• Incidence: 150.00 cases per 100,000 person-years
  • Peak incidence: 40-50 years
  • Sex ratio: more common in males 3:1
Condition Relative
Renal stones1
Ruptured abdominal aortic aneurysm0.07
<1 1-5 6+ 16+ 30+ 40+ 50+ 60+ 70+ 80+


Risk factors
  • dehydration
  • hypercalciuria, hyperparathyroidism, hypercalcaemia
  • cystinuria
  • high dietary oxalate
  • renal tubular acidosis
  • medullary sponge kidney, polycystic kidney disease
  • beryllium or cadmium exposure

Risk factors for urate stones
  • gout
  • ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid

Drug causes
  • drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline
  • thiazides can prevent calcium stones (increase distal tubular calcium resorption)


Type of stonesFeaturesPercentage of all calculi
Calcium oxalateHypercalciuria is a major risk factor (various causes)
Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes with calcium making it more soluble
Stones are radio-opaque (though less than calcium phosphate stones)
Hyperuricosuria may cause uric acid stones to which calcium oxalate binds
CystineInherited recessive disorder of transmembrane cystine transport leading to decreased absorption of cystine from intestine and renal tubule
Multiple stones may form
Relatively radiodense because they contain sulphur
Uric acidUric acid is a product of purine metabolism
May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown e.g. malignancy
More common in children with inborn errors of metabolism
Calcium phosphateMay occur in renal tubular acidosis, high urinary pH increases supersaturation of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2 and 4 do not)
Radio-opaque stones (composition similar to bone)
StruviteStones formed from magnesium, ammonium and phosphate
Occur as a result of urease producing bacteria (and are thus associated with chronic infections)
Under the alkaline conditions produced, the crystals can precipitate
Slightly radio-opaque

Effect of urinary pH on stone formation
Urine pH will show individual variation (from pH 5-7). Post prandially the pH falls as purine metabolism will produce uric acid. Then the urine becomes more alkaline (alkaline tide). When the stone is not available for analysis the pH of urine may help to determine which stone was present.

Stone typeUrine acidityMean urine pH
Calcium phosphateNormal- alkaline>5.5
Calcium oxalateVariable6
Uric acidAcid5.5

Clinical features



Initial investigations
  • urine dipstick and culture
  • serum creatinine and electrolytes: check renal function
  • FBC / CRP: look for associated infection
  • calcium/urate: look for underlying causes
  • also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis

  • BAUS now recommend that non-contrast CT KUB should be performed on all patients, within 14 hours of admission
  • if a patient has a fever, a solitary kidney or when the diagnosis is uncertain an immediate CT KUB should be performed. In the case of an uncertain diagnosis, this is to exclude other diagnoses such as ruptured abdominal aortic aneurysm
  • CT KUB has a sensitivity of 97% for ureteric stones and a specificity of 95%
  • ultrasound still has a role but given the wider availability of CT now and greater accurary it is no longer recommend first-line. The sensitivity of ultrasound for stones is around 45% and specificity is around 90%

The table below summarises the appearance of different types of renal stone on x-ray

TypeFrequencyRadiograph appearance
Calcium oxalate40%Opaque
Mixed calcium oxalate/phosphate stones25%Opaque
Triple phosphate stones*10%Opaque
Calcium phosphate10%Opaque
Urate stones5-10%Radio-lucent
Cystine stones1%Semi-opaque, 'ground-glass' appearance
Xanthine stones<1%Radio-lucent

*stag-horn calculi involve the renal pelvis and extend into at least 2 calyces. They develop in alkaline urine and are composed of struvite (ammonium magnesium phosphate, triple phosphate). Ureaplasma urealyticum and Proteus infections predispose to their formation


The British Association of Urological Surgeons (BAUS) published guidelines in 2018 on the management of acute ureteric/renal colic.

Initial management of renal colic

  • the BAUS recommend an NSAID as the analgesia of choice for renal colic
  • whilst diclofenac has been traditionally used the increased risk of cardiovascular events with certain NSAIDs (e.g. diclofenac, ibuprofen) should be considered when prescribing
  • the CKS guidelines suggest for patients who require admission: 'Administer a parenteral analgesic (such as intramuscular diclofenac) for rapid relief of severe pain'
  • BAUS no longer endorse the use of alpha-adrenergic blockers to aid ureteric stone passage routinely. They do however acknowledge a recently published meta-analysis advocates the use of α-blockers for patients amenable to conservative management, with greatest benefit amongst those with larger stones

Management of renal stones

Stones < 5 mm will usually pass spontaneously. Lithotripsy and nephrolithotomy may be for severe cases.

Most renal stones measuring less than 5mm in maximum diameter will typically pass within 4 weeks of symptom onset. More intensive and urgent treatment is indicated in the presence of ureteric obstruction, renal developmental abnormality such as horseshoe kidney and previous renal transplant. Ureteric obstruction due to stones together with infection is a surgical emergency and the system must be decompressed. Options include nephrostomy tube placement, insertion of ureteric catheters and ureteric stent placement.

In the non-emergency setting, the preferred options for treatment of stone disease include extra corporeal shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy, open surgery remains an option for selected cases. However, minimally invasive options are the most popular first-line treatment.

Shockwave lithotripsy
  • A shock wave is generated external to the patient, internally cavitation bubbles and mechanical stress lead to stone fragmentation. The passage of shock waves can result in the development of solid organ injury. Fragmentation of larger stones may result in the development of ureteric obstruction. The procedure is uncomfortable for patients and analgesia is required during the procedure and afterwards.

  • A ureteroscope is passed retrograde through the ureter and into the renal pelvis. It is indicated in individuals (e.g. pregnant females) where lithotripsy is contraindicated and in complex stone disease. In most cases a stent is left in situ for 4 weeks after the procedure.

Percutaneous nephrolithotomy
  • In this procedure, access is gained to the renal collecting system. Once access is achieved, intra corporeal lithotripsy or stone fragmentation is performed and stone fragments removed.

Therapeutic selection

Stone burden of less than 2cm in aggregateLithotripsy
Stone burden of less than 2cm in pregnant femalesUreteroscopy
Complex renal calculi and staghorn calculiPercutaneous nephrolithotomy
Ureteric calculi less than 5mmManage expectantly

Prevention of renal stones

Calcium stones may be due to hypercalciuria, which is found in up to 5-10% of the general population.
  • high fluid intake
  • low animal protein, low salt diet (a low calcium diet has not been shown to be superior to a normocalcaemic diet)
  • thiazides diuretics (increase distal tubular calcium resorption)

Oxalate stones
  • cholestyramine reduces urinary oxalate secretion
  • pyridoxine reduces urinary oxalate secretion

Uric acid stones
  • allopurinol
  • urinary alkalinization e.g. oral bicarbonate