What a Kidney Stone Actually Is, and Why It Forms

SEPTEMBER 10, 2026

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I wanted to understand kidney stones from the beginning, and the beginning turned out to be a question I had never actually asked: what is a kidney stone, and why does one form? Not "how do I avoid one" — that's the next entry, and it has an answer that is less settled than the usual advice suggests — but the thing itself. It is a common enough object. In the United States about one adult in eleven has had one [1] — a figure that has roughly tripled since 1980 [3] — and in the most recent survey years around 11% of adults reported one ever and 2.1% reported passing one in the previous twelve months [2]. Men still make more than women, but the gap has been closing for a decade [3]. So: what is it?

What is a kidney stone made of?

A kidney stone is a hard lump of crystals, held together with a small amount of protein, that formed inside the kidney out of substances that are normally dissolved in urine. It can be the size of a grain of sand or it can fill the whole branching interior of the kidney like a cast — the coral-shaped "staghorn" at the lower left of the plate above. Cut one open and it has rings, because a stone grows in layers around whatever it started on. Brödel painted those rings in 1909 and they are the single most useful thing to know about a stone: it is not a thing that appears, it is a thing that accumulates.

What it accumulates out of depends on the person. The largest modern count I found is from the Mayo Clinic's laboratory, which analysed the first stone submitted by each of 43,545 patients in a single year [4]:

• Calcium oxalate — 67%. The ordinary stone. Calcium and oxalate (a small organic acid that the liver makes and that is also in food) bind into a crystal that is nearly insoluble in water.
• Calcium phosphate (hydroxyapatite) — 16%. The same mineral as bone; favours alkaline urine.
• Uric acid — 8%. The waste product of purine metabolism, the same molecule behind gout. Needs acidic urine to crystallise, which is the whole story of who gets these (below).
• Struvite — 3%. Magnesium ammonium phosphate, made by certain bacteria during a urinary infection. These are the ones that grow into staghorns.
• Brushite — 0.9% (another calcium phosphate) and cystine — 0.35% (an inherited defect in amino-acid transport).

Two things follow. First, "kidney stone" is really "calcium stone" nine times out of ten — among first-time stone formers in one Minnesota county, 93.5% made a calcium stone of one kind or another [5]. Older textbooks put struvite at around 10% [6]; it has fallen as urinary infections get treated sooner. Second, the kind matters for what happens next: in that same county, the ten-year chance of a second symptomatic stone was about 30% for calcium oxalate and calcium phosphate stones but about 50% for brushite, struvite and uric acid [5]. You cannot reason about your stone until you know which one you make — which is why the guideline says to have one analysed at least once [7], and why I would keep it.

Why do kidney stones form?

Urine is a strange solution. It carries calcium, oxalate, phosphate and uric acid at concentrations that would already be crystallising if you dissolved the same amounts in plain water — it is supersaturated, most of the time, in most people [6]. It stays liquid because the kidney also puts inhibitors into it: citrate, which grabs calcium before oxalate can; magnesium; and a set of proteins that coat any crystal that does start and stop it growing. A stone is what you get when, in one kidney, the supersaturation outruns the inhibition for long enough.

That takes four steps, and the last one is the one that matters. Crystals nucleate; they grow; they aggregate into clumps; and then they have to be retained. A crystal that washes out with the urine was never a stone — most of us pass microscopic crystals routinely. Something has to hold it in place long enough for the layers to build. For the common calcium oxalate stone, that something has a name and a discoverer.

Randall's plaque

In the 1930s Alexander Randall noticed small white deposits of calcium phosphate at the tips of the renal papillae — the points where the kidney's collecting ducts open into the urine-filled space — and proposed that stones grew on them. It took seventy years to show how. In 2003 a group at Indiana University took papillary biopsies from calcium stone formers during surgery and traced the deposits to their origin: they begin in the basement membrane of the thin limbs of the loop of Henle, deep in the medulla, and spread outward through the tissue until they sit just under the papilla's lining [8]. Where that lining erodes, the plaque is exposed to urine, and calcium oxalate — for which the urine is already supersaturated — grows on it. Stones removed at surgery are often found still attached, with a small dimple on one face where they sat on the papilla. Non-stone-formers biopsied in the same study had no plaque at all.

