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[[Image:Kidney Stone1.jpg|thumb|left|8mm Kidney Stone]]'''Kidney stones''', or ''renal [[Calculus (medicine)|calculi]]'', are solid concretions ([[crystal aggregation]]s) of dissolved [[dietary mineral|minerals]] in [[urine]]; calculi typically form inside the [[kidney]]s or [[ureter]]s. The terms ''nephrolithiasis'' and ''urolithiasis'' refer to the presence of calculi in the kidneys and urinary tract, respectively. Renal calculi can vary in size from as small as grains of sand to as large as grapefruit. 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 before passage--on the order of at least 2-3 millimeters--they can cause obstruction of the ureter. The resulting distention with urine can cause severe episodic [[Pain and nociception|pain]], most commonly felt in the [[flank]], lower abdomen and groin (a condition called [[renal colic]]). Renal colic can be associated with nausea and vomiting due to the embyrological association of the kidneys and the intestinal tract. Recurrence rates are estimated at about 10% per year.
[[Image:Kidney Stone1.jpg|thumb|left|8mm Kidney Stone]]'''Kidney stones''', or ''renal [[Calculus (medicine)|calculi]]'', are solid concretions ([[crystal aggregation]]s) of dissolved [[dietary mineral|minerals]] in [[urine]]; calculi typically form inside the [[kidney]]s or [[ureter]]s. The terms ''nephrolithiasis'' and ''urolithiasis'' refer to the presence of calculi in the kidneys and urinary tract, respectively. Renal calculi can vary in size from as small as grains of sand to as large as grapefruit. 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 before passage--on the order of at least 2-3 millimeters--they can cause obstruction of the ureter. The resulting distention with urine can cause severe episodic [[Pain and nociception|pain]], most commonly felt in the [[flank]], lower abdomen and groin (a condition called [[renal colic]]). Renal colic can be associated with nausea and vomiting due to the embyrological association of the kidneys and the intestinal tract. Recurrence rates are estimated at about 10% per year.


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[[Image:Bladder Stone 08783.jpg|thumb|Star shaped bladder urolith]]
[[Image:Bladder Stone 08783.jpg|thumb|Star shaped bladder urolith]]
Kidney stones are most commonly composed of [[calcium oxalate]] crystals, and factors that promote the precipitation of crystals in the urine are associated with the development of renal calculi. Conventional wisdom and common sense has long held that consumption of too much [[calcium]] can promote the development of kidney stones. However, current evidence suggests that the consumption of low-calcium diets is actually associated with a higher overall risk for the development of kidney stones. This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation, about 15 times stronger than calcium.
Kidney stones are most commonly composed of [[calcium oxalate]] crystals, and factors that promote the precipitation of crystals in the urine are associated with the development of renal calculi. Conventional wisdom and common sense has long held that consumption of too much [[calcium]] can promote the development of kidney stones. However, current evidence suggests that the consumption of low-calcium diets is actually associated with a higher overall risk for the development of kidney stones. This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation, about 15 times stronger than calcium.
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Some patients show no symptoms until their urine turns bloody—this may be the first symptom of a kidney stone. The amount of blood may not be sufficient to be seen, and thus the first warning can be microscopic hematuria, when red blood cells are found in the microscopic study of a urine sample, during a routine medical test. However, not every kidney stone patient demonstrates blood in urine, even microscopically. About 15% of proven kidney stone patients may not show even microscopic hematuria so this is not considered a definitive diagnostic sign.
Some patients show no symptoms until their urine turns bloody—this may be the first symptom of a kidney stone. The amount of blood may not be sufficient to be seen, and thus the first warning can be microscopic hematuria, when red blood cells are found in the microscopic study of a urine sample, during a routine medical test. However, not every kidney stone patient demonstrates blood in urine, even microscopically. About 15% of proven kidney stone patients may not show even microscopic hematuria so this is not considered a definitive diagnostic sign.
they smell bad like shit nd fuck u


==Diagnosis & Investigation==
==Diagnosis & Investigation==

Revision as of 13:15, 28 March 2007

Kidney stone disease
SpecialtyUrology, nephrology Edit this on Wikidata
8mm Kidney Stone

Kidney stones, or renal calculi, are solid concretions (crystal aggregations) of dissolved minerals in urine; calculi typically form inside the kidneys or ureters. The terms nephrolithiasis and urolithiasis refer to the presence of calculi in the kidneys and urinary tract, respectively. Renal calculi can vary in size from as small as grains of sand to as large as grapefruit. 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 before passage--on the order of at least 2-3 millimeters--they can cause obstruction of the ureter. The resulting distention with urine can cause severe episodic pain, most commonly felt in the flank, lower abdomen and groin (a condition called renal colic). Renal colic can be associated with nausea and vomiting due to the embyrological association of the kidneys and the intestinal tract. Recurrence rates are estimated at about 10% per year.

