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Definition of Nephrolithiasis

Nephrolithiasis: The process of forming a kidney stone, a stone in the kidney (or lower down in
the urinary tract).
Kidney stones are a common cause of blood in the urine and pain in the abdomen, flank, or
groin. Kidney stones occur in 1 in 20 people at some time in their life.
The development of the stones is related to decreased urine volume or increased excretion of
stone-forming components such as calcium, oxalate, urate, cystine, xanthine, and phosphate. The
stones form in the urine collecting area (the pelvis) of the kidney and may range in size from tiny
to staghorn stones the size of the renal pelvis itself.
The cystine stones (below) compared in size to a quarter (a U.S. $0.25 coin) were obtained from
the kidney of a young woman by percutaneous nephrolithotripsy (PNL), a procedure for crushing
and removing the dense stubborn stones characteristic of cystinuria.

The pain with kidney stones is usually of sudden onset, very severe and colicky (intermittent),
not improved by changes in position, radiating from the back, down the flank, and into the groin.
Nausea and vomiting are common.

Factors predisposing to kidney stones include recent reduction in fluid intake, increased exercise
with dehydration, medications that cause hyperuricemia (high uric acid) and a history of gout.
Treatment includes relief of pain, hydration and, if there is concurrent urinary infection,
antibiotics.
The majority of stones pass spontaneously within 48 hours. However, some stones may not.
There are several factors which influence the ability to pass a stone. These include the size of the
person, prior stone passage, prostate enlargement, pregnancy, and the size of the stone. A 4 mm
stone has an 80% chance of passage while a 5 mm stone has a 20% chance. If a stone does not
pass, certain procedures (usually by a urology specialist doctor) may be needed.
The process of stone formation, nephrolithiasis, is also called urolithiasis. "Nephrolithiasis" is
derived from the Greek nephros- (kidney) lithos (stone) = kidney stone "Urolithiasis" is from the
French word "urine" which, in turn, stems from the Latin "urina" and the Greek "ouron" meaning
urine = urine stone. The stones themselves are also called renal caluli. The word "calculus"
(plural: calculi) is the Latin word for pebble

Kidney stone
From Wikipedia, the free encyclopedia
(Redirected from Nephrolithiasis)
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"Bladder stone" redirects here. For bladder stones in animals, see Bladder stone
(animal).

Kidney stone
Classification and external resources

An 8-mm kidney stone.

ICD-10

N20.0

ICD-9

592.0

DiseasesDB

11346

MedlinePlus

000458

eMedicine

med/1600

MeSH

D007669

Kidney stones (ureterolithiasis) result from stones or renal calculi (from Latin ren, renes,
"kidney" and calculi, "pebbles")[1] in the ureter. The stones are solid concretions or calculi
(crystal aggregations) formed in the kidneys from dissolved urinary minerals. Nephrolithiasis
(from Greek (nephros, "kidney") and o (lithos, "stone")) refers to the condition of
having kidney stones. Urolithiasis refers to the condition of having calculi in the urinary tract
(which also includes the kidneys), which may form or pass into the urinary bladder.
Ureterolithiasis is the condition of having a calculus in the ureter, the tube connecting the
kidneys and the bladder. The term bladder stones usually applies to urolithiasis of the bladder in
non-human animals such as dogs and cats.
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
obstruction causes dilation or stretching of the upper ureter and renal pelvis (the part of the
kidney where the urine collects before entering the ureter) as well as muscle spasm of the ureter,
trying to move the stone. This leads to 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. There can be blood in the urine, visible with the naked eye or under the microscope
(macroscopic or microscopic hematuria) due to damage to the lining of the urinary tract.
There are several types of kidney stones based on the type of crystals of which they consist. The
majority are calcium oxalate stones, followed by calcium phosphate stones. More rarely, struvite
stones are produced by urea-splitting bacteria in people with urinary tract infections, and people
with certain metabolic abnormalities may produce uric acid stones or cystine stones.
The diagnosis of a kidney stone can be confirmed by radiological studies and/or ultrasound
examination; urine tests and blood tests are also commonly performed. When a stone causes no
symptoms, watchful waiting is a valid option. In other cases, pain control is the first measure,
using for example non-steroidal anti-inflammatory drugs or opioids. Using soundwaves, some
stones can be shattered into smaller fragments (this is called extracorporeal shock wave
lithotripsy). Sometimes a procedure is required, which can be through a tube into the urethra,
bladder and ureter (ureteroscopy), or a keyhole or open surgical approach from the kidney's side.
Sometimes, a tube may be left in the ureter (a ureteric stent) to prevent the recurrence of pain.
Preventive and structive measures are often advised such as drinking sufficient amounts of water
and milk although the effect of many dietary interventions has not been rigorously studied.
Contents