Why the plaque forms is not settled. The current picture is that it resembles the calcification of an artery more than it resembles a rock in a pipe: the deposits sit in an organic matrix with the same proteins that show up in vascular calcification, and the tissue around them carries the marks of inflammation and oxidative stress [9]. A stone, on this reading, is the end product of a slow injury to the deep kidney rather than a simple precipitate — which is one reason the "dissolve it with X" folk remedies for calcium stones have never worked.

Who gets kidney stones, and why?

Everything that raises supersaturation, or lowers inhibition, or keeps a crystal in the kidney longer, raises the risk. The list is long; the ones with real numbers behind them are these.

Not enough urine

The single biggest one. Concentration is amount divided by volume, and stone formers make less urine. In the Italian trial that established the point, men presenting with a first calcium stone were passing about 1.06 litres a day against 1.40 in controls, and women about 0.99 against 1.24 [10]. Across three large American cohorts totalling 192,126 people, low fluid intake accounted for an estimated 26% of all first stones — more than any other modifiable factor — and five such factors together (fluid, body weight, diet pattern, dietary calcium, sugary drinks) accounted for more than half [11]. Whether telling people to drink more actually prevents stones is a different question from whether low volume causes them, and it is the subject of the next entry, because a large 2026 trial gave an answer that surprised me.

Too much calcium in the urine — and the trap in the obvious fix

High urinary calcium is the most common measurable abnormality in calcium stone formers [6]. The intuitive response, and the standard medical advice until the 1990s, was to eat less calcium. This turned out to be exactly backwards, and the evidence for that is some of the cleanest in the whole subject.

First the cohorts. In 45,619 men followed for four years, those eating the most dietary calcium had a lower risk of a first stone than those eating the least [12]. In 91,731 women followed for twelve years, with 864 stones, the highest fifth of dietary calcium intake had 35% lower risk than the lowest — while calcium taken as a supplement, on its own, carried a 20% higher risk, and high sodium intake a 30% higher risk [13].

Then the trial. Borghi and colleagues randomised 120 men with recurrent calcium oxalate stones and high urinary calcium to either the traditional low-calcium diet, or a diet with normal calcium (about 1,200 mg a day) but restricted salt and animal protein, and followed them for five years. On the low-calcium diet 23 of 60 relapsed (38%); on the normal-calcium, low-salt, low-protein diet, 12 of 60 (20%) — a relative risk of 0.49 [14]. Urinary calcium fell equally in both groups. What differed was oxalate: it rose on the low-calcium diet and fell on the other. The mechanism is in the gut. Calcium eaten with a meal binds the oxalate in that meal, so it leaves in the stool instead of being absorbed and excreted in the urine; take the calcium away and the oxalate walks straight through. That is also why supplemental calcium, swallowed between meals with nothing to bind, behaves differently from calcium in food.

Salt is the other lever on urinary calcium: the kidney handles sodium and calcium together, and the more sodium it excretes the more calcium goes with it. In a three-month trial of 210 stone formers, a low-salt diet cut urinary calcium from 361 to 271 mg a day and brought it into the normal range in 62% of patients, against 34% on water alone [15]. The American guideline's current advice for calcium stone formers with high urinary calcium is accordingly 1,000–1,200 mg a day of dietary calcium, with sodium limited [7] — not less calcium, but less salt.

Oxalate, citrate, and the acidity of the urine

Oxalate comes from food — spinach, rhubarb, almonds, beets, chocolate, tea are the famous ones — and from the liver's own metabolism, and either can run high. Citrate is the chief inhibitor and runs low when the body is handling an acid load, which a diet heavy in animal protein produces. And urine pH decides which crystal can form at all: calcium phosphate needs it alkaline, uric acid needs it acid. Each of these deserves its own entry; here they are just the other three dials.

