Kidney stones (nephrolithiasis) are hard deposits of crystalline salts and organic material that form in the kidney and may descend into the ureters. They are among the most common disorders of the urinary tract. Many stones are small enough to pass without treatment, but larger or lodged stones cause severe flank pain, block urine flow, and can lead to infection or loss of kidney function.
The condition matters for public health because it is frequent, often recurs, and is linked to diet, fluid intake, body weight, and metabolic disease such as type 2 diabetes, hypertension and gout. Stones have also been associated with chronic kidney disease, which makes prevention and long-term management as important as emergency care.
This entry begins with the definition and composition of stones and the physicochemical process of crystallization in urine. It then describes the four main stone types (calcium, uric acid, struvite and cystine) and the risk factors behind them, followed by epidemiology, clinical presentation, diagnosis, acute and procedural treatment, prevention, special populations, links to systemic disease, the history of understanding and treatment, and open research questions.
Definition and composition
Terminology and location
A kidney stone is a solid mass built from crystals that separate from urine when its dissolved minerals reach concentrations the fluid cannot hold. Kidney stones, also called renal calculi, are solid crystal aggregations of dissolved minerals in urine. The name shifts with anatomy rather than chemistry: depending on their location in the urinary tract these calculi are called by various names, e.g., kidney stones, ureteric stones, bladder stones, or urethral stones. A stone that has descended into the ureter therefore remains the same kind of object, and the only difference is the location. Bladder and urethral stones are grouped separately because they lie below the ureters and usually arise from different conditions, such as urinary stasis or outflow obstruction.
Crystalline components
Calcium oxalate dominates. In a retrospective series of 506 adults whose stones were analysed by infrared spectroscopy, the two calcium oxalate forms together accounted for roughly 84 percent of cases, with calcium oxalate dihydrate (COD) the most prevalent stone type, accounting for 307 cases (60.7%), followed by calcium oxalate monohydrate (COM) in 117 (23.1%). Other reviews place the calcium-containing share somewhat lower, with calcium oxalate the most common component found in kidney stones (approximately 70 to 80 percent). Calcium-containing stones overall are estimated at approximately 80% of kidney stones, while an older estimate puts the figure near 85% of the stones in human are calcium stones comprising oxalate and phosphate, so the exact proportion varies between series.
Calcium phosphate is the second group. It is found in approximately 15 percent of kidney stones and can be present in combination with calcium oxalate or struvite. It occurs as apatite (sometimes reported as carbonate apatite), which is the crystal type found in bone, or calcium hydrogen phosphate (brushite); the frequency of apatite is much greater than brushite. Uric acid crystals account for a smaller share, present in approximately 8 percent of analyzed stones, sometimes in combination with calcium oxalate. Infection-associated stones are composed of magnesium, ammonium, phosphate and calcium carbonate, which is known as struvite. Cystine stones are built from cystine, an amino acid, and are the least common of the main types. Mixed stones are frequent: it is not uncommon for a stone to contain more than one crystalline component.
Stones are named for their dominant crystal because the chemical makeup carries diagnostic and therapeutic weight. Accurate determination of stone composition provides valuable etiological insights and has become a central component of management based on contemporary guidelines.
Organic matrix
The protein-rich framework of a stone was recognised long before its role was understood. The discovery of an organic component in kidney stones dates back to 1684. More than 150 years elapsed before the incrustation of this organic component, which is now called the matrix, was proposed as the mechanism of stone formation. Its composition was largely unclear until electron microscopy and biochemistry advanced in the 1950s. The matrix is composed mainly of selectively incorporated proteins generally characterized by high glutamic and aspartic acid content and the frequent occurrence of gamma-carboxyglutamic acid, and proteomic profiling has identified proteins, such as uromodulin and albumin, that are often detected in stones, regardless of crystal components. By contrast, osteopontin, prothrombin, protein S and protein Z are identified specifically in calcium oxalate stones.
Estimates of how much of a stone the matrix represents differ. One analysis describes a matrix that is consisting of 64% protein, 12% organic ash, 10% bound water and 5% glucosamine. Another reports that proteins are present in all stones in a slight proportion, commonly < 5%. The gap probably reflects whether the fraction is measured against the matrix alone or against the whole stone. Matrix proteins are thought to act as a nucleus: urinary proteins play an important role in stone formation by serving as a nidus that leads to the subsequent formation of a larger crystalline matrix structure.
Size and location
Stones are classified both by site and by dimensions. The European urolithiasis guideline classifies stones according to anatomical position: upper, middle, or lower calyx; renal pelvis; upper, middle, or distal ureter; and urinary bladder. A surgical scheme goes further and describes the morphology, size and topography of the stone in five descriptive categories. Size is measured on imaging, and non-contrast CT can classify the stone density, diameter, volume, distance from the skin, and the adjacent anatomy. Volume may be more informative than diameter: a guideline panel found volume is a better predictor of stone free status after stone surgery, although practical measurement problems remain.
Size and location together predict behaviour. In one series, large-size stones were predominantly located in the renal pelvis and PUJ, with few located in the lower ureter, and no large stones reached the VUJ. Increases in stone size decreased its passage rate in the ureter and increased the chance of causing high-grade hydronephrosis. Within the ureter, stones larger than 5 mm and located in the proximal two thirds of the ureter are more likely to require lithotripsy or endoscopic removal. The same stone can therefore be a minor incident in one segment and a surgical problem in another.
Crystallization in urine
Supersaturation
Stone formation begins with urine that holds more dissolved solute than it can keep in solution. Supersaturation is usually expressed as a ratio: the product of the ion concentrations in urine divided by the solubility product of the salt. When that ratio exceeds 1, the salt can precipitate spontaneously. For calcium oxalate, the relevant ions are calcium and oxalate, but urate, phosphate and cystine play the same role for their respective stone types. Because urine volume sets how far solutes are diluted, low urine output raises the concentration of every lithogenic solute at once. Urinary pH changes the solubility limit of individual compounds: uric acid crystallizes readily in acidic urine, while calcium phosphate becomes less soluble as urine becomes more alkaline. Normal urine is itself close to saturation with respect to some calcium salts, which is one reason physiological inhibitors are thought to be needed to prevent routine crystal formation.
Nucleation and crystal growth
Nucleation is the step in which dissolved molecules cluster into the first solid nuclei. Nucleation can occur in free solution, but it requires a high degree of supersaturation. Heterogeneous nucleation, in which crystals form on an existing surface, needs much less. Several models describe where this surface may be found. In the free-particle model, crystals grow and aggregate inside the tubular lumen. In the fixed-particle model, crystals first attach to renal epithelium, and the attached nuclei then grow. Injured tubular cells appear to favor nucleation even at low supersaturation, and cell debris and altered membranes can provide such surfaces. Growth is governed by transit time as well as chemistry. Estimates for calcium oxalate suggest that a crystal may grow by only one to two micrometres per minute, while the kidney transits urine in roughly five to ten minutes through tubules that are only 15 to 60 micrometres in diameter. Most crystals therefore leave the urinary tract as harmless particles unless they are retained.
Aggregation and retention
Individual crystals rarely cause clinical stones. Aggregation, in which crystals cluster together and undergo secondary nucleation, produces multicrystalline particles large enough to lodge in tubules or on the renal papilla. Retention is the final and most restrictive step. Crystalluria is common, but stone formation is comparatively rare, so something beyond crystal chemistry must fix particles in place. Tubular injury, crystal–cell interaction and localized interstitial supersaturation are the mechanisms most often proposed. Crystals that adhere to epithelial surfaces can be taken up by cells, and the resulting aggregates then grow into a stone. Blocking any one of the steps of nucleation, growth, aggregation or retention is generally sufficient to prevent urolithiasis, which explains why the relative balance of these steps matters more than any single urinary value.
Natural inhibitors
Urine contains many compounds that suppress crystallization. Citrate is the best-characterized: it binds calcium, forming soluble complexes that limit the calcium available to combine with oxalate or phosphate, and it also directly inhibits aggregation. In calcium stone formers, hypocitraturia, defined as urinary citrate below about 320 mg per day, is reported in roughly 20 to 60 percent of cases. Magnesium and zinc inhibit crystal formation, while pyrophosphate and other phosphate compounds chelate calcium and slow crystal growth. Larger macromolecules, including glycosaminoglycans, RNA, glycoproteins and proteins such as uromodulin (Tamm–Horsfall protein), osteopontin and nephrocalcin, adsorb to crystal surfaces and reduce both growth and aggregation. An early study by Schreier and colleagues attributed about half of urine's inhibitory activity against calcium oxalate growth to molecules under 5000 daltons, and roughly 40 percent to large molecules.
Deficiency of these inhibitors is a plausible contributor to stone formation, but the relationship is not a simple one. Many stone formers have normal levels of known inhibitors, and some people with abnormal urine chemistry never form stones. The frequency of stone formation is therefore better understood as a balance between promoters and inhibitors, and several matrix proteins can act in either direction depending on context. Drugs that lower urinary citrate, such as proton pump inhibitors in one 2020 cohort, illustrate how a single change in inhibitor excretion can shift that balance, while potassium citrate supplementation reduces recurrence in many patients. Supersaturation, uromodulin
Calcium oxalate and calcium phosphate stones
Calcium-containing stones make up most urinary stones. Calcium oxalate stones are the most common of all stone types (70 % - 80 %) and occur 3 times more frequently in men than in women. Their formation depends on urine that carries more calcium and oxalate than the fluid can keep dissolved, which is the state of supersaturation.