Star shaped bladder urolith

Kidney stones are most commonly composed of calcium oxalate crystals, and factors that promote the precipitation of crystals in the urine are associated with the development of renal calculi. Conventional wisdom and common sense has long held that consumption of too much calcium can promote the development of kidney stones. However, current evidence suggests that the consumption of low-calcium diets is actually associated with a higher overall risk for the development of kidney stones. This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation, about 15 times stronger than calcium.

Other components of kidney stones include struvite (magnesium, ammonium and phosphate), uric acid, calcium phosphate, or cystine (found only in high urinary concentrations in people suffering from cystinuria). The formation of struvite stones is associated with the presence of urea-splitting bacteria, most commonly Proteus mirabilis (but also Klebsiella, Serratia, Providencia species). These organisms are capable of splitting urea into ammonia, decreasing the acidity of the urine and resulting in favorable conditions for the formation of struvite stones. The formation of calcium phosphate stones is associated with conditions such as hyperparathyroidism and renal tubular acidosis. The formation of uric acid stones is associated with conditions that cause high blood uric acid levels, such as gout, leukemias/lymphomas treated by chemotherapy (secondary gout from the death of leukemic cells), and acid/base metabolism disorders.

Renal calculi can occur due to other underlying conditions, such as renal tubular acidosis, Dent's disease and medullary sponge kidney, Many centers will screen for such disorders in patients with recurrent nephrolithiasis.

Symptoms

Kidney stones are usually asymptomatic until they obstruct the flow of urine. Symptoms can include acute flank pain (renal colic), nausea and vomiting, restlessness, dull pain, hematuria, and possibly fever if an infection is present. Acute renal colic is described as one of the worst types of pain that a patient can suffer. Note that the pain is generally due to the stone's presence in the ureter, and not—as is commonly believed—the urethra and lower genitals.

Some patients show no symptoms until their urine turns bloody—this may be the first symptom of a kidney stone. The amount of blood may not be sufficient to be seen, and thus the first warning can be microscopic hematuria, when red blood cells are found in the microscopic study of a urine sample, during a routine medical test. However, not every kidney stone patient demonstrates blood in urine, even microscopically. About 15% of proven kidney stone patients may not show even microscopic hematuria so this is not considered a definitive diagnostic sign.

Diagnosis & Investigation

Staghorn calculus

Diagnosis is usually made on the basis of the location and severity of the pain, which is typically colic in nature (comes and goes in spasmodic waves). Radiological imaging is used to confirm the diagnosis and a number of other tests can be undertaken to help establish both the possible cause and consequences of the stone. Ultrasound imaging is also useful as it will give details about the presence of hydronephrosis (swelling of the kidney - suggesting the stone is blocking the outflow of urine). It can also be used to show the kidneys during pregnancy when standard x-rays are discouraged. About 10% of stones do not have enough calcium to be seen on standard x-rays (radiolucent stones) and may show up on ultrasound although they typically are seen on CT scans.

The relatively dense calcium renders these stones radio-opaque and they can be detected by a traditional X-ray of the abdomen that includes Kidneys, Ureters and Bladder—KUB. This may be followed by an IVP (Intravenous Pyelogram; IntraVenous Urogram (IVU) is the same test by another name) which requires about 50ml of a special dye to be injected into the bloodstream that is excreted by the kidneys and by its density helps outline any stone on a repeated X-ray. These can also be detected by a Retrograde pyelogram where similar "dye" is injected directly into the ureteral opening in the bladder by a surgeon, usually a urologist. Computed tomography (CT or CAT scan), a specialized X-ray, is considered the gold-standard diagnostic test for the detection of kidney stones, and in this setting does not require the use of intravenous contrast, which carries some risk in certain people (eg, allergy, kidney damage). All stones are detectable by CT except very rare stones composed of certain drug residues in urine. The non-contrast "renal colic study" CT scan has become the standard test for the immediate diagnosis of flank pain typical of a kidney stone. If positive for stones, a single standard x-ray of the abdomen (KUB) is recommended. This additional x-ray provides the physicians with a clearer idea of the exact size and shape of the stone as well as its surgical orientation. Further, it makes it simple to follow the progress of the stone without the need for the much more expensive CT scan just by doing another single x-ray at some point in the future.

