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Axial CT scan of abdomen without contrast, showing a 3 mm stone (marked by an arrow) in the left proximal ureter
Classification and external resources
Specialty urology
ICD-10 N21.0-N21.9
ICD-9-CM 594.0, 594.1, 594.2, 594.8, 594.9
DiseasesDB 31859
eMedicine ped/2371
Patient UK Urolithiasis
MeSH D001744

Urolithiasis is the formation of urinary calculi (urinary stones), which are calculi formed or located anywhere in the urinary system.[1] It comprises nephrolithiasis (the formation of kidney stones), ureterolithiasis (the formation of stones in the ureters), and cystolithiasis (the formation of bladder stones).[2]

Urinary stones are typically classified by their location or by their chemical composition (calcium-containing, struvite, uric acid, or other compounds). In humans, calcium oxalate is a major constituent of most urinary stones. About 80% of those with kidney stones are men. Men most commonly experience their first episode between 20–30 years of age, while for women the age at first presentation is somewhat later. The term is from Greek oûron, "urine", + lithos, "stone", + -iasis.

Signs and symptoms[edit]

In the kidney, fixed renal pain (flank pain) is common. In the ureter (according to localisation of stone): If in the upper one-third of the ureter - pain radiates to the perineum, if at the pelvic brim - pain radiates to the inner aspect of the thigh, if present in the middle one-third of ureter - pain radiates to the iliac fossa. If the stone is localised in the bladder neck or urethra - pain may present as tip of penis pain. Frequency of urination, oliguria, dribbling of urine, and hematuria may increase.


The development of urinary stones is most commonly related to:

  • Decreased urine volume
  • Increased excretion of stone-forming components
  • Inadequate urine drainage, which may lead to stasis
  • Decrease in urinary citrate levels leading to deposition of calcium
  • Deficiency of vitamins A or C - these conditions can also lead to the "hyper triad": hyperparathyroidism, hypercalcaemia, and hyperuricosuria.

Nephrolithiasis and ureterolithiasis[edit]

Main article: Kidney stone
Kidneys, ureters, and bladder x-ray with bilateral kidney stones

A kidney stone, also known as a renal calculus is a solid concretion or crystal aggregation formed in the kidneys from dietary minerals in the urine. Kidney stones typically leave the body by passage in the urine stream, and many stones are formed and passed without causing symptoms. If stones grow to sufficient size (usually at least 3 millimeters (0.12 in)) they can cause obstruction of the ureter. Ureteral obstruction causes postrenal azotemia and hydronephrosis (distension and dilation of the renal pelvis and calyces), as well as spasm of the ureter. This leads to pain, most commonly felt in the flank (the area between the ribs and hip), lower abdomen, and groin (a condition called renal colic). Renal colic can be associated with nausea, vomiting, fever, blood in the urine, pus in the urine, and painful urination. Renal colic typically comes in waves lasting 20 to 60 minutes, beginning in the flank or lower back and often radiating to the groin or genitals. The diagnosis of kidney stones is made on the basis of information obtained from the history, physical examination, urinalysis, and radiographic studies. Ultrasound examination and blood tests may also aid in the diagnosis.


Urolithiasis deaths per million persons in 2012

When a stone causes no symptoms, watchful waiting is a valid option. For symptomatic stones, pain control is usually the first measure, using medications such as nonsteroidal anti-inflammatory drugs or opioids. More severe cases may require surgical intervention. For example, some stones can be shattered into smaller fragments using extracorporeal shock wave lithotripsy. Some cases require more invasive forms of surgery. Examples of these are cystoscopic procedures such as laser lithotripsy or percutaneous techniques such as percutaneous nephrolithotomy. Sometimes, a tube (ureteral stent) may be placed in the ureter to bypass the obstruction and alleviate the symptoms, as well as to prevent ureteral stricture after ureteroscopic stone removal.