Body weight, diabetes, and uric acid

In the same three cohorts — 4,827 stones over a combined 46 years of follow-up — men over 220 lb had 44% more stones than men under 150 lb, and heavier women roughly 90% more, after adjusting for diet and fluid [16]. Part of the reason is specific to uric acid. Insulin resistance impairs the kidney's ability to excrete ammonium, which is what normally buffers acid in urine; the urine turns unusually acidic, and uric acid — which stays dissolved at a pH of 6.5 and largely does not at 5.3 — comes out of solution. Thirteen recurrent uric acid stone formers put through a formal insulin-clamp study were severely insulin resistant, and in healthy volunteers infusing insulin raised urine pH from 6.1 to 6.8 [17]. It is why uric acid stones cluster with obesity and diabetes, and why after age 55 they overtake calcium phosphate as the second most common kind [4].

Family

In 37,999 men followed for eight years, a family history of stones carried a relative risk of 2.57 (95% CI 2.19–3.02), after adjusting for diet and everything else measured [18]. Some of that is shared kitchens, but not all of it — urinary calcium handling is heritable, and the rare single-gene stone diseases (cystinuria, primary hyperoxaluria) run in families outright.

Heat

Sweat is water that did not become urine. The Mayo laboratory received more calcium oxalate and uric acid stones in July and August than in any other months [4]; the American South has long been called the "stone belt"; and a 2008 analysis projected that a warming climate would push the high-risk zone north — from 40% of the US population living in it in 2000 to 56% by 2050 — adding 1.6 to 2.2 million lifetime stone cases by mid-century [19]. A model, not a measurement — but the seasonal signal underneath it is real.

Infection

Certain bacteria — Proteus above all — carry an enzyme that splits urea into ammonia. That drives urine pH up and floods it with ammonium, and magnesium ammonium phosphate (struvite) crystallises in bulk. These are the stones that fill the kidney's whole interior, and they are a different disease: the bacteria live inside the stone, so it cannot be treated without removing it.

How likely is a second kidney stone?

Less likely than the older textbooks say, and more likely than most first-timers assume. The classic figures — 35% by five years, 52% by ten [20] — came from stone clinics, which see the people who keep coming back. When the Mayo group instead followed every adult in Olmsted County, Minnesota with a first symptomatic stone from 1984 on (2,239 of them), the rate of a second symptomatic episode was 11% at two years, 20% at five, 31% at ten, and 39% at fifteen [21]. It compounds: the recurrence rate per hundred person-years was 3.4 after a first stone, 7.1 after a second, 12.1 after a third, and 17.6 after a fourth [22]. And those are symptomatic stones; when the same group put first-time formers through a CT scan five years later, a new stone had formed in 35% of them and some manifestation of recurrence — new stone, growth, or passage — was present in 67% [23]. Most stones never announce themselves.

So what does a first stone actually tell you?

Not much, on its own — which is the honest answer, and the guideline's. The American Urological Association's evaluation for a first stone is a detailed history, blood chemistries and a urinalysis; a stone analysis at least once whenever a stone can be caught; and a 24-hour urine collection — measured for volume, pH, calcium, oxalate, uric acid, citrate, sodium, potassium and creatinine — for recurrent stone formers and for first-timers who are either at high risk or interested [7]. That last phrase is the door. The 24-hour urine is the one test that tells you which of the dials above is turned up in your particular kidney, and every recommendation in the next entry depends on which one it is.

Postscript: three questions about water and pills

Three questions arrived the moment the above was written, and they turn out to be the same question in three costumes: does the calcium you drink, or swallow, become the calcium in a stone? They are worth their own answers, because the intuitive answer to all three is yes and the measured answer is mostly no.

Do people in hard-water areas get more kidney stones?