1 Signs and symptoms

2 Causes

2.1 Calcium oxalate stones

2.2 Uric acid (urate)

2.3 Other types

3 Diagnosis
o

3.1 X-rays

3.2 Computed tomography

3.3 Ultrasound

3.4 Other

3.5 Gallery

4 Prevention
o

4.1 Restricting oxalate consumption

4.2 Diuretics

4.3 Allopurinol

4.4 Decreased-protein diet

4.5 Other modifications

4.6 Calgranulin

4.7 Medical management

5 Management
o

5.1 Conservative

5.2 Analgesia

5.3 Alpha adrenergic blockers

5.4 Urologic interventions

5.4.1 Ureteral (double-J) stents

6 Epidemiology

7 History

8 See also

9 References

10 External links

[edit] Signs and symptoms

Symptoms of kidney stones include:[2][3]

Localization of kidney stone pain

Colicky pain: "loin to groin". Often described as "the worst pain [...] ever
experienced." This can also occur in the lower back. [4]

Nausea/vomiting: embryological link with intestine stimulates the vomiting

center.

Hematuria: blood in the urine, due to minor damage to inside wall of kidney,
ureter and/or urethra.

Pyuria: pus in the urine.

Dysuria: burning on urination when passing stones (rare). More typical of

infection.

Oliguria: reduced urinary volume caused by obstruction of the bladder or

urethra by stone, or extremely rarely, simultaneous obstruction of both
ureters by a stone.

Postrenal azotemia: the blockage of urine flow through a ureter.[5]

Hydronephrosis:[6] the distension and dilation of the renal pelvis and calyces.

[edit] Causes

Kidney stones do not have single, well-defined cause, but are the result of a combination of
factors. A stone is created when the urine does not have the correct balance of fluid and a
combination of minerals and acids. When the urine contains more crystal-forming substances
than the fluid can dilute, crystals can form. Normally the urine contains components that prevent

these crystals from attaching to each other. However, when these substances fall below their
normal proportions, stones can form out of an accumulation of crystals.[7]
Kidney stones or calcium oxalate crystals in kidney can be due to underlying metabolic
conditions, such as renal tubular acidosis,[8] Dent's disease,[9] hyperparathyroidism,[10] primary
hyperoxaluria[11] and medullary sponge kidney.[12] Kidney stones are also more common in
patients with Crohn's disease.[13] Patients with recurrent kidney stones should be screened for
these disorders. This is typically done with a 24 hour urine collection that is chemically analyzed
for deficiencies and excesses that promote stone formation.[14]
There has been some evidence that water fluoridation may increase the risk of kidney stone
formation. In one study, patients with symptoms of skeletal fluorosis were 4.6 times as likely to
develop kidney stones.[15]
A 1998 paper in the Archives of Internal Medicine examined the sources of a widely-held belief
in the medical community that vitamin C can cause kidney stones, and found it to be based on
several circular references, ultimately attributing the belief to a wider pattern of skepticism
regarding efficacy of vitamin supplements.[16] A more recent study suggested a causal
relationship may exist, but it was not conclusive.[17]
The American Urological Association has projected that increasing global temperatures will lead
to greater future prevalence of kidney stones, notably by expanding the "kidney stone belt" of the
southern United States.[18] Astronauts seem to show a higher risk of developing kidney stones
during or after long duration space flights.[19]
[edit] Calcium oxalate stones

The most common type of kidney stone is composed of calcium oxalate crystals, occurring in
about 80% of cases,[8] and the factors that promote the precipitation of crystals in the urine are
associated with the development of these stones.
Perhaps counter-intuitively, current evidence suggests that the consumption of low-calcium diets
is associated with a higher overall risk for the development of kidney stones.[2] 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.
[edit] Uric acid (urate)

About 510% of all stones are formed from uric acid.[8] Uric acid stones form in association with
conditions that cause hyperuricosuria with or without high blood serum uric acid levels