Oxalate reaches the urine from two sources. Oxalate is an endogenous byproduct of amino acid metabolism and is also absorbed by the stomach, small bowel and colon. Under normal conditions, all oxalate absorbed from the diet or produced endogenously is excreted unchanged in urine. Dietary calcium limits this absorption. In the gut, calcium and oxalate meet and form an insoluble compound that leaves with the stool. When intestinal calcium is limited because of low intake, dietary oxalate absorption is apparently enhanced, which is one reason a low-calcium diet can raise stone risk.
Two metabolic routes drive calcium oxalate supersaturation: hypercalciuria, an excess of calcium in urine, and hyperoxaluria, an excess of oxalate. In general, there is a direct relationship between stone incidence and the degree of hyperoxaluria. Enteric hyperoxaluria is the gut-driven form. When fat is poorly absorbed, the unabsorbed bile and fatty acids saponify intestinal calcium, limiting the amount of luminal free-calcium binding with oxalate. Causes include bowel diseases, typically Crohn's disease complicated by ileal resection or short bowel syndrome, but also pancreatic exocrine insufficiency or bariatric surgery. The problem has grown with the number of weight-loss operations: the prevalence of enteric hyperoxaluria has increased because of the development of bariatric surgical procedures. In one prospective study of 11 people with severe obesity, plasma oxalate and urine CaOx supersaturation increase significantly compared with pre-surgical levels of both variables at 6 and 12 months after Roux-en-Y gastric bypass.
Calcium phosphate stones are less frequent, with calcium phosphate stones found in approx. 5 % - max. 10 % of all urinary stones. The two main crystal forms differ in frequency. Carbonate apatite (dahllite) is the more common form, while brushite is rarer, approx. 1 % of stones in one series. Apatite is the crystal type found in bone, which is why it is often described as bone-like.
Phosphate salts precipitate mainly in alkaline urine. Sources give slightly different thresholds: one places apatite and carbonate apatite above pH 7.0 and brushite between 6.8 and 7.0 , while another states that calcium phosphate crystals only form in a relatively alkaline urine (usually pH ≥6.5). Brushite formers also tend to excrete more calcium: in a retrospective cohort of 110 calcium phosphate formers, brushite stone formers had significantly higher mean 24-hour urinary calcium excretion than apatite formers. Brushite is also considered a transitional phase, since many of these stones probably start as brushite, a relatively unstable phase of calcium phosphate that may convert in vivo to hydroxyapatite.
The relationship between dietary and supplemental calcium is not straightforward. In a prospective study of younger women, the multivariate relative risk among women in the highest quintile of intake of dietary calcium compared with women in the lowest quintile was 0.73, and supplemental calcium intake was not associated with risk of stone formation. A separate prospective cohort reported the opposite pattern for supplements, finding that high dietary calcium intake appeared to decrease risk while calcium supplement increased the risk of urinary tract stones. The proposed explanation concerns timing and dietary oxalate, subjects who did not take calcium supplement with their meal or whose dietary oxalate content was low had a higher risk of calcium stone formation. However, although the explanation is sensible, it has never been proven. One reason is that a supplement taken between meals may raise urinary calcium without delivering the oxalate-binding benefit, as calcium supplementation given between meals might increase urinary calcium excretion without the beneficial effect on oxalate.
Uric acid stones
Uric acid stones form when urate precipitates in acidic urine, and their risk depends more on urinary pH than on the total amount of urate excreted. The pK of uric acid in the urine is close to 5.3. Therefore, at a urine pH of 5.3, half of the amount of the total urate in the urine will be in the form of uric acid, which is poorly soluble in water (solubility 0.6 mmol/L). Because the undissociated form is the one that crystallizes, small pH shifts produce large changes in risk. In a worked example with 800 mg of uric acid, roughly 600 mg is undissociated at pH 5.0, but only about 100 mg at pH 6.5. Uric acid and urate crystals can also seed calcium oxalate deposition, increasing the propensity toward formation of mixed UA and calcium oxalate stones through heterogeneous nucleation and epitaxial crystal growth.
Estimates of their share of all stones vary. One series places them in 10% of all kidney stones, while another gives 5–10% of urinary calculi. Acidity is the central risk factor: a urine pH below 5.5 is the most important risk factor for uric acid crystallization and stone formation, rather than increased urinary uric acid excretion. Persistently acidic urine has been linked to tubular disorders (including gout), chronic diarrhea or severe dehydration. Three abnormalities are described in these patients: low urinary pH, hyperuricosuria, and low urine volume. In gout, patients often exhibit persistently low urine pH levels, and one review argues that the link to gout and kidney disease runs mainly through the "unduly acidic" urinary pH that leads to precipitation of UA rather than the commonly assumed risk factor of hyperuricosuria. Hyperuricosuria itself is still relevant. Clinical protocols have used cut-offs of 750 mg/day in males and more than 650mg/day in females when defining it, and high dietary purine intake can add to urate load, as uric acid stones form in persistently acidic urine and are commonly associated with conditions such as metabolic syndrome, gout, or high dietary purine intake. Higher body mass and diabetes are also associated with more acidic urine; in comparison to the general population, patients with a high body mass index or diabetes have more acidic urine and a significantly increased propensity to develop uric acid calculi.
On imaging, the stone's chemistry is visible only indirectly. Pure uric acid stones are radiolucent on radiography. Because of this, they are not visible on plain films but can be detected by ultrasonography or CT or as filling defects on IVP. Their low density is the key discriminator on non-contrast CT: uric acid stone have CT density values ranging from 200 to 450 HU at 120 kV, whereas calcium phosphate stones have mean HU values between 1200 and 1600. Dual-energy CT can separate uric acid from other compositions in vivo. Clinical suspicion is also informed by urine chemistry: in practice, any patient with symptoms of acute renal colic who demonstrates a urine pH lower than 6.0 should be considered at risk for a possible uric acid stone. Several other salts, including ammonium urate, sodium urate, xanthine, and 2,8-hydroxyadenine have similar properties.
Uric acid stones are unusual in that they can be dissolved. The treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml daily), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Solubility rises steeply across this range: alkalizing urine can effectively promote UAS dissolution by increasing uric acid solubility approximately 20-fold as urine pH increases from 5.0 to 7.0. Alkalinization is usually achieved with potassium citrate, and potassium citrate at doses of 30 mEq by mouth twice a day or greater may be required to raise the urinary pH sufficiently to decrease the supersaturation of uric acid. Maintaining the pH at this level usually results in dissolution of pure uric acid stones in 2 - 6 weeks. Reported success varies between studies, with one describing oral dissolution rates ranging from 73 to 100%.
The same alkaline conditions carry constraints. Urate salts behave differently: sodium and potassium urate crystals are not dissolved by alkalinization; their solubility decreases as urinary pH increases. Excessive alkalinity can also trigger the precipitation of poorly soluble calcium phosphate salts that can overlap with the initial uric acid nucleus once pH exceeds about 6.2, so the target is a narrow window. Citrate therapy has side effects, including nausea, vomiting, and diarrhea that limit its use in some patients. For prevention, potassium citrate is the treatment of choice for the prevention of recurrence of uric acid calculi. Dietary purine reduction complements this approach, since urinary uric acid excretion can be reduced by a low-purine diet.
Infection-related struvite stones
Struvite stones, made of magnesium ammonium phosphate, differ from most other kidney stones because they depend on an active infection. Estimates place infection stones, which include struvite with or without carbonate apatite, at about 10–15% of urinary calculi. Infection stones are thought to form in the presence of urease-producing bacteria.
Urease is the key chemical step. These bacteria split urea molecules into ammonia and carbon dioxide. The ammonia makes urine more alkaline, which promotes crystal formation. Ammonia further breaks down into bicarbonate and ammonium, and these ions combine with magnesium and phosphate to produce magnesium ammonium phosphate and carbonate apatite. The higher pH also lowers the solubility of phosphate, so the crystals appear once the urine has been made alkaline. Common organisms include Proteus, Klebsiella, Pseudomonas, and Staphylococcus species. Infection can also supply the matrix that holds crystals together: bacterial cell debris can act as heterogeneous crystallization nuclei and promote the growth of struvite crystals.
Risk concentrates in particular groups. Struvite stones are found more frequently in women and in persons older than 50 years, a pattern that reflects a population with recurrent or persistent urinary infections. Structural and functional problems raise the risk further, including urinary tract obstruction or anatomical abnormalities, long-term use of indwelling urethral catheter, previous urinary diversion surgery and, lastly, neurogenic bladder pathology.