Investigations typically carried out include:

  • Microscopic study of urine, which may show proteins, red blood cells, pus cells, cellular casts and crystals.
  • Culture of a urine sample to exclude urine infection (either as a differential cause of the patient's pain, or secondary to the presence of a stone)
  • Blood tests: Full blood count for the presence of a raised white cell count (Neutrophilia) suggestive of infection, a check of renal function and if raised blood calcium blood levels (hypercalcaemia).
  • 24 hour urine collection to measure total daily urinary volume, magnesium, sodium, uric acid, calcium, citrate, oxalate and phosphate.

Treatment

An 8-mm kidney stone.

90% of stones 4 mm or less in size usually will pass spontaneously, however the majority of stones greater than 6 mm will require some form of intervention. In most cases, a smaller stone that is not symptomatic is often given up to 30 days to move or pass before consideration is given to any surgical intervention as it's been found that waiting longer tends to lead to additional complications. Immediate surgery may be required in certain situations such as in people with only one working kidney, intractable pain or in the presence of an infected kidney blocked by a stone which can rapidly cause severe sepsis and toxic shock.

Management of pain from kidney stones varies from country to country and even from physician to physician, but may require intravenous medication (eg, narcotic or nonsteroidal anti-inflammatories) in acute situations. Similar classes of drugs may be effectve orally in an outpatient setting for less severe discomfort. Intravenous ketorolac (Toradol) has been found to be quite effective in many cases of acute renal colic to control the pain without the need for narcotic medications. Ketorolac is a non-steroidal anti-inflammatory that is related to aspirin and ibuprofen. Most acute kidney stone pain will last less than 24 hours and not require hospitalization. Patients are encouraged to strain their urine so they can collect the stone when it eventually passes and send it for chemical composition analysis.

In many cases non-invasive Extracorporeal Shock Wave Lithotripsy or (ESWL) may be used. Otherwise some form of invasive procedure is required; with approaches including ureteroscopic fragmentation (or simple basket extraction if feasible) using laser, ultrasonic or mechanical (pneumatic, shock-wave) forms of energy to fragment the stones. Percutaneous nephrolithotomy or open surgery may ultimately be necessary for large or complicated stones or stones which fail other less invasive attempts at treatment.

A single retrospective study in the USA, at the Mayo Clinic, has suggested that lithotripsy may increase subsequent incidence of diabetes and hypertension,[1] but it has not been felt warranted to change clinical practice at the clinic.[2] The study reflects early experience with the original lithotripsy machine which had a very large blast path, much larger than what is used on modern machines. Further study is believed necessary to determine how much risk this treatment actually has using modern machines and treatment regimens.

Prevention

Preventive strategies include dietary modifications and sometimes also taking drugs with the goal of reducing excretory load on the kidneys:[3]

  • Drinking enough water to make 2 to 2.5 liters of urine per day.
  • A diet low in protein, nitrogen and sodium intake.
  • Restriction of oxalate-rich foods and maintaining an adequate intake of dietary calcium is recommended. There is equivocal evidence that calcium supplements increase the risk of stone formation, though calcium citrate appears to carry the lowest, if any, risk.
  • Taking drugs such as thiazides, potassium citrate, magnesium citrate and allopurinol depending on the cause of stone formation.
  • Depending on the stone formation disease, vitamin B-6 and orthophosphate supplements may be helpful, although these treatments are generally reserved for those with Hyperoxaluria. Cellulose supplements have also shown potential for reducing kidney stones caused by hypercalciuria (excessive urinary calcium) although today other means are generally used as cellulose therapy is associated with significant side effects.

Certain foods may increase the risk of stones: spinach, rhubarb, chocolate, peanuts, cocoa, tomato juice, grapefruit juice, apple juice, soda (acidic and contains phosphorus), and berries (high levels of oxalate). In the United States, the South has the highest incidence of kidney stones, a region where sweet tea consumption is very common. Other drinks are associated with decreased risk of stones, including wine, lemonade and orange juice, the latter two of which are rich in citrate, a stone inhibitor.