(hyperuricemia); and with acid/base metabolism disorders where the urine is excessively acidic
(low pH) resulting in uric acid precipitation. A diagnosis of uric acid nephrolithiasis is supported
if there is a radiolucent stone, a persistent undue urine acidity, and uric acid crystals in fresh
urine samples.[20]
[edit] Other types

Other types of kidney stones are composed of struvite (magnesium, ammonium and phosphate);
calcium phosphate; and cystine.
Struvite stones are also known as infection stones, urease or triple-phosphate stones. About 10
15% of urinary calculi consist of struvite stones.[21] The formation of struvite stones is associated
with the presence of urea-splitting bacteria,[22] 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. Struvite stones are always associated with urinary tract infections.[21]
The formation of calcium phosphate stones is associated with conditions such as
hyperparathyroidism and renal tubular acidosis.
Formation of cystine stones is uniquely associated with people suffering from cystinuria, who
accumulate cystine in their urine. Cystinuria can be caused by Fanconi's syndrome.
Urolithiasis has also been noted to occur in the setting of therapeutic drug use, with crystals of
drug forming within the renal tract in some patients currently being treated with Indinavir,
Sulfadiazine or Triamterene.[citation needed]
[edit] Diagnosis

Clinical diagnosis is usually made on the basis of the location and severity of the pain, which is
typically colicky in nature (comes and goes in spasmodic waves). Pain in the back occurs when
calculi produce an obstruction in the kidney.[3]
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.
[edit] X-rays

The relatively dense calcium renders these stones radio-opaque and they can be detected by a
traditional X-ray of the abdomen that includes the kidneys, ureters and bladderKUB.[23] This
may be followed by an IVP (intravenous pyelogramintravenous urogram (IVU) is the same
test by another name) which requires about 50 ml 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.
About 10% of stones do not have enough calcium to be seen on standard X-rays (radiolucent
stones).
[edit] Computed tomography

Computed tomography without contrast is considered the gold standard diagnostic test for the
detection of kidney stones. All stones are detectable by CT except very rare stones composed of
certain drug residues in the urine.[23] If positive for stones, a single standard X-ray of the
abdomen (KUB) is recommended. This gives 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 by doing another X-ray in the future.
Drawbacks of CT scans include radiation exposure and cost.
[edit] Ultrasound

Ultrasound imaging is useful as it gives details about the presence of hydronephrosis (swelling of
the kidneysuggesting the stone is blocking the outflow of urine).[23] It can also be used to
detect stones during pregnancy when x-rays or CT are discouraged. Radiolucent stones may
show up on ultrasound however they are also typically seen on CT scans.
Some recommend that US be used as the primary diagnostic technique with CT being reserved
for those with negative US result and continued suspicion of a kidney stone. This is due to its
lesser cost and avoidance of radiation.[24]
[edit] Other

Other investigations typically carried out include:[23]

Microscopic study of urine, which may show proteins, red blood cells,
bacteria, 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 to look for
abnormally high blood calcium blood levels (hypercalcaemia).

24 hour urine collection to measure total daily urinary volume, magnesium,

sodium, uric acid, calcium, citrate, oxalate and phosphate.

Catching of passed stones at home (usually by urinating through a tea

strainer or stonescreen) for later examination and evaluation by a doctor. [25][26]

[edit] Gallery

Staghorn calculus

Multiple kidney
stones composed of Star-shaped bladder urolith
uric acid and a small on an X-ray of the pelvis.
amount of calcium
oxalate.

Bilateral kidney
stones on abdominal
X-ray. Not to be
confused with
phleboliths seen in
the pelvis.

Three-dimensional
CT of abdomen without
reconstructed CT scan image
contrast showing right
of a ureteral stent in the left
proximal ureteric stone A kidney stone at the kidney (indicated by yellow
tip of an ultrasonic arrow). There is a kidney
causing mild
instrument.
obstruction and
stone in the pyelum of the
hydronephrosis
lower pole of the kidney
(marked by an arrow).
(highest red arrow) and one
in the ureter beside the stent
(lower red arrow).
[edit] Prevention

Preventive strategies may include dietary modifications and medication with the goal of reducing
excretory load on the kidneys:[2][27]

Drinking enough water to make 2 to 2.5 liters of urine per day.