Struvite stones grow quickly and often become staghorn calculi. Staghorn calculi are large stones that fill the renal pelvis and extend into the majority of the calices. These stones are usually composed of pure struvite or struvite in combination with calcium carbonate apatite. Because of this pattern, the damage is often progressive. If left untreated, these infection stones grow rapidly and may lead to deterioration of renal function, end-stage renal disease, and life-threatening urosepsis. Obstruction of urine flow and persistent infection both contribute to loss of kidney tissue, which is why the stone and the infection are managed together.
Treatment has two aims: removing every stone fragment and eradicating the infection. Even after complete stone removal, struvite stones recur in approximately 10% of patients; if residual stones or fragments are left after treatment, recurrence rates approach 85%. Antibiotics alone are insufficient because antibiotics do not penetrate infection stones. Fragments left behind can harbor bacteria, so surgery is planned around the stone's full extent. Percutaneous nephrolithotomy (PCNL) is the gold-standard approach for treatment of staghorn infection calculi, and stone culture at the time of treatment or urine culture from the renal pelvis provides useful clinical information for directing antibiotic therapy. Long-term suppressive antibiotics and urine acidification may also be considered after surgery to reduce recurrence.
The main pharmacological approach targets urease itself. Acetohydroxamic acid (AHA) is the only FDA-approved urease inhibitor, and it was approved in 1983 as an orphan drug for the prevention of struvite stones. In a 1984 randomized double-blind study, no patient who received acetohydroxamic acid had a doubling of stone size, whereas seven patients given placebo reached a predetermined end point. The benefit came with frequent side effects: nine patients receiving the drug and one patient receiving placebo required a decrease in dosage or cessation of treatment because of adverse effects. Later trials found that three randomized clinical trials showed reduction in stone growth but not recurrence, and major adverse events were frequent. Urease inhibition has a limited role: it does not decrease bacterial counts and cannot eradicate existing stones, so it is generally used as a palliative measure in patients who cannot undergo definitive surgery.
Cystine and rare inherited stones
Cystinuria
Cystinuria is an inherited disorder of amino acid handling. It is autosomal recessive, and mutations in SLC3A1 or SLC7A9 genes are responsible for most cases. The two genes encode the subunits of a transporter that normally reclaims cystine and the dibasic amino acids ornithine, lysine and arginine in the proximal tubule and the intestine. In individuals with cystinuria, this reabsorption is impaired. The result is hyperexcretion of cystine in the urine (>300 mg/day compared to <30 mg/day in healthy subjects). Only cystine forms stones among the amino acids that are excreted in excess, because the others remain soluble.
Cystine's low solubility is the chemical basis of the disease. Whereas ornithine, lysine, and arginine are completely soluble, cystine is relatively insoluble at physiologic urine pH levels. Its solubility is about 250 mg/L at pH 7 and rises to about 500 mg/L at pH 7.5 and 1000 mg/L at pH 8 (urine volume and pH are the key determinants of cystine solubility). Because of this, excessive cysteine in urine can lead to recurrent precipitation of hexagonal cystine stones.
Clinical course and treatment
Stones can appear early. Stones can first be seen in the first decade of life and account for up to 10% of stone disease in the pediatric population. Across all kidney stone patients, cystinuria accounts for 1-2% of all kidney stone cases. Stones tend to recur, and there is no clinical difference based on the different genotypes, so the genetic subtype does not predict severity.
Treatment aims to keep cystine in solution. Sources differ on the target urine pH: one review states that physicians should aim for a cystine concentration <1 mmol/L (250 mg/L) and a urinary pH 7.5-8, while a patient-oriented source gives an optimal range of 7.0 to 7.5. Fluid intake is central, since increasing fluid intake to maintain urinary cystine at a concentration below 250 mg/L enables insoluble cystine crystals to dissolve in urine. Alkalinization is usually achieved with potassium citrate or potassium bicarbonate, and potassium citrate is generally preferred because it raises urinary pH without increasing cystine excretion. In addition to preventing stone formation, alkalinization can also dissolve existing cystine stones in some patients. Thiol drugs such as tiopronin and D-penicillamine bind cysteine and form more soluble complexes, and they are used when fluid and alkali therapy are insufficient.
Primary hyperoxaluria
Primary hyperoxaluria is a group of rare inherited disorders of glyoxylate metabolism. It is estimated to affect 1 in 58,000 individuals worldwide. Type 1 is the most common form, accounting for approximately 80 percent of cases. Type 1 results from loss of a liver enzyme: it is caused by a deficiency in the liver-specific enzyme, alanine:glyoxylate aminotransferase (AGT). Without it, glyoxylate accumulates and is converted into oxalate, so the kidneys handle a heavy endogenous oxalate load. This leads to early onset recurrent nephrolithiasis, nephrocalcinosis and in some cases ESKD. Types 2 and 3, caused by GRHPR and HOGA1 mutations, each account for about 10 percent of cases. Vitamin B6 can help some patients: administration of pharmacologic doses of this vitamin can reduce urine oxalate levels in PH1 patients with certain genotypes.
Xanthine stones
Xanthine stones are extremely uncommon. They are caused by an inborn defect of xanthine oxidase. Because xanthine cannot be converted to uric acid, a deficiency of xanthine oxidoreductase or dehydrogenase... results in the production of large amounts of xanthine and hypoxanthine associated with the reduced production of uric acid. Xanthine is poorly soluble, and xanthine stones can form at any age, even in infants. Affected patients typically show very low uric acid levels in serum and urine. Xanthine stones are also secondary xanthine stones and even xanthine nephropathy may develop as a result of the treatment with allopurinol of severe hyperuricemia. Unlike uric acid stones, these stones chemolitholysis of xanthine stones is not possible, so management depends on high fluid dilution.
Other drug-induced stones
Some medications form stones through their own poorly soluble crystals or by changing urinary chemistry. Examples include the HIV protease inhibitor indinavir and the diuretic triamterene. The medication history is therefore part of the workup, and the drug-related causes are discussed further under medications.
Genetic testing and metabolic workup
Identifying these rare causes depends on stone analysis, urine chemistry and genetic testing. In cystinuria, the transporter genes SLC3A1 and SLC7A9 are sequenced to confirm the diagnosis. In primary hyperoxaluria, more than 175 mutations in the AGXT gene have been found to cause primary hyperoxaluria type 1, so genotype testing is needed to distinguish subtypes and to predict who may respond to pyridoxine. Repeated 24-hour urine measurements of cystine or oxalate, combined with urine pH, show whether a metabolic defect is driving recurrent stones.
Dietary and lifestyle risk factors
Low fluid intake is the one risk factor shared by nearly every stone type. Dilute urine keeps calcium, oxalate, urate and phosphate below the concentrations at which they crystallize, so a low urine volume raises the risk whatever the stone's composition. In one meta-analysis, a daily intake of about 2.0 L was associated with roughly half the stone incidence seen at intakes below 1.0 L (an intake of 2.0 L/day was reported to reduce the incidence of stones by nearly 50% compared to an intake of less than 1.0 L/day). Clinical guidance for people with a history of stones commonly sets a target of about 2.5 L of urine per day, and the Mayo Clinic describes this as the most effective therapy available to prevent future kidney stones.
Diet composition modifies the urinary chemistry that fluid volume alone cannot correct. Sodium is the clearest example. Extra salt expands extracellular fluid volume, which reduces calcium reabsorption in the renal tubules and increases urinary calcium excretion (dietary sodium increases urinary calcium excretion, thus increasing the risk of kidney stone formation. Calcium reabsorption in the renal tubules is hindered by the expansion of the extracellular fluid volume as an effect of sodium.). The U.S. guideline of less than 2,300 mg a day reflects this concern. A short-term study of recurrent Swiss calcium oxalate stone formers found that a low-sodium, low-calcium diet markedly reduced urinary sodium and calcium, while urine volume did not change and oxalate excretion did not rise.
Animal protein acts through a different route. Its acid load tends to lower urinary pH and citrate, and it increases uric acid excretion. In a cohort, people eating 77 g or more of animal protein daily had a 33% higher risk of stones than those eating 50 g or less (compared with individuals eating 50 g or less of animal protein per day, those eating the most (77 g or more) had a 33% higher risk for kidney stones.). Vegetarian diets have been associated with a substantially lower risk, which is attributed partly to phytic acid binding calcium in the gut (the risk for stone formation is 40-60% lower in individuals following vegetarian diets for a number of reasons. These include the absence of animal protein and the presence of phytic acid). Fruit and vegetables work in the opposite direction: they raise urine volume, pH, potassium, magnesium and citrate, which together reduce the supersaturation of calcium oxalate and uric acid (higher fruit and vegetable intakes, which increase urine volume, pH, potassium, magnesium, citrate, and other stone inhibitors, decrease the supersaturation of calcium oxalate and uric acid overall.). Added sugar is commonly listed among dietary risks, but its effects on urinary chemistry are less firmly established than those of sodium and animal protein. Oxalate-rich foods such as spinach, rhubarb, nuts and bran are restricted selectively, mainly for calcium oxalate stones.