Hard water is water carrying dissolved calcium and magnesium; the intuition is that drinking calcium makes calcium stones. The intuition has been tested for forty years, and it fails. In 1982 a study of 2,295 patients compared the Carolinas — soft water, one of the highest stone rates in the country — with the Rockies, hard water and one of the lowest; across the United States as a whole, the authors noted, hardness and stone rates run in opposite directions, and comparing stone patients with hernia patients from the same towns found no difference in the calcium, magnesium or sodium of their tap water [24]. (The one signal they did find: private-well users had about 1.5 times the risk — the wells' minerals were not the reason, and nobody has since shown what was.) In 2002 a stone clinic matched 4,833 calcium stone formers to the hardness of their public water by zip code: patients in the softest tenth had formed 3.4 stones each in their lifetimes, patients in the hardest tenth 3.0 — fewer, not more — and urinary calcium did rise with harder water, but so did urinary magnesium and citrate, the two inhibitors [25]. The largest and most recent look is the UK Biobank: 288,041 people with no prior stone, followed prospectively, 3,298 first stones. Water hardness and water calcium had no association with stones overall; the magnesium in water did — people in the highest quartile (above 5 mg/L) had 12% fewer stones — and the one dissonant note is a subgroup finding that hard water carried 18–34% more risk in women and in people over 60, which is worth watching but is the kind of result that appears in one cohort and not the next [26].

Why doesn't the calcium in water behave like the calcium in a supplement? Partly it does: in a crossover trial, 18 stone formers who drank two litres a day of very hard bottled water (255 mg of calcium per litre) between meals raised their urinary calcium by about half compared with soft water, with no change in oxalate [27] — the same "calcium with nothing to bind" effect the supplement section below returns to. But the amounts are small (see the distiller question), and hard water brings magnesium and bicarbonate along with the calcium, both of which push urinary citrate up. A 2020 systematic review of three decades of this literature concluded that hard water and calcium-rich mineral water are, if anything, slightly helpful to calcium stone formers [28]. Short answer: no. The American stone belt is a soft-water region.

Would a water distiller prevent kidney stones — and what percentage of them?

I looked for the trial and there isn't one: nobody has randomised people to distilled or reverse-osmosis water and counted stones, so the honest percentage is unmeasured. What has been measured lets me estimate it, and the estimate is close to zero.

Start with how much calcium a distiller actually removes. Across the UK Biobank the average tap water carried 53 mg of calcium per litre [26] — two litres a day is about 105 mg, a tenth of the 1,000–1,200 mg the guideline wants a calcium stone former to eat [7]. Even genuinely hard water at 100–150 mg per litre gives 200–300 mg a day in two litres, roughly one glass of milk. A distiller removes that and nothing else that matters. Then ask whether that calcium was doing harm: in the population it is not — no association in 288,000 people, slightly fewer stones with harder water in 4,833 stone formers — and the distiller also strips out the magnesium, the one water mineral with a measurable protective association [26]. The single scenario in which distilling could plausibly help is a person with high urinary calcium who drinks a great deal of very hard water between meals, on the strength of that 50% rise in the crossover trial [27] — and even there the lever is smaller than salt's, which moved urinary calcium from 361 to 271 mg a day [15], and no one has shown it changes stones.

What a distiller cannot change is the litre count, and the litre count is the whole game: low fluid intake accounts for an estimated 26% of first stones [11], against a mineral effect indistinguishable from zero. If owning one makes someone drink more water, it prevented stones — through volume, not purity. Short answer: a percentage I can't give because nobody has measured it; from what has been measured, close to nil; and the number that does matter is how much comes out of the tap, not what was taken out of it.

Do calcium and mineral supplements cause kidney stones over the years?

This is the one of the three where the intuition is partly right, and there is a proper randomised trial to say by how much. The Women's Health Initiative gave 36,282 postmenopausal women either 1,000 mg a day of elemental calcium as calcium carbonate — the form in most supermarket supplements and antacids — with 400 IU of vitamin D₃, or placebo, for an average of seven years. Stones were reported by 449 women on the supplement and 381 on placebo — a hazard ratio of 1.17 (95% CI 1.02–1.34) [29] [30]. In absolute terms that is 2.5% against 2.1%: about one extra stone for every 270 women taking the pill for seven years. Real, and small. The Nurses' cohort had found the same direction a decade earlier — supplemental calcium, RR 1.20 — and noticed that two-thirds of the women taking it took it away from meals or with meals that had little oxalate to bind [13].