A diet low in protein, nitrogen and sodium intake. The National Institutes of
Health website disputes the notion that specific foods can cause formation of
kidney stones in everyone, although "in some people, a diet high in protein

may lead to kidney stones because extra protein causes calcium to be

excreted from the body, raising calcium levels in the urine." [28]

People with urinary tract infections, kidney disorders such as cystic kidney diseases, and certain
rare, inherited metabolic disorders are also more likely to develop kidney stones. In some of
these susceptible people, the foods they eat can have an influence on the development of their
kidney stones. For example, if you are at higher risk for kidney stones, your doctor may tell you
to limit or avoid foods containing higher levels of oxalate, which include chocolate, coffee, beer,
dairy products, and some fruits and vegetables.

Restriction of oxalate-rich foods, such as chocolate, nuts, soybeans,[29]

rhubarb and spinach,[30] plus maintenance of an adequate intake of dietary
calcium. Recent research has shown that low-calcium diets may be harmful,
and a diet that includes recommended calcium levels has been shown to
prevent kidney stones in men better than a low-calcium diet appears to. [31]
Calcium helps rid the body of oxalate, and calcium citrate appears to carry
the lowest, if any, risk for kidney stones.

Taking drugs such as thiazides, potassium citrate, magnesium citrate and

allopurinol, depending on the cause of stone formation.

Some fruit juices, such as orange, blackcurrant, and cranberry, may be useful
for lowering the risk factors for specific types of stones. Orange juice may
help prevent calcium oxalate stone formation, black currant may help prevent
uric acid stones, and cranberry may help with UTI-caused stones. [32][33]

Limit intake of caffeinated beverages, such as coffee.[34][35]

Avoidance of cola beverages.[36][37]

Avoiding large doses of vitamin C.[38]

On the Indian subcontinent, there is a popular cultural belief that spinach

should not be cooked along with tomatoes, since spinach is rich in calcium
and oxalates, and reacts with the chemicals in tomatoes, causing deposits in
those prone to kidney stone formation. However, this theory is not
scientifically proven and is controversial.[citation needed]

For those patients interested in optimizing their kidney stone prevention options, a 24 hour urine
test can be a useful diagnostic.[citation needed]
[edit] Restricting oxalate consumption

Calcium plays a vital role in body chemistry so limiting calcium may be unhealthy. Since
calcium in the intestinal tract will bind with available oxalate, thereby preventing its absorption
into the blood stream, some nephrologists and urologists recommend chewing calcium tablets
during meals containing oxalate foods. However, a more reliable approach is to restrict the intake

of food that is high in oxalate (see oxalate for a list). This is only helpful in those patients who
are absorbing excess oxalate which is a minority of patients as most oxalate excreted in the urine
is actually made by the liver.[citation needed]
[edit] Diuretics

Although it has been claimed that the diuretic effects of alcohol can result in dehydration, which
is important for kidney stone 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.[39]
One of the recognized medical therapies for prevention of stones is thiazides, a class of drugs
usually thought of as diuretics. These drugs prevent calcium 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 restriction is
necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Thiazides
work best for renal leak hypercalciuria - a condition in which the high urinary calcium levels are
from a primary kidney defect. They work well initially for absorptive hypercalciuria - a condition
in which high urinary calcium is a result of excess absorption from the GI tract. With this
condition they lose effectiveness over time, typically around 2 years, and patients need a period
off treatment to regain effectiveness. Thiazides will cause hypokalemia and reduced urinary
citrate levels so should be given with supplements for each, usually as a potassium citrate
preparation.
[edit] Allopurinol

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.[40]
However, hyperuricemia is not the critical feature of uric acid stones, which can occur in the
presence of hypouricemia. Uric acid stones are more often caused by a combination of high urine
uric acid and low urine pH.[41] 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 (in the form of Shohl's solution (sodium citrate),
sodium bicarbonate, potassium citrate, potassium bicarbonate or acetazolamide, a carbonic
anhydrase inhibitor).
Allopurinol is reserved for patients in whom alkalinization is difficult. For patients with
increased uric acid levels and calcium stones, allopurinol is one of the few treatments that has
been shown in double-blinded placebo controlled studies to actually reduce kidney stone