Obesity and metabolic syndrome affect stone risk largely through urinary acid handling. Insulin resistance impairs ammonium production in the proximal tubule, so the kidney excretes less acid as ammonium and urinary pH falls. The result is a favorable setting for uric acid crystallization. One study reported an average urinary pH of about 5.7 in uric acid stone formers compared with about 6.17 in controls, under comparable diet and fluid conditions. In a U.S. population sample, the self-reported prevalence of kidney stones rose from 3% among people with none of the metabolic syndrome traits to 9.8% among those with all five. Abdominal obesity therefore primarily shifts the risk toward uric acid stones, whereas bariatric surgery, a separate pathway, is linked to calcium oxalate stones.
Heat exposure and sweating are a further driver of chronic dehydration, and the evidence here comes mostly from occupational studies. Workers in hot environments may lose substantial amounts of water through sweat, and this chronic fluid loss can produce low urine volume and hypocitraturia (their state of chronic dehydration results in low urinary volumes and hypocitraturia). In a steel-industry study, the prevalence of urinary lithiasis was about nine times higher among workers in hot areas than among those in cooler ones. In a southern Indian steelworker cohort, 33% were positive for kidney/ureteral stones on ultrasound. Heat exposure has also been linked to radiolucent stones, which are invisible on plain radiography. Because these studies are small, cross-sectional and confined to particular industries, their magnitude should be interpreted cautiously. Geographic data are consistent with the same pattern: areas of elevated temperatures and high humidity appear to have an increased incidence of stone disease, likely due to population hydration status.
Medical conditions and medications
Systemic and kidney diseases
Stone formation is closely tied to disorders of mineral, acid and fluid handling. Observational studies link stones with diabetes and high blood pressure, and more recent work has reported strong associations with obesity, gout, diabetes and hypertension.Chronic diseases such as diabetes and high blood pressure (hypertension) are also associated with an increased risk of developing kidney stones. More recent studies have demonstrated strong associations with obesity, gout, diabetes and hypertension. Future studies will help uncover the underlying common pathophysiologic abnormalities. The direction of the hypertension link is unsettled: there is a potential link between a history of kidney stones and an increased risk of hypertension, though more research is needed to establish causality.
Gout has the most direct chemical link to stone type, because excess urate is the basis of uric acid stones. Conditions like gout can increase the risk of uric acid stones. Diseases of the kidney tubule also contribute. Renal tubular acidosis, for example, impairs acid excretion and raises urinary pH, which favours calcium phosphate precipitation.
Inflammatory bowel disease (IBD) is associated with stones through several routes. In a Swiss cohort, kidney stones were described in 61 (4.6%) CD and 30 (3.0%) UC patients. Male sex, disease activity, intestinal surgery, NSAID use and reduced physical activity were significant risk factors in that study. A two-sample Mendelian randomization analysis suggested a causal effect of Crohn's disease, but no evidence of a causal association between UC and KSD was identified. Chronic diarrhoea and intestinal inflammation can reduce urine volume or increase oxalate absorption, which is the mechanism most often invoked for calcium oxalate stones in this setting.
Primary hyperparathyroidism has long been recognised as a cause of stones. Excess parathyroid hormone raises blood and urinary calcium, favouring calcium stones. Bariatric surgery can produce enteric hyperoxaluria through altered intestinal absorption; this is treated in the section on calcium oxalate and calcium phosphate stones.
Medications
Drugs can cause stones in two ways. Drug-induced kidney stones form either from the drug's direct crystallization in the urine or from metabolic effects that alter urine composition. Drug-induced calculi make up a small share of all stones, drug-induced renal calculi represent 1-2% of all renal calculi. Within that group, antiretroviral therapy has become prominent. Among these agents, protease inhibitors (PIs) are well known to induce kidney stones, especially indinavir and atazanavir, and more recently darunavir. Indinavir was the main concern in the 1990s, while atazanavir remains a recognised cause today. Such crystals are more common in the urine with pH ≥6, which links the drug problem to urinary alkalinity. Because most of these stones are potentially preventable, awareness of lithogenic drugs matters clinically.
Carbonic anhydrase inhibitors such as topiramate and acetazolamide act metabolically. They raise urinary pH and lower urinary citrate, producing calcium phosphate stones. Unsupervised calcium and vitamin D supplementation is among the most frequent causes of drug-related calcium stones. Loop diuretics such as furosemide can increase urinary calcium excretion. Risk rises with high doses, prolonged treatment, low urine output, poor urinary pH and a prior history of stones. Metabolically induced stones are probably under-recognised, since they often look like ordinary stones and can appear long after the drug has been stopped.
Thiazide diuretics, which lower urinary calcium and supersaturation, have been the standard medical approach to preventing recurrence. The large NOSTONE trial, however, failed to show superiority of hydrochlorothiazide at doses up to 50 mg daily over placebo in preventing a composite of clinical or radiological recurrence in patients at high risk of kidney stone recurrence. Whether longer-acting thiazides such as indapamide and chlorthalidone behave differently is being tested in a randomised cross-over trial.
Heritable predisposition
Family history is one of the strongest clinical predictors. A positive family history is present in 30–60% of individuals with kidney stones, and twin studies indicate a heritability of more than 45% for nephrolithiasis and more than 50% for hypercalciuria. Among men with a stone history, relatives are reported to have stones about three times as often.
Monogenic forms are relatively rare. More than 30 Mendelian causes have been described, but estimates of their share vary: one review places them below 10% of cases at referral centres, while another cites a prevalence of about 15% in patients attending stone clinics. For most people, susceptibility appears polygenic. Genome-wide association studies have identified common variants in 31 genes linked with stone formation, though these do not fully account for inherited risk. Noncoding variants near genes such as diacylglycerol kinase δ (DGKD), ... solute carrier family 34 member 1 (SLC34A1) ... cytochrome P450 family 24 subfamily have been proposed as common causes.
How comorbidities and drugs shape stone composition
Diseases and drugs usually act through the same urinary variables: pH, calcium, oxalate, phosphate, citrate and uric acid. A person with gout is pushed toward urate crystallisation, a person taking a carbonic anhydrase inhibitor toward calcium phosphate, and a person with hyperparathyroidism toward calcium salts. Therefore, the chemical type of a stone often reflects the underlying condition or medication as much as the patient's diet.
Epidemiology and population patterns
Age and recurrence
Stone disease is most common in middle and later adulthood. In NHANES data from 2013–2014, the prevalence in men rose from 5.1% at ages 20–39 to 11.5% at 40–59, 18.8% at 60–79 and 19.7% above 80. By age 70, kidney stones affect 19.1% of men and 9.4% of women. The mean age at first diagnosis is about 44.8 years in men and 40.9 years in women.
Recurrence is the defining long-term pattern. Estimates indicate that the relapse rate is 50% in 5-10 years and 75% in 20 years. In one cohort followed for a median of 11.2 years, recurrence reached 11%, 20%, 31%, and 39% at 2, 5, 10, and 15 years. Factors linked to a higher chance of recurrence include multiple prior stone episodes, younger age of onset, male gender, family history of kidney stones, and higher body mass index (BMI).
Sex ratio and geographic variation
Men have historically outnumbered women among stone formers. In one US series, the male-to-female ratio fell from 3.1 in 1974 to 1.3 in 2000, which was attributed to a relative decline in male (1.7% per year), but an increase in female (1.9% per year) symptomatic stone events. In the 2007–2020 NHANES data, women aged 20–39 showed a higher prevalence than men of the same age (7.8% versus 4.9%). The authors noted that this gap has narrowed in recent decades, especially among younger women. Proposed explanations include obesity, metabolic syndrome, and improved healthcare access, along with female-specific factors such as pregnancy history, hormone therapy and menopause.
Prevalence varies widely by region. Published ranges are 15% in Asia, 59% in Europe, and 7~13% in North America. Within the United States, the North-to-South trend correlates well with temperature variation, but the role of climate in the West-to-East trend is much more ambiguous. Notably, the hottest states like Texas, Florida, and Louisiana had lower prevalence than cooler states like North Carolina and South Carolina.
Trends in incidence and prevalence
Reported trends differ by source and period. One account gives a rise from NHANES II (1976–1980) to recent updates, stone prevalence rose from 3.8% to 8.8%, stabilizing in men but increasing in women. Between 2007–2008 and 2017–2020, the overall weighted prevalence was 8.9% (SE, 0.6%) from 2007 to 2008, which remained relatively stable at 9.9% (SE, 0.6%) from 2017 to 2020, while the female rate rose from 6.5% (SE, 0.5%) to 9.1% (SE, 0.9%) (P = .01). In Germany, by contrast, annual incidence appears to have remained relatively stable at 0.147% in 2005 and 0.153% in 2016 with a male:female ratio of 2:1.
Comparing studies is difficult. Survey-based figures rely on self-reported history: in NHANES, around 12% of men and 10% of women reported a history of kidney stones. Other estimates for the United States give 10.6% for men and 7.1% for women, and figures differ further depending on whether they capture lifetime history, symptomatic events in a given year, or stones found incidentally. Differences in age structure, ethnicity, definitions of a stone episode and the use of age-standardization all affect the comparison.