That timing is the mechanism, and it has been tested directly. Thirty-two healthy men took three grams of calcium carbonate a day (about 1,200 mg of calcium) for a week, either as one gram with each meal or as the whole dose at bedtime, then crossed over. With meals, urinary calcium rose but urinary oxalate fell and citrate rose, and the calculated tendency of the urine to form calcium oxalate did not change. At bedtime, urinary calcium rose the same amount, oxalate did not move, and the tendency to form calcium oxalate rose significantly [31]. Calcium in food is protective because it meets oxalate in the gut; calcium in a pill on an empty stomach is the same calcium arriving with nothing to bind. The supplement is not the villain; the empty stomach is. The other common form, calcium citrate, has only been tested on urine, not stones: in 18 postmenopausal women, 400 mg of calcium as citrate twice a day raised urinary calcium and citrate together, lowered oxalate, and left the urine's calcium oxalate saturation unchanged [41] — a plausible advantage over the carbonate, with no stone-count trial behind it.

The other pills, briefly. Vitamin D on its own has not shown a stone signal in trials: 5,110 adults given 100,000 IU a month (about 3,300 IU a day) for a median 3.3 years had a hazard ratio of 0.90 [32], and a meta-analysis of 22 trials at 3,200–4,000 IU a day in 12,952 people found hypercalcaemia doubled (four extra cases per thousand) but no excess of stones [33] — with the caveat that people already spilling calcium into their urine are exactly who those trials didn't enrich for, and in the Women's Health Initiative the combination did raise stones. Vitamin C is the supplement with the clearest signal, because the body turns part of it into oxalate: across 156,735 women and 40,536 men, a total intake of 1,000 mg a day or more carried 43% more stones in men — and none in women [34]; a Swedish cohort of 23,355 men put ascorbic-acid tablet users at roughly double the risk, though letters to the journal argued part of that is men on high-dose vitamin C being scanned more readily [35]. Magnesium runs the other way in every dataset that has it — but it matters which magnesium, because three different things have gone by that name above.

In water it is the dissolved ion, leached from dolomite and magnesium-bearing limestone, and the UK Biobank's 12% fewer stones above 5 mg per litre is about that [26]. In the cohorts it is magnesium in food — nuts, seeds, beans, whole grains, leafy greens — where the highest fifth of intake had 29% fewer stones in men [36]. Neither is a pill. The pills have been tested, and the result depends on the salt. Magnesium hydroxide — milk of magnesia — is the one magnesium salt ever put on its own against a placebo for stone recurrence: at 650 or 1,300 mg a day it did no better than the placebo, in a trial that also watched the placebo group form 56% fewer stones than their own histories predicted — a lesson in why "I started taking it and the stones stopped" proves nothing [37]. Potassium-magnesium citrate did work: 64 recurrent stone formers, three years, new stones in 63.6% on placebo and 12.9% on the salt [38]. But that salt carries 63 mEq of citrate and 42 of potassium alongside its 21 of magnesium, and citrate salts with no magnesium in them cut new stones by a similar margin across seven trials [39] — so the citrate is the likely active half. The only head-to-head between magnesium salts is on urine, not stones: 90 stone formers with high urinary oxalate were randomised to magnesium oxide, magnesium citrate or placebo, 120 mg three times a day with meals for eight weeks; both lowered urinary oxalate, the citrate about twice as much (−17 against −8 mg a day), and only the citrate significantly lowered the calcium oxalate supersaturation [40]. So the magnesium with evidence behind it is the magnesium already in food and hard water; as a pill, the citrate salt — and probably as much for its citrate as its magnesium; and the hydroxide failed the one fair test it was given. Short answer: the calcium pill most people take for their bones raises stone risk by about a sixth over seven years — small in absolute terms, and avoidable in principle by taking it with food; the supplement to be genuinely wary of is high-dose vitamin C, in men.

Next in this series: does drinking more water prevent kidney stones? The 1996 trial that halved recurrence, the 2026 trial in 1,658 people that couldn't, and what the difference between them means.

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This is one reader's reading of the research, not medical advice. If something here touches on your own health, take it to a clinician who knows you — and read how these entries are put together.