recurrences. 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.
[edit] Decreased-protein diet
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A high-protein diet might be partially to blame.[original research?] 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).
[citation needed]
The kidney filters the liberated calcium which may then form insoluble crystals (i.e.,
stones) in urine with available oxalate (partly from metabolic processes, partly from diet) or
phosphate ions, depending on conditions.[citation needed] High protein intake is therefore associated
with decreased bone density as well as stones.[citation needed] The acid load is associated with
decreased urinary citrate excretion;[citation needed] citrate competes with oxalate for calcium and can
thereby prevent stones.[original research?]
In addition to increased fluid intake, one of the simplest fixes is to moderate animal protein
consumption.[original research?] However, despite epidemiologic data showing that greater protein
intake is associated with more stones, randomized controlled trials of protein restriction have not
shown reduced stone prevalence.[citation needed] In this regard, it is not just dietary calcium per se that
may cause stone formation, but rather the leaching of bone calcium.[original research?] Some diseases
(e.g., 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.[citation needed]
[edit] Other modifications

Potassium citrate is also used in kidney stone prevention. This is available as both a tablet and
liquid preparation. The medication increases urinary pH (makes it more alkaline), as well as
increases 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 against the formation of
stones.[42]
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. Oxalaterich 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
hypotheses.
[edit] Calgranulin

Crystallization of calcium oxalate (CaOx) appears to be reduced by molecules in the urine that
retard the formation, growth, aggregation, and renal cell adherence of calcium oxalate. By
purifying urine using salt precipitation, preparative isoelectric focusing, and sizing
chromatography, some researchers have found that the molecule calgranulin is able to inhibit
calcium oxalate crystal growth.[43] Calgranulin is a protein formed in the kidney. Given the large
amounts of calcium oxalate in the urine, and considering its potency, calgranulin could become
an important contribution to the normal urinary inhibition of crystal growth and aggregation. If
so, it will be an important tool in the renal defense against kidney stones.
[edit] Medical management

There has been some debate regarding the usefulness of medical management overall in the
treatment of stone forming patients. Despite this debate, it is clear that repeat stone formers do
benefit from more intense management, including proper hydration and use of certain
medications. Additionally, it is also clear that careful surveillance is required in order to
maximize the clinical course for patients who are unlucky enough to be stone formers.[44][45]
[edit] Management
[edit] Conservative

About 90% of stones 4 mm or less in size usually will pass spontaneously; however, 99% of
stones larger than 6 mm will require some form of intervention.[46] There are various measures
that can be used to encourage the passage of a stone. These can include increased hydration,
medication for treating infection and reducing pain, and diuretics to encourage urine flow and
prevent further stone formation. Caution should be exercised in eating certain foods, such as
starfruit, with high concentrations of oxalate which may precipitate acute renal failure in patients
with chronic renal disease.[47]
In most cases, a smaller stone that is not symptomatic is often given up to four weeks[2] to move
or pass before consideration is given to any surgical intervention as it has 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, bilateral obstructing stones,

intractable pain or in the presence of an infected kidney blocked by a stone which can cause
sepsis.
Straining the urine allows collection of the stone when it passes. Analysis can help establish
preventative options.
[edit] Analgesia

Management of pain often requires intravenous administration of NSAIDS or opioids in an

emergency room setting. Orally-administered medications are often effective for less severe
discomfort (NSAIDs or opioids). Intravenous acetaminophen also appears to be effective.[48]
After treatment, the pain may return if the stone moves but re-obstructs in another location.
[edit] Alpha adrenergic blockers

Alpha adrenergic blockers such as tamsulosin (Flomax) may increase the spontaneous passage of
the stone by 30%. Recent studies have, however, questioned this claim, finding no benefit from
these medications.[49]
[edit] Urologic interventions

Most kidney stones do not require surgery and will pass on their own. Surgery is necessary when
the pain is persistent and severe, in renal failure and when there is a kidney infection. It may also
be advisable if the stone fails to pass or move after 30 days. Finding a significant stone before it
passes into the ureter allows physicians to fragment it surgically before it causes any severe
problems. In most of these cases, non-invasive extracorporeal shock wave lithotripsy (ESWL)
will 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 larger stones.
Percutaneous nephrolithotomy or rarely 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,[50] but it has not been felt warranted
to change clinical practice at the clinic.[51] 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.
More common complications related to ESWL are bleeding, pain related to passage of stone
fragments, failure to fragment the stone, and the possible requirement for additional or
alternative interventions.
[edit] Ureteral (double-J) stents