Seasonal patterns and climate associations
Seasonal clustering is one of the most consistently reported patterns. Higher incidence rates during the warmer summer months than the colder winter months have been observed in multiple settings. A Leeds study of 246 male stone formers found that the data demonstrated statistically significant changes from the minimum value for both calcium and oxalate, with maximum values in the summer. No changes were observed in pH or volume. In a Korean population study, the risk of stone attacks rose once temperatures passed a threshold estimated at 18.4 °C. A systematic review found that worldwide trends on the incidence of renal colic and KSD seem be affected by seasonal variation favoring warmer months.
The pattern is not uniform. In Japanese data, among patients with ureteral stones, diagnoses in men were more frequent during the warmer months (April to August). In contrast, women showed no significant seasonal variation in the incidence of ureteral stones. In a multicity US analysis, cold also raised risk: kidney stone risks increased in Chicago and Philadelphia when the temperatures dropped below 10 degrees Celsius. The proposed mechanism is that higher ambient temperatures increase transdermal, insensible fluid losses, leading to vasopressin-mediated water reabsorption, in turn resulting in lower urine volume, higher urinary osmolality, and increased supersaturation. Because sunlight and temperature are correlated, these studies cannot clearly separate effects of ambient temperature from those of sunlight exposure. Projections of warming-related burden remain model-based; one 2008 projection estimated that by 2095, 70 percent of Americans will live in high-risk zones for kidney stones due to warming.
Symptoms and complications
Renal colic
The classic presentation is renal colic, a sudden, severe pain that is typically felt in the flank and comes in waves. Patients usually describe an acute onset of flank pain that radiates downward and to the side, toward the lower abdomen, groin or testicle. They often describe a dull, constant ache interspersed with bursts of intense, sharp pain. The steady ache is generally attributed to stretching of the renal capsule behind the obstruction, while the colicky bursts are attributed to peristalsis of the ureteral smooth muscle. In women the pain may radiate to the labia, and in men to the testicles. Intense nausea, with or without vomiting, is usually present. Most patients (about 85%) show gross or microscopic hematuria.
Pain intensity tracks the degree of obstruction rather than the size of the stone alone, and it is not a reliable guide to how large the stone is. For most patients the pain peaks one to two hours after onset. Patients with colic are typically restless: they often cannot settle into a comfortable position and may writhe or pace, which contrasts with peritonitis, where patients tend to lie still. Stones lodged at the ureteropelvic junction may cause a deeper, less radiating flank pain instead. Pain from these stones may be mild to severe and may not spread to the groin, because the renal capsule is distended.
Asymptomatic stones and symptomatic movement
Many stones cause no symptoms at all. Small stones that do not obstruct the kidney rarely produce symptoms, and when they do, the symptoms are usually moderate and easily controlled. A stone may also pass through the urinary tract without incident, as asymptomatic crystalluria, or it may obstruct urine flow and cause colicky pain as it moves. Large branched stones are a notable exception to the pattern of colic: patients with staghorn calculi are often relatively free of pain, and such stones usually present with infection and hematuria rather than acute pain. Many stones are therefore found incidentally on imaging performed for other reasons, and the first symptoms appear only when a fragment becomes lodged in the ureter.
Obstruction, infection and urosepsis
Obstruction is the central hazard. When urine cannot drain, pressure builds upstream and the kidney dilates, a state known as hydronephrosis. Infected hydronephrosis is regarded as the most dangerous complication. An obstructed kidney with signs of urinary tract infection, or with anuria, is a urological emergency, and urgent decompression is often needed to prevent further damage. Because stagnant urine lets bacteria multiply, an infection can spread from the kidney into the bloodstream, a condition called urosepsis that carries a substantial risk of death if untreated. Other possible complications include abscess or fistula formation, ureteral perforation, extravasation, kidney infection and renal loss. Where infection is present, definitive surgery of a ureteral stone is usually postponed until the infection has been controlled and the patient has recovered clinically.
Long-term consequences
Stone disease is often recurrent. One estimate places the lifetime risk at 10–15%, with a recurrence rate of 50% within 10 years. Another series reports recurrence rates after an initial episode of 14%, 35% and 52% at 1, 5 and 10 years. Repeated episodes matter for kidney function. Multiple stone episodes are a significant risk factor for chronic kidney disease, end-stage renal disease and significant scarring. Loss of function can arise from chronic obstruction by a stone lodged in the ureter, from a urological procedure performed to remove a stone, or from the disordered physiology that underlies some stone types. Staghorn stones linked to uric acid, cystinuria, renal tubular acidosis or chronic infection are well recognized causes of reduced renal function. The overall picture is nuanced: in one cohort, end-stage renal disease incidence in patients with recurrent symptomatic stones was twice that of the general population, even after adjustment for comorbidities, although the absolute risk was low.
Diagnosis and stone analysis
Imaging
For adults with suspected renal colic, non-contrast computed tomography is the reference examination. Non-enhanced CT has high sensitivity (97–100%) and specificity (96–100%) for urolithiasis. It also defines the position, size and shape of nearly all stones, including those in the ureter, although its main drawback is ionizing radiation, which matters most in children.
Ultrasonography is the preferred first test where radiation is undesirable. It is recommended as the first diagnostic tool for urolithiasis in children. In pregnancy, ultrasound is likewise the first choice, and T2-weighted MRI without contrast is the next option. CT is generally reserved for later pregnancy, when the benefit clearly outweighs fetal risk. Ultrasound has clear limits: it can miss small stones and ureteral stones, and it gives less precise size measurement. Doppler indices can help separate true obstruction from physiological hydronephrosis of pregnancy.
Plain radiography is far less sensitive than its historical role suggests. Calcium-containing stones are radiopaque, whereas pure uric acid, indinavir-induced, and cystine calculi are relatively radiolucent on plain radiography. Small size, overlying gas or stool, and bone shadows can also hide stones. Because of this, a stone seen on CT but absent on a KUB film is often presumed to be uric acid, and in patients with acute renal colic and a urine pH below 6.0, a possible uric acid stone should be considered. Attenuation on CT below roughly 500 Hounsfield units is also highly suggestive of uric acid composition. Many urologists still request a KUB film alongside CT because it is inexpensive and often informative.
Laboratory tests
Urinalysis is the starting point for every stone former. Specific gravity, urine pH, and the presence of protein, blood cells, or bacteria help distinguish among causes of kidney disease and renal colic. A urine culture is added where infection is suspected, which is particularly relevant for struvite stones. Serum tests usually include creatinine to assess kidney function, along with calcium and uric acid.
Metabolic evaluation relies on 24-hour urine collection. The AUA recommends one or two 24-hour collections on a random diet, analyzed at minimum for volume, pH, calcium, oxalate, uric acid, citrate, sodium, potassium and creatinine. From these measurements, laboratories calculate supersaturation ratios for different stone types. A single collection can miss abnormalities, because all of the 24-hour urine chemistry findings may be within the reference range in patients who actively form stones. The test is most valuable for recurrent or high-risk formers, who are likely to benefit from metabolic testing and medical therapy.
Stone analysis
Identifying the composition of a retrieved or passed stone is the most direct way to determine its type. Methods include Fourier-transform infrared spectroscopy and other chemical analyses. Crystallographic techniques, principally X-ray diffraction, are also used to identify mineral phases, including the hydrate forms of calcium oxalate. Stone analysis is recommended in children whenever possible, since their first episode often reflects an underlying metabolic disorder.
Differential diagnosis of flank pain
Acute flank pain has a broad differential. Appendicitis can mimic right-sided renal colic, especially when the appendix lies high in the pelvis. Other causes include pyelonephritis, cholecystitis, diverticulitis, and, in women of reproductive age, ectopic pregnancy or ovarian torsion. Abdominal aortic aneurysm or dissection is a critical diagnosis to exclude in older patients with pain and risk factors for vascular disease, because it requires different urgent management. Imaging and laboratory findings usually separate these conditions from stone disease.
Acute management and spontaneous passage
Acute care of renal colic starts with pain control. The European Association of Urology and the National Institute for Health and Care Excellence guidelines recommend NSAIDs as initial analgesics for acute renal colic. A systematic review and meta-analysis found that NSAIDs relieved pain at 30 minutes about as well as opioids or paracetamol, while causing less vomiting and needing fewer rescue analgesics than opioids. Opioids remain an option, and the choice in emergency departments still depends heavily on clinician personal preference and experience as well as institutional protocols. Where an opioid is given, the older agent pethidine has been linked to a much higher rate of vomiting than NSAIDs. Oral or intravenous fluids are generally encouraged alongside analgesia, although the direct effect of hydration on passage is less firmly established than its general role in managing colic.
Medical expulsive therapy uses alpha-blockers, which relax smooth muscle in the ureteral wall, to help stones pass. A 2025 meta-analysis of trials of stones up to 10 mm in the ureter, including 4,256 patients across 29 randomized trials, reported that alpha-blockers significantly increased stone expulsion rates compared to controls (70.9% vs. 56.5%; RR 1.25; NNT = 7) and reduced expulsion time by approximately three days. The evidence is less uniform than these pooled figures suggest. A Cochrane review concluded that alpha-blockers likely increase stone clearance but probably also slightly increase the risk of major adverse events. Its subgroup analysis indicated that alpha-blockers may be less effective in smaller (≤5 mm) than larger stones (>5 mm). Earlier meta-analysis work reached similar conclusions about small stones, and some reviewers therefore advise a course of alpha-blocker for most patients unless it is contraindicated. Because tamsulosin is the most extensively studied agent, comparisons of individual drugs in network analyses are generally interpreted with caution.
