Kidney stones form when minerals in your urine become so concentrated that they crystallize and stick together into solid masses. The specific cause depends on the type of stone, but the underlying problem is always the same: too much of a particular substance in too little liquid. About 1 to 2% of adults under 65 develop stones in any given year, and that number climbs to 3 to 5% for people over 65.
How Stones Actually Form
Your kidneys filter waste from your blood and flush it out in urine. When certain minerals or salts become too concentrated, the urine becomes “supersaturated,” meaning it can no longer keep those substances dissolved. At that point, tiny crystals begin to form, a process called nucleation. These crystals don’t appear out of thin air. They usually latch onto something already present, like a cell or another crystal, and use it as a foundation to grow.
Once a crystal forms and anchors itself to the wall of the kidney, additional mineral layers build on top of it. This growth stage can continue as long as the urine stays supersaturated. Crystals also clump together, which is how a microscopic speck eventually becomes a stone large enough to block a urinary passage and cause pain. The whole process can take weeks to months.
The Four Main Types and Their Causes
Calcium Oxalate and Calcium Phosphate Stones
Roughly 80% of kidney stones contain calcium, most commonly paired with oxalate. These form when your urine has too much calcium, too much oxalate, or not enough of the natural inhibitors (like citrate) that normally prevent crystals from forming. High-oxalate foods are a well-known contributor. Spinach is the single biggest dietary source of oxalate for most people, followed by rhubarb, beets, chard, nuts, bran, and star fruit.
Here’s the counterintuitive part: eating too little calcium actually raises your risk. Calcium binds to oxalate in your gut, preventing it from being absorbed into your bloodstream and reaching your kidneys. When people cut dietary calcium from 1,000 mg to 400 mg per day, their urinary oxalate excretion jumped by 20 to 50%. The current recommendation is to eat 300 to 400 mg of calcium with each meal rather than avoiding it.
Uric Acid Stones
Uric acid stones form when urine is persistently too acidic, with a pH at or below 5.5. At that acidity level, uric acid can’t stay dissolved and precipitates into crystals. The biggest driver of overly acidic urine is insulin resistance and metabolic syndrome, the cluster of conditions that includes obesity, high blood pressure, high blood sugar, and abnormal cholesterol. People with type 2 diabetes produce more acid than their kidneys can buffer, which pushes urine pH down into the danger zone. Obesity alone is associated with low urine pH in stone formers, even without a full diabetes diagnosis.
Struvite Stones
Struvite stones are caused by urinary tract infections with specific types of bacteria, most commonly Proteus species. These bacteria produce an enzyme called urease that breaks down urea (a normal waste product in urine) into ammonia and carbon dioxide. The ammonia makes the urine alkaline, and under those alkaline conditions, magnesium, phosphate, and ammonium ions combine to form struvite crystals. These stones can grow rapidly and become very large because the infection continuously feeds the crystallization process. Treating the underlying infection is essential to stopping them.
Cystine Stones
Cystine stones are the rarest type and are entirely genetic. They’re caused by inherited mutations in two genes that build a transport channel in kidney cells. When this channel doesn’t work properly, the amino acid cystine can’t be reabsorbed back into the body as urine is being filtered. Cystine accumulates in the urine, and because it’s relatively insoluble, it crystallizes into stones. People with cystinuria typically start forming stones in childhood or adolescence and need to drink 3.5 to 4 liters of fluid daily to keep cystine dissolved.
Dehydration Is the Single Biggest Risk Factor
No matter what type of stone you’re prone to, insufficient fluid intake makes everything worse. Less water means more concentrated urine, which pushes mineral levels past the point where crystals can form. Major urological associations recommend drinking 2.5 to 3 liters of fluid per day, enough to produce at least 2 to 2.5 liters of urine. That’s noticeably more than the “eight glasses a day” many people aim for. The goal is pale, dilute urine with a low specific gravity, not the dark yellow that signals concentration.
Diet Beyond Oxalate
Two other dietary patterns significantly raise stone risk: high sodium intake and high animal protein consumption.
Sodium increases the amount of calcium your kidneys excrete. The more salt you eat, the more calcium ends up in your urine, creating conditions for calcium stones. Animal protein works through a different mechanism. When researchers increased protein intake from about 47 to 112 grams per day while holding other nutrients constant, urinary calcium rose by roughly 60%. High-protein diets also decreased urinary citrate, one of the body’s natural defenses against stone formation. The culprit is the acid load that comes with metabolizing animal protein. That extra acid forces the kidneys to pull calcium from the body to help buffer it, and that calcium gets dumped into the urine.
Your Gut Bacteria Play a Role
A bacterium called Oxalobacter formigenes lives in the intestines of a large portion of the healthy adult population. Its job, from a stone-prevention perspective, is useful: it eats oxalate. When this bacterium is present and thriving, it breaks down dietary oxalate in the gut before it can be absorbed into the bloodstream and filtered through the kidneys. When it’s absent, more oxalate gets absorbed and excreted in urine, raising the risk of calcium oxalate stones. Frequent courses of antibiotics can wipe out this bacterium, which may partly explain why antibiotic use is listed among drug-related risk factors for stones.
Medications That Increase Risk
Several common medications can promote stone formation through different mechanisms:
- Loop diuretics and glucocorticoids increase urinary calcium, promoting calcium stones.
- Topiramate and other carbonic anhydrase inhibitors lower citrate levels and raise urine pH, favoring calcium phosphate stones.
- High-dose vitamin C supplements increase oxalate production, promoting calcium oxalate stones.
- Laxative abuse raises urinary ammonium, which can lead to ammonium urate stones.
- Certain antibiotics and antiviral drugs can themselves crystallize in urine and form stones directly.
Medical Conditions That Cause Stones
Some people form stones because of an underlying condition that alters their urine chemistry. Primary hyperparathyroidism, where one or more parathyroid glands overproduce hormone, is found in about 3 to 5% of stone formers. The excess hormone pulls calcium from bones and increases how much calcium the kidneys filter, creating a steady supply of raw material for stones. This is a treatable condition, and correcting it can stop recurrent stones.
Type 2 diabetes, obesity, gout, chronic diarrhea (which causes dehydration and changes urine chemistry), and inflammatory bowel disease all independently increase stone risk. Chronic diarrhea is particularly problematic because it causes the body to lose fluid and bicarbonate, making urine both concentrated and acidic.
Recurrence Is Extremely Common
One of the most important things to understand about kidney stones is that having one dramatically increases your odds of having another. Recurrence rates reach as high as 50% within five years and 80 to 90% within ten years. This is why identifying your specific cause matters so much. A 24-hour urine collection can reveal whether your urine has excess calcium, oxalate, uric acid, or too little citrate, and that information points directly to the dietary or medical change most likely to prevent the next stone. Men over 65 are the most affected group, with prevalence rising from 4.3% to 6.4% between 2012 and 2021, though the gender gap has narrowed among younger adults.