Other animals[edit]

Among ruminants, uroliths more commonly cause problems in males than in females; the sigmoid flexure of the ruminant male urinary tract is more likely to obstruct passage. Early-castrated males are at greater risk, because of lesser urethral diameter.[3]

Low Ca:P intake ratio is conducive to phosphatic (e.g. struvite) urolith formation.[3] Incidence among wether lambs can be minimized by maintaining a dietary Ca:P intake ratio of 2:1.[3][4]

Alkaline pH favors formation of carbonate and phosphate calculi. For domestic ruminants, dietary cation:anion balance is sometimes adjusted to assure a slightly acidic urine pH, for prevention of calculus formation[3]

Differing generalizations regarding effects of pH on formation of silicate uroliths may be found.[3][5] In this connection, it may be noted that under some circumstances, calcium carbonate accompanies silica in siliceous uroliths.[6]

Pelleted feeds may be conducive to formation of phosphate uroliths, because of increased urinary phosphorus excretion. This is attributable to lower saliva production where pelleted rations containing finely ground constituents are fed. With less blood phosphate partitioned into saliva, more tends to be excreted in urine.[7] (Most saliva phosphate is fecally excreted.[8])

Oxalate uroliths can occur in ruminants, although such problems from oxalate ingestion may be relatively uncommon. Ruminant urolithiasis associated with oxalate ingestion has been reported.[9] However, no renal tubular damage or visible deposition of calcium oxalate crystals in kidneys was found in yearling wether sheep fed diets containing soluble oxalate at 6.5 percent of dietary dry matter for about 100 days.[10]

Conditions limiting water intake can be conducive to urolith formation.[11]

Various surgical interventions, e.g. amputation of the urethral process at its base near the glans penis in male ruminants, perineal urethrostomy, or tube cystostomy may be considered for relief of obstructive urolithiasis.[11]


  1. ^ Pearle MS, Calhoun EA and Curhan GC (2007). "Chapter 8: Urolithiasis". In Litwin, MS; Saigal, CS. Urologic Diseases in America (NIH Publication No. 07–5512) (PDF). Bethesda, Maryland: US Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. pp. 283–319. Retrieved 2011-06-04. 
  2. ^ McNutt, WF (1893). "Chapter VII: Vesical Calculi (Cysto-lithiasis)". Diseases of the kidneys and bladder: a text-book for students of medicine. IV: Diseases of the Bladder. Philadelphia: J.B. Lippincott Company. pp. 185–6. Retrieved 2011-06-04. 
  3. ^ a b c d e Pugh, D. G. 2002. Sheep and goat medicine. Saunders, Philadelphia. 468 pp.
  4. ^ Bushman, D. H., R. J. Emerick and L. B. Embry. 1965. Urolithiasis: relationships involving dietary calcium, phosphorus and magnesium. J. Nutr. 87: 499-504.
  5. ^ Stewart, S. R., R. J. Emerick and R. H. Pritchard. 1991. Effects of dietary ammonium chloride and variations in calcium to phosphorus ratio on silica urolithiasis in sheep. J. Anim. Sci. 69: 2225-2229.
  6. ^ Forman, S. A., F. Whiting and R. Connell. 1959. Silica urolithiasis in beef cattle. 3. Chemical and physical composition of the uroliths. Can. J. Compar. Med. 23(4):157-162.
  7. ^ Scott, D. and W. Buchan. 1988. The effects of feeding pelleted diets made from either coarsely or finely ground hay on phosphorus balance and on the partition of phosphorus excretion between urine and faeces in the sheep. Q. J. Exp. Physiol. 73: 315-322.
  8. ^ Bravo, D., D. Sauvant, C. Bogaert and F. Meschy. 2003. III. Quantitative aspects of phosphorus excretion in ruminants. Reprod. Nutr. Dev. 43: 285-300.
  9. ^ Waltner-Toews, D. and D. H. Meadows. 1980. Case report: Urolithiasis in a herd of beef cattle associated with oxalate ingestion. Can. Vet. J. 21: 61-62
  10. ^ James, L. F. and J. E. Butcher. 1972. Halogeton poisoning of sheep: effect of high level oxalate intake. J. Anim. Sci. 35: 1233-1238
  11. ^ a b Kahn, C. M. (ed.) 2005. Merck veterinary manual. 9th Ed. Merck & Co., Inc., Whitehouse Station.

External links[edit]

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