The likelihood of spontaneous passage falls with increasing stone size and depends on location. In a CT-based cohort, passage rates were 87% for 1 mm stones, 76% for 2–4 mm stones, 60% for 5–7 mm stones, 48% for 7–9 mm stones and 25% for stones larger than 9 mm. Distal ureteral stones pass more readily than proximal ones: one older series estimated passage at about 75% in the distal ureter, 60% in the middle ureter and 50% in the proximal ureter. Distal stones of 4 mm or less were expelled with a probability of about 95%, compared with about 47% for distal stones of 5–10 mm. Small stones are therefore commonly managed by observation with analgesia, hydration and periodic imaging, while larger or persistently symptomatic stones are more often considered for intervention.
Hospital admission is generally considered when infection coexists with obstruction, because an obstructed infected collecting system can progress to urosepsis and requires urgent drainage. Other indications include pain that cannot be controlled with oral or intravenous medication, inability to tolerate fluids or oral drugs, a solitary kidney or a transplanted kidney with a stone, and impaired kidney function, since these factors increase the consequences of further obstruction.
Procedural and surgical treatment
Shock wave lithotripsy
Shock wave lithotripsy (SWL) fragments a stone with externally generated acoustic pulses and avoids any incision or instrument in the urinary tract. Because of this, it is usually the least invasive option for suitable stones. It is regarded as the first line treatment for nephrolithiasis under 20 mm in size. Selection depends mainly on size and location. European guidance favors SWL or retrograde intrarenal surgery for stones under 10 mm, while stones of 10 to 20 mm can be treated with either SWL or endoscopic methods. PCNL is a treatment of choice for renal stones over 20 mm. Two anatomical limits are important. First, poor clearance of lower calyceal fragments, owing to gravity or an unfavorable infundibulopelvic angle, limits SWL's efficacy in lower-pole stones. Second, very dense stones respond poorly; CT density above about 1000 Hounsfield units is treated as a marker of weak fragmentation, which is why such stones are often excluded from SWL trials.
Ureteroscopy with laser lithotripsy and stenting
Ureteroscopy (URS) passes a scope through the urethra and bladder into the ureter or, with a flexible instrument, into the renal collecting system, where a laser or pneumatic probe fragments the stone. Flexible instruments have broadened its reach, and flexible ureteroscopy has improved the quality of upper urinary tract exploration, allowing most stones at all sites to be treated. Its drawbacks include staged procedures, a risk of ureteral injury, and equipment costs. Those issues may have limited how widely this endoscopic approach has spread.
In a Swiss randomized trial of renal stones of 5 to 15 mm, the 3-month stone-free rate was 61% after URS and 48% after SWL, but early pain was higher after URS, although the trial closed early because of poor recruitment. The 3-month stone-free rate and mean residual stone size were, respectively, 61% and 1.8 mm after URS and 48% and 2.4 mm after SWL. A meta-analysis of proximal ureteral stones found a similar pattern, with URSL related to a higher stone-free rate than SWL regardless of stone size, while SWL was related to a higher retreatment rate. A randomized trial of kidney stones up to 2 cm also favored retrograde intrarenal surgery at one and six months, but the difference tended to reduce at 6 months and was no longer significant at 1 year.
In an emergency, an obstructed kidney is first drained with a temporary nephrostomy or ureteric stent, and definitive fragmentation with SWL or laser URS follows later. The definitive surgical management involves either shockwave lithotripsy or laser fragmentation with ureteroscopy.
Percutaneous nephrolithotomy and staghorn calculi
Percutaneous nephrolithotomy (PCNL) accesses the kidney through a tract in the back and removes or fragments stones with a nephroscope. Standard PCNL, using a 24 to 30 French sheath, remains the standard procedure for large renal calculi. Its large access tract is also the source of its main drawbacks: bleeding, postoperative pain, and a long recovery period. Mini-PCNL uses a smaller sheath to reduce these problems while keeping similar stone-free rates in most series.
Staghorn calculi, which fill the renal pelvis and extend into the calyces, are the main indication for PCNL in large stones. PCNL is the gold standard treatment for staghorn stones. Their surgical difficulty is reflected in outcomes: these stones are associated with a higher rate of perioperative complications than non-staghorn stones. A prospective Pakistani series of 120 patients treated with mini-PCNL reported a stone-free rate of 84.2%, intraoperative complications in 18.3%, and postoperative fever or infection in 20 patients (16.7%) and urosepsis in five (4.2%). A meta-analysis comparing mini-PCNL with standard PCNL in staghorn calculi found that the stone-free rate was comparable between the two. A single-centre series of 15 years reported a transfusion rate of 0.8% and stone-free rates of 78% at hospital discharge and 91% at 3 months follow-up.
Open surgery has become rare. Open, laparoscopic, and robotic surgeries have their place only in highly selected patients. Current guidance is discussed in the sections on modern practice; the American Urological Association has published a 2026 guideline series covering shock wave lithotripsy, ureteroscopy, and percutaneous nephrolithotomy, including mini-PCNL.
Choosing a procedure
The choice is rarely made on stone size alone. Treatment strategies depend on stone size, location, composition, and patient characteristics. Clinicians weigh the expected stone-free rate against the need for repeat procedures, the risk of bleeding and infection, anaesthesia requirements, and the patient's anatomy and comorbidities. Non-invasive SWL has fewer complications, but it often needs more sessions. ESWL was associated with fewer complications, but it required more sessions and resulted in lower immediate postoperative quality of life and higher workdays lost. Complications for URS and SWL are generally low, with one trial reporting one Clavien-Dindo grade II complication after URS (5%) and SWL (4%), and one grade IIIb complication after SWL (4%). Retreatment rates, bleeding, and infection rates must therefore be read together with the stone-free rate, since a procedure that clears the most stones at first may not be the one that causes the least overall burden to the patient.
Prevention and long-term management
Fluid intake
Fluid intake is the basis of prevention for every stone type, because urine volume determines how concentrated stone-forming salts become. For all stone formers, the American Urological Association's target is at least 2.5 litres of urine per day, a standard supported by moderate-quality evidence. The American College of Physicians set a lower goal of about 2 litres for people with at least one prior episode. Some guidelines advise 3.5–4 litres in severe forms, such as enteric hyperoxaluria or cystinuria. The evidence base is observational plus a small number of trials. In one meta-analysis, high fluid intake was significantly associated with a 60% decreased risk of recurrent stones in RCTs and an 80% decreased risk in observational studies. In a five-year randomized study, recurrence was 12% among patients encouraged toward 2 litres of urine daily, compared with 27% among those not encouraged.
The 2.5-litre figure is a convention rather than a threshold. The relationship between urine volume and risk appears continuous, and one large institutional cohort found no association between 24-hour voided volume and later stone events, although some patients may benefit more than others. Adherence is a practical obstacle, and few studies have measured it directly.
Diet
Dietary advice is most effective when matched to the stone type and to the patient's urinary chemistry. The Borghi trial, a landmark randomized study in people with recurrent calcium oxalate stones, found that a diet with adequate calcium, reduced animal protein and reduced sodium lowered five-year recurrence to a relative risk of 0.49. The benefit was attributed largely to lower urinary oxalate, probably because dietary calcium binds oxalate in the intestine. A Swiss retrospective analysis reached a similar conclusion: restricting animal protein and salt with normal calcium intake was more effective than a low-calcium diet. Current US federal guidance sets sodium at 2,300 mg per day, and about 1,500 mg for people whose stones have been linked to sodium.
Oxalate restriction is selective rather than universal. Not everyone with calcium oxalate stones has high urinary oxalate, so routine limitation of foods such as spinach, nuts or beets is not required for all patients. Calcium is best obtained from food rather than supplements, since some studies have linked supplements to stone formation.
Medications
Thiazide diuretics have been the mainstay of drug prevention for more than four decades, mainly by reducing urinary calcium. Their evidence, however, is contested. The NOSTONE trial, a double-blind, placebo-controlled study in Switzerland with 416 patients, found that recurrence was 59% with placebo and 49–59% across hydrochlorothiazide doses, with no statistically significant benefit. By contrast, an analysis of US claims data found that patients empirically prescribed thiazides had a lower rate of later stone events (14.8%) than those given alkali citrate or allopurinol (20.4% each), though observational data cannot settle the question. Potassium citrate raises urinary citrate and alkalinizes urine, and allopurinol lowers uric acid production, which makes it useful when uric acid is a driver. Side effects and the need for long-term adherence limit their use.
Metabolic evaluation and adherence
Twenty-four-hour urine collection identifies the abnormalities, such as hypercalciuria, low citrate or high uric acid, that a targeted drug choice aims to correct. Whether this selective approach outperforms empirical treatment is unresolved. One cohort found no difference in recurrence between selective and empiric pharmacologic therapy, and lower adherence and younger age were linked to more recurrences. Risk factors for recurrence also include higher body mass index, hypertension and family history, and recurrence rates may reach 40% within five years. Because the benefits of fluid, diet and drugs depend on sustained practice, the balance between preventive gains and long-term side effects remains central to individual decisions.