One modern medical technique uses a ureteral stent (a small tube between the bladder and the
inside of the kidney) to provide immediate relief of a blocked kidney. This is especially useful in
saving a failing kidney due to swelling and infection from the stone. Ureteral stents vary in
length and width but most have the same shape usually called a "double-J" or "double pigtail",
because of the curl at both ends. They are designed to allow urine to drain around any stone or
obstruction. They can be retained for some length of time as infections recede and as stones are
dissolved or fragmented with ESWL or other treatment. The stents will gently dilate or stretch
the ureters which can facilitate instrumentation and they will also provide a clear landmark to
help surgeons see the stones on x-ray. Most stents can be removed easily during a final office
visit. Discomfort levels from stents typically range from minimal associated pain to moderate
discomfort. However, it isn't uncommon for patients to experience severe discomfort too,
especially upon removal of said stent.
The use of ureteral stents is of particular significance in the treatment of ureteral stones. Their
use, non use, and circumstances peculiar to stents should be well understood in order to
maximize the benefits.[52]
[edit] Epidemiology

Within the United States, about 1015% of adults will be diagnosed with a kidney stone,[53] and
the total cost for treating this condition was US$2 billion in 2003.[23] The incidence rate increases
to 2025% in the Middle East, because of increased risk of dehydration in hot climates. (The
typical Arabian diet is also 50% lower in calcium and 250% higher in oxalates compared to
Western diets, increasing the net risk.)[54] Recurrence rates are estimated at about 10% per year,
totalling 50% over a 510 year period and 75% over 20 years.[8] Men are affected approximately
4 times more often than women. Recent evidence has shown an increase in pediatric cases.[55]
[edit] History

The existence of kidney stones has been recorded since the beginning of civilization, and
lithotomy for the removal of stones is one of the earliest known surgical procedures.[56] In 1901, a
stone was discovered in the pelvis of an ancient Egyptian mummy, and was dated to 4,800 BC.
Medical text from ancient Mesopotamia, India, China, Persia, Greece and Rome all mentioned
calculous disease. Part of the Hippocratic oath contains an admonition about the dangers of
operating on the bladder for stones. The Roman medical treatise De Medicina by Cornelius
Celsus contained a description of lithotomy, and this work served as the basis for this procedure
up until the 18th century.[57]
New techniques in lithotomy began to emerge starting in 1520, but the operation remained risky.
It was only after Henry Jacob Bigelow popularized the technique of litholapaxy in 1878 that the
mortality rate dropped from about 24% down to 2.4%. However, other treatment techniques were
developed that continued to produce a high level of mortality, especially among inexperienced

urologists.[57][58] In 1980, Dornier MedTech introduced extracorporeal shock wave lithotripsy for
breaking up stones via acoustical pulses, and this technique has come into widespread use.[59]

Nephrolithiasis
Author: J Stuart Wolf Jr, MD, FACS, The David A Bloom Professor of Urology, Director of
Division of Minimally Invasive Urology, Department of Urology, University of Michigan
Medical School
Contributor Information and Disclosures
Updated: Jul 16, 2010

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Overview

Differential Diagnoses & Workup

Treatment & Medication

Follow-up

Multimedia

References

Keywords

Introduction

Background

Nephrolithiasis is a common disease that is estimated to produce medical costs of $2.1 billion per
year in the United States.1 Nephrolithiasis specifically refers to calculi in the kidneys, but this
article discusses both renal calculi, shown below, and ureteral calculi (ureterolithiasis). Ureteral
calculi almost always originate in the kidneys, although they may continue to grow once they
lodge in the ureter.

Small renal calculus that would likely respond to extracorporeal shockwave

lithotripsy.
[ CLOSE WINDOW ]

Small renal calculus that would likely respond to extracorporeal shockwave

lithotripsy.

Urinary tract stone disease has been a part of the human condition for millennia; in fact, bladder
and kidney stones have even been found in Egyptian mummies. Some of the earliest recorded
medical texts and figures depict the treatment of urinary tract stone disease.
Pathophysiology

Urinary tract stone disease, depicted below, is likely caused by two basic phenomena.