Although it has been claimed that the diuretic effects of alcohol can result in dehydration, which is important for kidney stones sufferers to avoid, there are no conclusive data demonstrating any cause and effect regarding kidney stones. However, some have theorized that frequent and binge drinkers create situations that set up dehydration, (alcohol consumption, hangovers, and poor sleep and stress habits). In this view, it is not the alcohol that creates a kidney stone but it is the alcohol drinker's associated behavior that sets it up. [4]

One of the recognized medical therapies for prevention of stones is thiazides, a class of drugs usually thought of as diuretic. These drugs prevent stones through an effect independent of their diuretic properties: they reduce urinary calcium excretion. Nonetheless, their diuretic property does not preclude their efficacy as stone preventive. Sodium restiction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Though some have said that the effect probably fades after two years or so of therapy (tachyphylaxis), in fact it is only randomized controlled trials lasting 2 years or more that show the effect; there is really no good evidence from studies of calcium metabolism that the thiazide effect does not last indefinitely. Thiazides are the medical therapy of choice for most cases of hypercalciuria (excessive urinary calcium) but may not be suitable for all calcium stone formers; just those with high urinary calcium levels.

Allopurinol (Zyloprim) is another drug with proven benefits in some calcium kidney stone formers. Allopurinol interferes with the liver's production of uric acid. Hyperuricosuria, too much uric acid in the urine, is a risk factor for calcium stones. Allopurinol reduces calcium stone formation in such patients. The drug is also used in patients with gout or hyperuricemia, but hyperuricosuria is not the critical feature of uric acid stones. Uric acid stones are more often caused by low urine pH. Even relatively high uric acid excretion will not be associated with uric acid stone formation if the urine pH is alkaline. Therefore prevention of uric acid stones relies on alkalinization of the urine with citrate. Allopurinol is reserved for patients in whom alkalinization is difficult. For patients with increased uric acid levels and calcium stones, alloprinol is one of the few treatments that has been shown in double-blinded placebo controlled studies to actually reduce kidney stone recurrences.[citation needed] Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/dL is often the goal of the drug's use in patients with gout or hyperuricemia.

Potassium citrate is also used in kidney stone prevention. This is available as both a tablet and liquid preparation. The medication will increase the urinary pH making it more alkaline as well as increasing the urinary citrate level which helps reduce calcium oxalate crystal aggregation. Optimal 24 hour urine levels of citrate are thought to be over 320 mg/liter of urine or over 600 mg per day. There are urinary dipsticks available that allow patients to monitor and measure urinary pH so patients can optimize their urinary citrate level.

Though caffeine does acutely increase urinary calcium excretion, several independent epidemiologic studies have shown that coffee intake overall is protective for stones.

Measurements of food oxalate content have been difficult and issues remain about the proportion of oxalate that is bio-available, versus a proportion that is not absorbed by the intestine. Oxalate-rich foods are usually restricted to some degree, particularly in patients with high urinary oxalate levels, but no randomized controlled trial of oxalate restriction has been performed to test that hypothesis.

A high protein diet might be partially to blame. Protein from meat and other animal products is broken down into acids, including uric acid. The most available alkaline base to balance the acid from protein is calcium phosphate (hydroxyapatite) from the bones (buffering). The kidney filters the liberated calcium which may then form insoluble crystals (ie, stones) in urine with available oxalate (partly from metabolic processes, partly from diet) or phosphate ions depending on conditions. High protein intake is therefore associated with decreased bone density as well as stones. The acid load is associated with decreased urinary citrate excretion; citrate competes with oxalate for calcium and can thereby prevent stones. One of the simplest fixes in addition to increased fluid intake is to moderate animal protein consumption. However, despite epidemiologic data showing that more protein intake is associated with more stones, randomized controlled trials of protein restriction have not shown reduced stone prevalence. In this regard, it is not just dietary calcium per se that may cause stone formation, but rather the leaching of bone calcium. Some diseases (eg, distal renal tubular acidosis) which cause a chronically acidic state also decrease urinary citrate levels; since citrates are normally present as potent inhibitors of stone formation, these patients are prone to frequent stone formation.

For those patients interested in optimizing their kidney stone prevention options, it's essential to have a 24 hour urine test performed. This should be done with the patient on his or her regular diet and activities. The results can then be analyzed for abnormalities and appropriate treatment given.

Though not a "cure", ease can sometimes be found during "mild" pain by walking (if possible), preferably in cold air.

