Kidney stones form when dissolved minerals in your urine become so concentrated that they solidify into crystals. This process, called supersaturation, is the starting point for every type of kidney stone. When your urine doesn’t have enough water to dilute these minerals, or lacks the natural chemicals that keep crystals from clumping together, small crystals can grow and bond into stones ranging from a grain of sand to a golf ball. Men develop stones at higher rates than women across all age groups, with the gap being widest in young adults.
From Dissolved Minerals to Solid Stones
Your kidneys filter waste from the blood and send it out as urine. That urine carries dissolved calcium, oxalate, uric acid, phosphate, and other substances. Normally, these stay dissolved because the water volume is high enough and natural inhibitors keep everything in check. But when the concentration of any stone-forming substance crosses a threshold, the urine becomes supersaturated, meaning it holds more dissolved material than it can support.
Once supersaturation occurs, the process unfolds in three stages. First, crystals begin to form in a step called nucleation, where molecules cluster together into tiny solid seeds. Second, those seeds grow as more molecules attach to their surface. Third, crystals clump together through aggregation, building into a structure large enough to lodge in the kidney or urinary tract. This entire sequence is a form of biomineralization, the same basic process that builds bone and teeth, just happening where you don’t want it.
Calcium Stones: The Most Common Type
About 80% of kidney stones contain calcium, usually paired with oxalate and sometimes with phosphate. These form when calcium and oxalate levels in the urine are high relative to the water volume. Eating large amounts of high-oxalate foods (spinach, rhubarb, nuts, chocolate) increases the oxalate available for crystal formation, while excess sodium forces your kidneys to excrete more calcium. Keeping sodium intake below 2,300 milligrams per day helps reduce the calcium your kidneys dump into urine.
Your body has a built-in defense against calcium stones: citrate. This molecule binds to calcium in urine, forming a soluble complex that keeps calcium from pairing with oxalate. Citrate also directly slows crystal growth and prevents small crystals from sticking together. When citrate levels drop, whether from a diet low in fruits and vegetables, chronic diarrhea, or certain metabolic conditions, calcium has a much easier path to crystallizing.
Uric Acid Stones and the Role of pH
Uric acid stones account for roughly 5 to 10% of all kidney stones, and they form through a different trigger: acidic urine. Uric acid dissolves well in urine with a pH around 6 to 6.5. Below about 5.5, nearly all uric acid molecules lose the electrical charge that keeps them dissolved in water. At that point, no more than about 90 milligrams can stay in solution, and anything above that starts to crystallize.
The overwhelming factor in uric acid stone formation is pH, not how much uric acid your body produces. People with insulin resistance or type 2 diabetes tend to produce more acidic urine, which puts them at higher risk. Low fluid intake compounds the problem. Even at a safe pH of 6, very low urine volumes can push uric acid past its saturation point. The combination of acidic, concentrated urine creates ideal conditions for these stones to form.
Infection Stones (Struvite)
Struvite stones don’t form from diet or dehydration. They’re caused by specific bacteria that infect the urinary tract, particularly species like Proteus, Klebsiella, Pseudomonas, and Staphylococcus. These bacteria produce an enzyme called urease, which breaks down urea (a normal waste product in urine) into ammonia. The ammonia makes urine sharply alkaline, which is the opposite of the acidic environment that drives uric acid stones.
In this alkaline urine, ammonia ions combine with magnesium and phosphate ions that are naturally present, forming struvite crystals. These stones can grow rapidly, sometimes filling the entire collecting system of the kidney in a branching shape called a staghorn stone. Because struvite stones are driven by active infection, they tend to recur unless the underlying bacterial infection is fully cleared.
Cystine Stones: A Genetic Condition
Cystine stones are rare, affecting about 1 to 2% of stone formers, but they’re significant because they’re caused by an inherited disorder called cystinuria. In a healthy kidney, an amino acid called cystine gets filtered into urine and then reabsorbed back into the bloodstream. In people with cystinuria, mutations in one of two specific genes (SLC3A1 or SLC7A9) disable that reabsorption, flooding the urine with cystine.
The problem is that cystine has very low solubility in water. At normal urine pH levels between 4 and 6, only about 160 milligrams per liter can stay dissolved. People with cystinuria routinely exceed that limit, so crystals form almost inevitably. These stones tend to appear in childhood or young adulthood and recur frequently throughout life without aggressive management focused on diluting urine and raising its pH.
Why Some People Form Stones and Others Don’t
Supersaturation alone doesn’t guarantee a stone. Many people walk around with supersaturated urine and never form one, because natural inhibitors in their urine, primarily citrate, keep crystals from gaining a foothold. Stone formation happens when the balance tips: too much of a stone-forming substance, too little water, too few inhibitors, or an unfavorable pH.
Several factors shift that balance. Chronic dehydration is the simplest and most common. When daily urine output falls below about 2 liters, concentrations of all dissolved substances rise. High-sodium diets increase urinary calcium. Obesity and insulin resistance lower urine pH, promoting uric acid stones. Recurrent urinary tract infections create the alkaline conditions for struvite. Genetics dictate cystine stone risk entirely and influence calcium stone risk through variations in how your kidneys handle calcium and citrate.
Geography and climate matter too. People living in hotter regions produce more concentrated urine from sweat losses, and stone rates are correspondingly higher. Seasonal patterns follow the same logic: emergency visits for kidney stones peak in late summer.
Hydration and Diet as the First Line of Defense
The single most effective way to prevent stones is to produce at least 2 liters of urine per day. That typically means drinking 2.5 liters or more of fluid, since you lose water through sweat and breathing. Water is ideal, though citrus-based drinks carry the added benefit of raising urine citrate levels.
Dietary adjustments target specific stone-forming pathways. Keeping sodium under 2,300 milligrams daily reduces calcium excretion. Eating calcium-rich foods (rather than supplements) at meals helps bind oxalate in the gut before it ever reaches the kidneys. Limiting high-oxalate foods matters most for people who’ve already had a calcium oxalate stone. For uric acid stone formers, reducing intake of red meat and organ meats lowers the acid load on the kidneys, helping maintain a healthier urine pH.
These strategies work because they address the root physics of stone formation: reducing the concentration of stone-forming substances, increasing the volume of solvent they’re dissolved in, and supporting the natural inhibitors that prevent crystals from growing into stones.