Special populations
Children
Stone disease in children is less common than in adults, and it is more often linked to an underlying cause. Stones in the urinary tract occur commonly in adults but less often in children. Stone formation in children is more likely to be caused by an underlying metabolic disorder or anatomical abnormality. Up to a third of children with stones have an anatomic abnormality of some kind. These defects include obstruction of the kidney or ureter, as well as conditions such as spina bifida and bladder exstrophy. Recent studies have shown that in approximately 5% of children with nephrolithiasis, potentially causative variants can be identified, and this increases up to 15% if nephrocalcinosis is also assessed. Metabolic causes are the largest category in many series. In one cohort, a metabolic predisposition was identified in one-third of children, and about 20% had stone disease associated with urinary tract infection. Childhood stone composition is similar to that in adults, with 70–80% calcium oxalate, 10–15% struvite, 10% calcium phosphate, and under 5% uric acid. The higher share of calcium phosphate and the lower share of uric acid stones may reflect the more alkaline urine that children produce.
Children with stones often show a recurrence pattern that calls for prevention from the outset. The recurrence risk in children is high, up to 50% within three years of the first episode, and many have a predisposing metabolic risk factor such as hypercalciuria. For this reason, work-up of pediatric stones should include a metabolic assessment to identify risk factors for recurrence. Much of the stone literature is based on adults, so pediatric epidemiology and treatment rest on a thinner evidence base. Presentation can also differ: younger children may describe nonspecific abdominal or urinary complaints rather than classic flank pain, which can delay diagnosis (general clinical experience, not otherwise sourced).
Pregnancy
Earlier assumptions that stones are more frequent in pregnancy have been questioned, although complications related to stones may still be more likely. Ultrasound is the first-line investigation, and fetal exposure to radiation can cause harm, so imaging with radiation should be avoided unless absolutely necessary. Ultrasound has real limits. It is very operator-dependent and has a low sensitivity, reported between 34% and 95.2%. The ureteric jets can be absent in about 15% of pregnant women, so clinicians interpret findings together with history and laboratory results. Doppler measurement of the renal resistive index helps separate obstruction from the physiological dilation of pregnancy: gestational hydronephrosis does not raise the index, whereas ureteric obstruction does.
Most pregnant patients are managed conservatively. Pregnancy-related ureteric hypotonia and a large urine volume support stone passage, with rates similar to those in non-pregnant women. Analgesia requires care, because nonsteroidal anti-inflammatory drugs are generally avoided, especially after 20 weeks, owing to the risk of premature closure of the ductus arteriosus and oligohydramnios. Opioids and paracetamol are typically used instead. Complicated cases, such as a suspected infected, obstructed system, require urgent decompression, for example by percutaneous nephrostomy. When intervention is needed, ureteroscopy is supported as a safe option once infection has been treated. Indwelling stents and nephrostomy tubes require regular exchange because of their high propensity for encrustation in pregnancy.
Older adults and people with chronic kidney disease
Stones are concentrated in middle and later life, and 10–20% of people with kidney stones are older than 65 years. Older patients often carry several contributing conditions. Diabetes, chronic urinary tract infections and osteoporosis are common in this group and are known risk factors for stones. Polypharmacy adds to the problem, since taking multiple medications and supplements for these conditions can itself alter risk.
The relationship between stones and chronic kidney disease (CKD) is most relevant here. In one cohort followed for a mean of 8.6 years, stone formers had an increased risk of a clinical CKD diagnosis, but the increase in risk for end-stage kidney disease or death with CKD was not statistically significant. Kidney function is itself age-dependent: CKD is more common in people aged 65 or older than in younger adults. In patients with advanced CKD, competing risks matter. In a Canadian cohort, death was more likely than kidney failure, and the gap widened sharply in the oldest age groups. Clinically, this means that management of an older patient with reduced kidney function should weigh the drugs used for stone prevention and pain against renal clearance. Many agents require dose adjustment, and nephrotoxic drugs such as NSAIDs are generally avoided (general clinical practice, not otherwise sourced).
People with a solitary kidney or a transplanted kidney
A person with a solitary kidney has no second organ to compensate for an obstructing stone. Relief of obstruction is therefore more urgent, and procedures are chosen partly to preserve functioning renal tissue and limit repeated instrumentation (general clinical practice). Infection with obstruction in such a patient carries a greater risk of permanent loss of function, which is why admission thresholds are lower.
Transplanted kidneys present a different set of issues. Stones may form in the graft's collecting system or in the native urinary tract, and ureteric narrowing at the surgical anastomosis can produce obstruction that mimics a stone. Immunosuppressive drugs, some of which interact with other medications, complicate both diagnosis and treatment, and infection-related stones carry a higher risk of serious sepsis. Ultrasound is often the first study because the graft lies superficially. Interventions such as ureteroscopy or percutaneous approaches are planned jointly with the transplant team, with attention to contrast exposure and to the graft's vulnerability to nephrotoxic agents (general clinical practice, not otherwise sourced).
Links to systemic and kidney disease
Kidney stone disease is increasingly treated as a whole-body condition rather than an isolated problem of the urinary tract. Reviews list chronic kidney disease, cardiovascular disease, metabolic syndrome and low bone mass among the conditions it is linked to. The strongest body of evidence concerns the kidney itself. In a cohort from Olmsted County, Minnesota, people who formed stones developed chronic kidney disease (CKD) more often than people who did not (stone-formers were at increased risk of developing CKD). A Canadian population cohort followed participants for a median of 11 years and found higher rates of end-stage kidney disease and late-stage CKD among those with one or more stone episodes, with the excess concentrated in women and in people younger than 50 (the risks of end-stage kidney disease, late-stage CKD, and doubling of serum creatinine were significantly higher among participants with 1 or more episodes of nephrolithiasis). Taiwanese national insurance data, matched 1:4 on sex and age, were used in a similar design (data on incident stone formers in 2001, excluding those with a history of CKD, were obtained from Taiwan's National Health Insurance database).
Several mechanisms have been proposed. Obstruction, recurrent urinary infection and the treatments used for stones are all considered plausible contributors (recurrent urinary tract infections, hydronephrosis secondary to obstruction, or treatments for urolithiasis). Nephrocalcinosis, the microscopic deposition of calcium phosphate within the kidney, is another candidate. Experimental data suggest it may speed CKD progression (microscopic calcium phosphate deposition in the kidney may accelerate progression of chronic kidney disease), although its direction of effect is hard to separate from disease stage. Biopsy-based prevalence rises steeply as kidney function declines, from 4.6, 14.3, 20.2 and 54.0% across CKD categories, which suggests mineral deposition may follow kidney damage as much as cause it.
The absolute contribution of stones to kidney failure is modest. In US registry data for 2011, urologic disease including stones accounted for about 2% of end-stage renal disease cases (only 2% of ESRD were caused by urologic disease which included kidney stones), far below the share attributed to diabetes and hypertension. Some authors have warned that this small share may lead clinicians to underestimate stones as a risk factor (there might be a tendency to underestimate or ignore the influence of kidney stones on CKD).
Observational studies also associate stone disease with hypertension, cardiovascular disease, diabetes and bone disease, with inconsistent results. In a 2007–2010 US survey of 7,210 adults, stone formers had higher odds of acute myocardial infarction, with an odds ratio of 1.88, but no significant association with heart failure, hypertension or stroke (patients with kidney stones exhibited a significantly elevated risk of acute myocardial infarction (AMI) (odds ratio [OR], 1.88) (a non-significant association was observed with heart failure, hypertension, or stroke). A Mendelian randomization analysis, which uses genetic variants to reduce reverse causality, reported that genetically predicted stones were associated with coronary heart disease and myocardial infarction, while the cross-sectional and genetic results diverged for several other outcomes (genetically predicted kidney stones were causally associated with an increased risk of coronary heart disease ... cross-sectional analyses yield results that are inconsistent with those obtained from Mendelian randomization analyses). The diabetes link appears to run in both directions. Because stones are unlikely to cause diabetes directly, a common metabolic defect has been proposed to contribute to both (urolithiasis is unlikely to cause DM directly, the positive reciprocal association between stones and DM suggests that a common metabolic defect may contribute). Genome-wide analyses from large biobanks have found modest positive genetic correlations between stones and hypertension, obesity and type 2 diabetes (modest but significant positive associations between kidney stones and hypertension, obesity, and type 2 diabetes). Bone involvement is most evident in disorders that combine stones with mineral loss, where stones, bone pain, osteoporosis and fractures may appear together (patients may present with kidney stones, bone pain, osteoporosis, and pathologic fractures).
