What causes kidney stones?

Stones form when urine becomes supersaturated with stone-forming salts and there is insufficient inhibitor activity to prevent crystals aggregating. The dominant modifiable factor is low urine volume — concentrated urine from inadequate fluid intake, hot climates, heavy sweating or chronic diarrhoea. Other contributors: high dietary sodium, which increases calcium loss in the urine; high animal protein intake, which raises acid load and lowers citrate; obesity, diabetes and metabolic syndrome, which lower urine pH and promote uric acid stones; primary hyperparathyroidism; inflammatory bowel disease and bariatric surgery, which cause enteric hyperoxaluria; recurrent urinary infection with urease-producing bacteria, which causes struvite stones; certain medications; and genetic conditions such as cystinuria and primary hyperoxaluria.

When is a kidney stone an emergency?

The critical emergency is an obstructing stone with infection. If a person with renal colic develops fever, rigors, confusion, a fast heart rate or low blood pressure, the obstructed kidney may be filling with pus — and this progresses to septic shock and death within hours. Antibiotics cannot fix it, because they cannot reach an obstructed system: the kidney must be drained urgently with either a stent passed up the ureter or a nephrostomy tube through the back. Other urgent situations: a stone obstructing a solitary kidney or both sides at once, causing acute kidney injury; uncontrollable pain or vomiting preventing oral intake; and stones in pregnancy. Otherwise, most stones can be managed with analgesia and observation.

Will my stone pass on its own?

Probably, if it is small. Stones under about 4-5mm pass spontaneously in roughly seventy to eighty per cent of cases; those between 5 and 10mm in about half; and stones larger than 10mm rarely pass and usually need treatment. Position matters too — stones already in the lower ureter, close to the bladder, pass much more readily than those higher up. Provided pain is controlled, there is no infection, kidney function is preserved and there is only one working kidney involved, it is reasonable to wait for up to four to six weeks. Tamsulosin may help passage specifically for larger stones in the lower ureter, though it was not shown to help overall in the large SUSPEND trial. If the stone has not passed within that window, intervention is usually offered.

Should I avoid calcium if I get calcium stones?

No — and this is one of the most damaging myths in the field. Restricting dietary calcium actually INCREASES the risk of calcium oxalate stones. The reason is that calcium in food binds oxalate in the gut, so the two are excreted together in the stool. If you eat less calcium, more oxalate is left free to be absorbed, and it ends up in the urine, where it is the limiting factor for stone formation. A landmark randomised trial found that a normal-calcium, low-sodium, low-animal-protein diet halved recurrence compared with a low-calcium diet. So the advice is normal dietary calcium (from food rather than high-dose supplements taken away from meals), less salt, moderate animal protein, and above all plenty of fluid.

How do I stop stones coming back?

Fluid is the foundation: drink enough to produce more than two to two and a half litres of urine a day, spread through the day and including before bed, with the simple target of keeping urine pale. This alone roughly halves recurrence in randomised trials. Reduce salt, which drives calcium into the urine. Keep animal protein moderate. Maintain normal dietary calcium. Limit high-oxalate foods such as spinach, rhubarb, nuts and strong tea only if hyperoxaluria has actually been demonstrated. Beyond diet, the stone itself should always be sent for analysis, because composition determines everything: uric acid stones can be dissolved with potassium citrate, struvite stones require complete surgical clearance and infection control, and cystine stones need specialist management. Recurrent formers should have a 24-hour urine metabolic assessment to target treatment such as thiazides or citrate precisely.

How does GMJ News cover kidney stones?

GMJ News covers the obstructed infected kidney as a decompression emergency, NSAIDs over opioids for renal colic, low-dose CT KUB and imaging in pregnancy and children, spontaneous passage rates by size and the SUSPEND trial on medical expulsive therapy, stone composition and analysis-directed prevention, uric acid stone dissolution, struvite and staghorn management, 24-hour urine metabolic evaluation, thiazides and citrate, surgical options (ESWL, ureteroscopy, PCNL), ureteric stent symptoms and the danger of forgotten stents, and the climate and occupational heat dimension of rising stone burden. Relevant to PHIG's kidney health, occupational health and climate-and-health programmes.

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Kidney Stones

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Urolithiasis — the formation of calculi within the urinary tract — has a lifetime prevalence approaching 10-15% and is rising globally, driven by obesity, diabetes, metabolic syndrome, dietary change and, increasingly, heat exposure, with recurrence rates of roughly 50% at ten years without preventive measures (WHO). Non-contrast CT of the kidneys, ureters and bladder is the diagnostic standard, and the critical clinical distinction in an acute presentation is between the great majority of stones that will pass spontaneously with analgesia — NSAIDs being more effective than opioids for renal colic — and the true urological emergency of an obstructed, infected kidney, where fever and obstruction together demand immediate decompression by ureteric stent or nephrostomy, since antibiotics alone cannot sterilise an obstructed system and delay leads rapidly to urosepsis and death.

