound one another.
Medical Conditions That Raise Your Risk
Diabetes and metabolic syndrome are strongly associated with uric acid stones because they tend to produce more acidic urine. Chronic diarrhea, whether from inflammatory bowel disease, celiac disease, or other digestive conditions, depletes fluid and can impair nutrient absorption, concentrating minerals in the urine and shifting its chemistry.
Recurrent urinary tract infections predispose people to struvite stones. Anyone who has frequent UTIs and develops a large or rapidly growing stone should be evaluated for this type. Hyperparathyroidism, a condition where the parathyroid glands produce too much hormone, causes elevated blood calcium levels that spill into the urine, promoting calcium stone formation.
Medications That Can Trigger Stones
Several common medications increase stone risk through different mechanisms. Loop diuretics (like furosemide) block calcium reabsorption in the kidneys, creating a high-calcium urine environment. Topiramate, an anti-seizure medication also used for migraines, acts as a carbonic anhydrase inhibitor that alters urine chemistry to favor calcium phosphate stones. Zonisamide, another anti-seizure drug, carries a similar risk.
Other medications can themselves crystallize in urine and form stones directly. These include certain antibiotics (ciprofloxacin and sulfa drugs like sulfamethoxazole), the potassium-sparing diuretic triamterene, the HIV medication indinavir, and over-the-counter preparations containing guaifenesin with ephedrine. Laxative abuse is another known trigger, associated with ammonium acid urate stones due to chronic fluid loss.
Genetics and Family History
Cystinuria is the clearest example of a genetic cause. It results from mutations in genes that encode the kidney’s cystine transport system. The condition can be inherited in several patterns depending on which gene is affected, and certain founder mutations are concentrated in specific populations, including Ashkenazi Jewish and Mennonite communities. People with cystinuria often begin forming stones in childhood or adolescence and deal with recurrences throughout their lives.
Beyond cystinuria, having a family history of any type of kidney stone raises your own risk. Genetic factors influence how your body handles calcium, oxalate, and uric acid, even when no single gene mutation is responsible. If a parent or sibling has had kidney stones, your chances of developing them are meaningfully higher, and paying attention to hydration and diet becomes that much more important.
Why Stones Come Back
The recurrence rate for kidney stones is striking: up to 50% at five years and 80% to 90% at ten years. This happens because the underlying metabolic conditions that caused the first stone, whether dietary habits, low fluid intake, or a genetic predisposition, don’t go away on their own. The composition of your first stone offers a roadmap for prevention. A calcium oxalate stone points toward hydration, sodium reduction, and balanced calcium and oxalate intake. A uric acid stone suggests reducing animal protein and increasing urine pH. Struvite stones require treating and preventing the UTIs that fuel them.
Knowing what your stone is made of, typically determined by analyzing a stone you’ve passed or had removed, is the single most useful piece of information for preventing the next one.