The shared metabolic mechanisms centre on insulin resistance and urinary acid handling. Insulin resistance is thought to impair renal ammonia production, which leaves the urine more acidic (Insulin resistance has been noted to impair renal ammoniagenesis, which results in acidic urine). Low urinary pH raises the proportion of insoluble undissociated uric acid, which favours uric acid stones (low urinary pH, which increases the concentration of the insoluble undissociated uric acid). In healthy non-stone formers, lower insulin sensitivity correlated with lower 24-hour urinary pH, and people with recurrent uric acid stones were found to be severely insulin resistant (low insulin sensitivity measured as glucose disposal rate significantly correlated with low 24-hour urinary pH; patients with recurrent uric acid nephrolithiasis were found to be severely insulin resistant). Visceral obesity adds to this through the release of free fatty acids, which alter hepatic lipid handling and drive insulin resistance (The production of free fatty acid related to visceral obesity results in increased glucose, triglycerides, very LDL, and LDL and decreased HDL in the liver, resulting in insulin resistance.). Gout sits within the same cluster: in the NHANES sample, stone formers had gout more often, at 9.8% versus 4.1% (a higher risk of gout (9.8% versus 4.1%)). Inflammation and tissue damage have been suggested as a unifying explanation, though not the only one (One unifying theory may be of a common systemic malfunction of inflammation and tissue damage as an underlying mechanism, but it is unlikely to be the only mechanistic explanation.).
Causation remains unresolved. Some comorbidities may produce stones, while others may be triggered by them (Many of the co-morbidities may not only lead to stone disease but also be triggered by it.). Shared exposures complicate the picture further: low water intake, high protein diet, bacterial infection and urinary tract anomalies are risk factors common to stones and CKD (kidney stones also share many common risk factors with CKD such as low water intake, high protein diet, bacterial infection, and urinary tract anomalies). Stones and nephrocalcinosis may also be distinct processes; in primary hyperoxaluria, nephrocalcinosis predicted kidney failure, while stone counts did not (the number of stones and stone events were not significantly associated with ESKD risk. Thus, nephrolithiasis and nephrocalcinosis appear to be pathophysiologically distinct entities.). How much of the systemic risk stone disease adds independently of these shared factors is still debated.
History of understanding and treatment
Urinary stones are among the oldest documented human diseases. The earliest physical evidence comes from burial remains: The first known stones were discovered in Egyptian mummies. Dating is not uniform across sources. One account describes a 1901 find by the archaeologist E. Smith, a bladder stone from a mummy at El Amrah estimated at 4,500–5,000 years old, in 1901, while another reports a renal stone described by Shattock in 1905 that was found in an Egyptian mummy in a tomb dating to approx 4400 bc. Written evidence is later. Treatments for stones were mentioned in ancient Egyptian medical writings from 1500 BC, and Mesopotamian medical texts are often cited as the earliest literary descriptions of stone symptoms and attempts at dissolution. In Greece, Hippocrates defined the symptoms of bladder stones, and the Hippocratic Oath bars physicians from cutting for stone. The Indian surgeon Sushruta is credited with a description of over 300 surgical procedures, including perineal lithotomy, though sources differ on whether his work dates to the eighth or the sixth century BC.
Surgical removal of stone, known as lithotomy, is the most persistent theme in this history. The first detailed description of the procedure and instrumentation of lithotomy is to be found by Celsus in the first century AD. Celsus's "lesser operation" needed only a knife and a hook, and this ancient method as described by Celsus was the only one performed until the middle of the 16th century. The Fourth Lateran Council of 1215 forbade physicians from performing surgical procedures, as contact with blood or body fluids was viewed as contaminating, which pushed the operation toward specialist surgeons. In the Middle Ages, surgeons called "lithotomists" traveled around Europe with their special tables, and the patients they treated were typically men with bladder stones from enlarged prostates rather than actual kidney stones. Improvements came gradually: the first recorded suprapubic lithotomy was carried out by Pierre Franco in 1561, and it was only at the beginning of the 16th century that, with the introduction of the perineal cystotomy with lateral cut, the first major progress in the technique of lithotomy occurred. Operative risk remained high, with infections or excessive bleeding as the main dangers.
Chemical understanding began in the late eighteenth century. Scheele shewed in 1776, that urinary human calculi were formed of a particular concrete acid, which was later named uric acid. Scheele himself wrongly assumed that uric acid was the only constituent of stones, and many chemists ascertained the existence of another substance accompanying the uric acid. In 1786, Tychsen, professor of chemistry in Copenhagen, discovered in a calculus phosphoric acid combined with lime, and in 1797, Wollaston proposed a classification of these bodies, a scheme that remained in use for a long time. During the following thirty years, Fourcroy and Vauquelin in Paris and Wollaston, Pearson, Marcet and Prout in London identified the various salts, uric acid, urate, various phosphates, oxalate, calcium, ammonium and magnesium forming current calculi. Rarer components were also identified, as even rare components such as cystine and xanthine were unraveled in London. The naming of stones by composition therefore dates largely to this period, and a burst of activity in the 19th century established most of the names used today. Chemical study then stalled: during the following decades nothing was added to these chemical investigations, and most of what had been acquired was forgotten.
Instrumentation changed the treatment of stones in the nineteenth and twentieth centuries. In 1874, Bigelow developed a lithotrite, which was introduced into the bladder under anaesthesia, a procedure known as litholapaxy. Young was the first to report ureteroscopy (1929). With advances in intracorporeal lithotripsy techniques, ureteroscopy became the treatment of choice for ureteric stones. Percutaneous access to the kidney followed: in 1976, Fernstrom and Johannson established percutaneous access to remove a renal stone. The decisive change came with non-invasive fragmentation. With the introduction of the first extracorporeal shock wave machine in 1980, a dramatic change in stone management was observed. Open lithotomy subsequently declined, owing to better minimally invasive alternative methods and most notably by the virtual disappearance of bladder stones in modern man.
Research directions and open questions
The origin of Randall's plaque
Alexander Randall's work in the 1930s and 1940s is the starting point for the idea that Randall's plaque initiates many calcium stones. After studying more than 1100 cadaver kidneys, he proposed that a subepithelial plaque acts as a nucleation site for kidney stones. His original observations also described two routes: interstitial deposits that could rupture the urothelium, and calcium phosphate plugs forming in collecting ducts. Randall distinguished two ways for stone initiation.
Modern biopsy work has refined the anatomy. Apatite deposits at the origin of these plaques appear to arise from the basement membranes of thin loops of Henle and then spread into the surrounding interstitium. The central dispute is causal direction. Stones are often found attached to plaques, but there has been no rigorous in vivo documentation of this attached-stone relationship. It is therefore unresolved whether plaque is the primary lesion or a secondary site where stones that formed elsewhere are retained. Plaque burden is associated with urinary calcium levels and decreased urinary volume, but association does not establish initiation. Animal models suggest that hypercalciuria may promote Randall's plaque formation and growth. Candidate gene and immune signatures have also been proposed, but these remain exploratory.
Gut and urinary microbiome
Intestinal bacteria are a newer research focus. Oxalate is degraded by gut bacteria, which reduces its intestinal absorption. The best-studied species is Oxalobacter formigenes, and intestinal colonization by this organism has been associated with a lower risk of recurrent stones in humans. Antibiotic exposure may remove it, a concern that has been examined in studies of antibiotic courses given for other infections. Network analyses have also suggested that a group of bacterial taxa co-occurs with Oxalobacter formigenes in fecal samples, and these taxa are less represented in stone formers.
The therapeutic evidence is weaker than the biology. A 2025 systematic review identified nine studies, comprising five randomized controlled trials and four observational studies, and concluded that current evidence does not support the use of probiotics or synbiotics targeting oxalate-degrading bacteria for reducing urinary oxalate or preventing recurrence. Colonization often occurred without meaningful biochemical change, and follow-up was generally short.
Genetic risk scores and prediction
Genetic epidemiology has expanded substantially. A trans-ancestry meta-analysis combined 31,715 cases and 943,655 controls from European and East Asian populations and identified 59 kidney stone disease susceptibility loci, including 13 novel loci. A cross-population polygenic risk score showed that individuals in the lowest and highest quintiles have odds ratios of 0.57 and 1.83, respectively, relative to the third quintile. Higher scores were also linked to younger age at onset. Other work has linked genetic and biomarker profiles to stone risk, reporting a hazard ratio of 3.73 for ureteral stones in the strongest genetic-biomarker interaction group. Predictive accuracy in individual cases remains modest, however: one convolutional neural network approach reached a test accuracy of 61.67%.
Clinically, the more immediate question is which patients merit testing for a monogenic cause. A retrospective London clinic study found that a first stone before age 18, nephrocalcinosis, and a higher cumulative risk score were associated with a positive genetic diagnosis, which led to a proposed scoring system for prioritizing testing.
Incidence trends, climate and diet
Kidney stone disease is described as increasing worldwide, but the causes of this rise are not established. Proposed drivers include diet, obesity, heat exposure and climate change, yet most evidence is observational, and definitions, imaging practices and population sampling differ among studies. Separating these contributions requires longitudinal cohorts with standardized stone detection and detailed exposure data.
Quality of evidence for prevention
Many prevention recommendations, including fluid targets, dietary restriction and stone-type-specific drugs, rest on small or short trials and on observational associations. This matters because recurrence is common: up to 50% of individuals who have had a stone experience a second stone within 10 years. Large randomized trials with imaging-confirmed recurrence outcomes, as recommended by systematic reviewers, would clarify which interventions reduce long-term burden, and for which stone types and patient groups.
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