Key messages

Obstruction plus infection is a urological emergency — decompress immediately

The single most important rule in stone disease. Fever, systemic upset or a raised white cell count in a patient with an obstructing ureteric stone indicates an obstructed, infected kidney (pyonephrosis) — a condition that progresses to septic shock and death within hours. Antibiotics alone cannot sterilise an obstructed collecting system. Management: resuscitation, blood cultures, IV antibiotics AND urgent decompression by either retrograde ureteric stent or percutaneous nephrostomy. Definitive stone treatment is deferred until the infection is controlled. Delay in decompression is the principal determinant of mortality.

NSAIDs beat opioids for renal colic

Non-steroidal anti-inflammatory drugs are more effective than opioids for the pain of renal colic and should be first-line unless contraindicated. The mechanism is specific: prostaglandin inhibition reduces both ureteric smooth muscle spasm and, importantly, the renal afferent arteriolar vasodilation that drives the rise in intrapelvic pressure causing the pain. Diclofenac (oral, rectal or intramuscular) or intravenous ketorolac are commonly used. Opioids are reserved for NSAID contraindication or inadequate relief. Caution with NSAIDs in acute kidney injury, dehydration, existing chronic kidney disease and in the elderly.

Non-contrast CT KUB is the diagnostic standard — but consider ultrasound first in specific groups

Non-contrast CT of the kidneys, ureters and bladder has near-perfect sensitivity and specificity, identifies stone size and position precisely (both of which determine management), and reveals alternative diagnoses. Low-dose protocols substantially reduce radiation exposure and should be standard. Ultrasound is preferred first-line in pregnancy (where CT is avoided and MRI is second-line) and in children, and is reasonable in young patients with recurrent typical colic to limit cumulative radiation. Point-of-care ultrasound showing hydronephrosis supports the diagnosis but cannot exclude a stone or size it reliably.

Stone size and position predict spontaneous passage

Most stones pass without intervention, and prediction guides management. Stones under 5mm pass spontaneously in roughly 70-80% of cases; 5-10mm in around 50%; above 10mm, spontaneous passage is unlikely and intervention is usually required. Distal ureteric stones pass more readily than proximal ones. Medical expulsive therapy with tamsulosin is now used selectively rather than routinely: the SUSPEND trial found no overall benefit, but meta-analyses suggest a genuine effect confined to larger distal ureteric stones (roughly 5-10mm), which is where guidelines now position it. Watchful waiting is appropriate for up to 4-6 weeks in a stable patient with controlled pain and no infection or renal impairment.

Recurrence is around 50% at ten years — and largely preventable

The most neglected part of stone care is what happens after the stone passes. Without preventive measures, roughly half of patients form another stone within a decade. The single most effective intervention is fluid intake sufficient to produce more than 2-2.5 litres of urine per day — proven in randomised trials to halve recurrence. Dietary measures: reduce sodium (which drives urinary calcium excretion); moderate animal protein; maintain NORMAL dietary calcium — restricting calcium paradoxically INCREASES calcium oxalate stone risk by leaving more oxalate free for absorption, a common and harmful piece of misinformation; and limit high-oxalate foods only in documented hyperoxaluria.

Metabolic evaluation and stone analysis change management

Every stone passed or retrieved should be sent for compositional analysis — it directs prevention entirely. Calcium oxalate (around 70-80%): fluid, sodium reduction, thiazides for hypercalciuria, potassium citrate for hypocitraturia. Uric acid (5-10%): radiolucent on plain film, associated with low urine pH, obesity, diabetes and gout — uniquely, these stones can be DISSOLVED with urinary alkalinisation to pH 6.5-7.0 using potassium citrate. Struvite: infection stones from urease-producing organisms (Proteus, Klebsiella), forming staghorn calculi — require complete surgical clearance since fragments perpetuate infection. Cystine: genetic, presenting in childhood, recurrent and treatment-resistant. Full 24-hour urine metabolic evaluation is indicated in recurrent formers, children, solitary kidneys, and non-calcium stones.

Key statistics

10-15%

lifetime prevalence of kidney stones, and rising globally

EAU/AUA

~50%

recurrence at 10 years without preventive measures

EAU/AUA

Fever + obstruction

equals emergency decompression by stent or nephrostomy — antibiotics alone are insufficient

EAU/AUA

>2-2.5 L/day

urine output halves stone recurrence — the single most effective preventive measure

RCT/EAU

NSAIDs

more effective than opioids for renal colic — first-line analgesia

Cochrane/EAU

Normal calcium

restricting dietary calcium INCREASES calcium oxalate stone risk — a harmful common myth

NEJM/EAU

Ureteric stones — spontaneous passage rate by size

Source: EAU/AUA. Size and position determine whether observation or intervention is appropriate.