Famous sufferers

  • French Renaissance essayist Montaigne suffered from kidney stones. British statesman Samuel Pepys also suffered from kidney stones and was operated on, pre-anesthesia, to remove a large stone which he carried with him and used to try to persuade fellow sufferers to endure the painful surgery. His contemporary, John Wilkins, Bishop of Chester, could not face the prospect and died as a result.
  • Dutch blacksmith Jan de Doot is remembered for having his portrait painted with the large stone that he removed from himself in 1651.
  • Author Isaac Asimov suffered from kidney stones, and wrote about how his pain was treated with morphine, saying that he feared becoming addicted to morphine if he ever needed it again.
  • Astronauts often get kidney stones because of an increase in the amount of calcium in their blood due to a loss of bone density in zero gravity.
  • Lyndon B. Johnson suffered from kidney stones at various times in his life. See Woods, "LBJ: Architect of American Ambition."
  • While DJ'ing at a student event, British DJ John Peel passed a kidney stone, and then proceeded to auction it off for charity at the same event.
  • On October 19, 2005, while working on the set of Boston Legal, actor William Shatner was taken to the emergency room for lower back pain. He eventually passed a kidney stone, but recovered and soon returned to work. Shatner sold his kidney stone in 2006 for $75,000 to GoldenPalace.com. The money will go to a housing charity. [1]
  • Minnesota Twins catcher Joe Mauer has also suffered from kidney stones. When asked about it he stated, "I don't wish that on anyone."
  • John Hart, signer of the Declaration of Independence, died of kidney stones.
  • Peter Baulman (Australia) had a kidney stone removed from his right kidney in December 2003 at The Gold Coast Hospital, Southport, Queensland, Australia, weighing 356 g (12.5 oz) and measuring at its widest point, 11.86 cm (4.66 in). It holds the Guinness world record for largest and heaviest kidney stone removed from a human being.

Fictitious sufferers

  • In the sixth season episode of Seinfeld, titled "The Gymnast," Kramer suffers from a kidney stone that he describes as "a stony mineral concretion, formed abnormally in the kidney. And this jagged shard of calcium pushes its way through the ureter into the bladder. It's forced out through the urine!" At the end of the episode, he passes the stone while in the washroom at a circus.
  • In third episode of season five of Friends, entitled "The One Hundredth", Joey suffers from kidney stones while at the hospital for Phoebe giving birth to the triplets.
  • In the 15th episode of the second season of Deadwood, Al Swearengen is diagnosed with a bladder stone, which has him crippled on the floor in pain, suffering from septic shock. He eventually passes the stone, thus avoiding being subjected to crude surgery with a 2 in 10 survival rate.
  • A sketch in Family Guy includes Muddy Waters as he plays in the bathroom screaming, trying to pass a kidney stone.
  • In an episode of Duckman, Duckman passes a kidney stone at his doctor's office. Upon examining it, the doctor touches it, and exclaims, "Ouch! I've never been cut by a urine sample before."
  • In an episode of Reba, Brock, Reba's ex-husband gets a kidney stone.
  • In Neal Stephenson's Baroque Cycle, the protagonist, Daniel Waterhouse, has a lithotomy performed by Robert Hooke to remove a bladder stone. His mentor, John Wilkins, dies of a bladder stone after refusing treatment in order to enable him to complete a particular work.

See also

References and notes

  • Coe FL, Evan A, Worcester E (2005). "Kidney stone disease". J Clin Invest. 115 (10): 2598–608. PMID 16200192.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  1. ^ Krambeck AE, Gettman MT, Rohlinger AL, Lohse CM, Patterson DE, Segura JW (2006). "Diabetes mellitus and hypertension associated with shock wave lithotripsy of renal and proximal ureteral stones at 19 years of followup". J Urol. 175 (5): 1742–7. PMID 16600747.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ Ed Edelson (2006). "Kidney Stone Shock Wave Treatment Boosts Diabetes, Hypertension Risk - Study suggests link, but doctors say it's too early to abandon this therapy". HealthFinder. National Health Information Center.
  3. ^ Goldfarb DS, Coe FL (1999, Nov 15). "Prevention of recurrent nephrolithiasis". Am Fam Physician. 60 (8): 2269–76. PMID 10593318. {{cite journal}}: Check date values in: |date= (help)
  4. ^ Rodman, John, S (May, 1997). "No More Kidney Stones". Prevention. {{cite journal}}: Check date values in: |date= (help)CS1 maint: multiple names: authors list (link)