Glossary of key terms

Stone composition
Urology/BiochemistryCalcium oxalate (70-80%): the commonest; radio-opaque; associated with hypercalciuria, hyperoxaluria, hypocitraturia and low urine volume. Calcium phosphate (5-10%): associated with higher urine pH, distal renal tubular acidosis, primary hyperparathyroidism and topiramate or acetazolamide use. Uric acid (5-10%): RADIOLUCENT on plain radiography though visible on CT; caused by persistently low urine pH rather than high uric acid alone; associated with obesity, type 2 diabetes, gout and chronic diarrhoea; the only stone type that can be dissolved medically. Struvite/magnesium ammonium phosphate: forms only in urine infected with urease-producing bacteria; grows rapidly into staghorn calculi. Cystine (1-2%): autosomal recessive cystinuria; presents young; recurrent and difficult to manage. Drug stones: indinavir, atazanavir, triamterene, ceftriaxone.

Surgical options for stones
UrologyExtracorporeal shockwave lithotripsy (ESWL): non-invasive, focused shockwaves fragment the stone; best for stones under about 2cm in the kidney or upper ureter; contraindicated in pregnancy, uncorrected coagulopathy, untreated infection and distal obstruction; less effective for hard stones (cystine, calcium oxalate monohydrate, brushite) and in obesity. Ureteroscopy (URS) with laser lithotripsy: highest single-procedure stone-free rate for ureteric stones and increasingly used for renal stones; requires anaesthesia and often a temporary stent. Percutaneous nephrolithotomy (PCNL): the standard for large (over 2cm) and staghorn renal stones, giving the best clearance but with the highest complication rate — bleeding, sepsis, injury to adjacent organs. The choice depends on stone size, position, composition, anatomy and patient factors.

Ureteric stent symptoms
Urology/Patient experienceUreteric stents are frequently placed for obstruction, after ureteroscopy, or to allow passive dilatation, and they are substantially more troublesome than patients are usually warned. Stent-related symptoms affect the majority: urinary frequency and urgency; suprapubic and flank pain, classically worse during voiding when reflux occurs up the stent; haematuria; and reduced work capacity and quality of life. Management: alpha-blockers (tamsulosin) and antimuscarinics both reduce stent discomfort; adequate analgesia; and, critically, minimising indwelling time. Every stent must be recorded on a stent register with a defined removal date — RETAINED FORGOTTEN STENTS encrust, obstruct, fragment and can destroy a kidney, and are a recurring and entirely preventable cause of serious harm and litigation.

Stones in pregnancy
Obstetrics/UrologySymptomatic stones complicate roughly 1 in 1,500 to 3,000 pregnancies, most commonly in the second and third trimesters, and must be distinguished from the physiological hydronephrosis of pregnancy (right-sided, from dextrorotation of the uterus and progesterone-mediated smooth muscle relaxation). Imaging: ultrasound first, including transvaginal for distal stones; MRI without gadolinium second-line; low-dose CT only where essential. Analgesia: paracetamol and opioids; NSAIDs are avoided, particularly after 30 weeks because of premature ductal closure and oligohydramnios. Most stones pass conservatively. Where intervention is required, ureteric stent or nephrostomy are the temporising options — noting that stents encrust rapidly in pregnancy and need frequent changes — with ureteroscopy increasingly performed safely in experienced hands. ESWL is contraindicated.

Heat, occupation and climate
Public healthStone disease is strongly climate-sensitive: the "stone belt" phenomenon — higher prevalence in hotter regions — reflects chronic mild dehydration and concentrated urine. This makes urolithiasis one of the more predictable health consequences of rising global temperatures, with modelling projecting meaningful increases in stone burden and associated cost as heat exposure rises. Occupational risk is concentrated in outdoor and hot indoor workers — agriculture, construction, foundries, kitchens, mining — where stone disease often coexists with heat stress and, in some settings, with chronic kidney disease of unknown aetiology. Workplace interventions are straightforward and effective: enforced hydration breaks, shade and cooling, work-rest cycling, and urine colour charts as a simple self-monitoring tool.

Thiazides and citrate in prevention
Pharmacology/PreventionThiazide diuretics (hydrochlorothiazide, indapamide, chlortalidone) reduce urinary calcium excretion by enhancing distal tubular calcium reabsorption, and reduce recurrence in patients with documented hypercalciuria — though the NOSTONE trial questioned benefit in unselected recurrent formers, reinforcing that they should be targeted using 24-hour urine data rather than given empirically. Potassium citrate raises urinary citrate, a natural inhibitor of calcium crystallisation, and raises urine pH: it is used for hypocitraturia, calcium oxalate recurrence, and — at higher doses to achieve pH 6.5-7.0 — for dissolving and preventing uric acid stones. Allopurinol is reserved for hyperuricosuric calcium oxalate stone formers. All preventive pharmacotherapy should follow, not precede, stone analysis and 24-hour urine assessment.