Distal ureteral stone observed through a small, rigid ureteroscope prior to ballistic
lithotripsy and extraction. The small caliber and excellent optics of today's
endoscopes greatly facilitate minimally invasive treatment of urinary stones.
[ CLOSE WINDOW ]

Distal ureteral stone observed through a small, rigid ureteroscope prior to ballistic
lithotripsy and extraction. The small caliber and excellent optics of today's
endoscopes greatly facilitate minimally invasive treatment of urinary stones.

The first phenomenon is supersaturation of the urine by stone-forming constituents, including

calcium, oxalate, and uric acid. Crystals or foreign bodies can act as nidi, upon which ions from
the supersaturated urine form microscopic crystalline structures. The overwhelming majority of
renal calculi contain calcium. Uric acid calculi and crystals of uric acid, with or without other

contaminating ions, comprise the bulk of the remaining minority. Other, less frequent stone types
include cystine, ammonium acid urate, xanthine, dihydroxyadenine, and various rare stones
related to precipitation of medications in the urinary tract. This is likely the underlying cause of
uric and cystine stones, but calcium-based stones (especially calcium oxalate stones) likely have
a more complex etiology.
The second etiology, which is most likely responsible for calcium oxalate stones, is deposition of
stone material on a renal papillary calcium phosphate nidus, typically a Randall plaque. Evan et
al (2007) recently proposed this model based on evidence accumulating from several
laboratories.2 Calcium phosphate precipitates in the basement membrane of the thin loops of
Henle, erodes into the interstitium, and then accumulates in the subepithelial space of the renal
papilla. The subepithelial deposits, which have long been known as Randall plaques, eventually
erode through the papillary urothelium. Stone matrix, calcium phosphate, and calcium oxalate
gradually deposit on the substrate to create a urinary calculus. Randall plaques are always
composed of calcium phosphate.
Frequency
United States

The lifetime prevalence of urinary tract stone disease in the United States is approximately 10%.
The annual incidence of urinary tract stones in the industrialized world is estimated to be 0.2%.
The likelihood that a white male will develop stone disease by age 70 years is 1 in 8. Stones of
the upper urinary tract are more common in the United States than in the rest of the world.
Roughly two million patients present on an outpatient basis with stone disease each year in the
United States, which is a 40% increase from 1994.1
International

The incidence of urinary tract stone disease in developed countries is similar to that in the United
States. Stone disease is rare in only a few areas, such as Greenland and the coastal areas of
Japan. In developing countries, bladder calculi are more common than upper urinary tract
calculi; the opposite is true in developed countries. These differences are believed to be dietrelated.
Mortality/Morbidity

The morbidity of urinary tract calculi is primarily due to obstruction with its
associated pain, although nonobstructing calculi can still produce
considerable discomfort.

Conversely, patients with obstructing calculi may be asymptomatic, which is

the usual scenario in patients who experience loss of renal function due to
chronic untreated obstruction.

Stone-induced hematuria is frightening to the patient but is rarely dangerous

by itself.

The most morbid and potentially dangerous aspect of stone disease is the
combination of urinary tract obstruction and upper urinary tract infection.
Pyelonephritis, pyonephrosis, and urosepsis can ensue. Early recognition and
immediate surgical drainage are necessary in these situations.

Race

Urinary tract calculi are far more common in Asians and whites than in Native Americans,
Africans, African Americans, and some natives of the Mediterranean region. Although some
differences may be attributable to geography (stones are more common in hot and dry areas) and
diet, heredity also appears to be a factor. This is suggested by the finding that, in regions with
both white and nonwhite populations, stone disease is much more common in whites.
Sex

In general, urolithiasis is more common in males (male-to-female ratio of

3:1).

Stones due to discrete metabolic/hormonal defects (eg, cystinuria,

hyperparathyroidism) and stone disease in children are equally prevalent
between the sexes.

Stones due to infection (struvite calculi) are more common in women than in
men.

Age

Most urinary calculi develop in persons aged 20-49 years.

Patients in whom multiple recurrent stones form usually develop their first
stones while in their second or third decade of life.

An initial stone attack after age 50 years is relatively uncommon.

Clinical
History

Patients with urinary calculi may report pain, infection, or hematuria. Small
nonobstructing stones in the kidneys only occasionally cause symptoms. If
present, symptoms are usually moderate and easily controlled.

The passage of stones into the ureter with subsequent acute obstruction,
proximal urinary tract dilation, and spasm is associated with classic renal
colic.

Renal colic is characterized by undulating cramps and severe pain and

is often associated with nausea and vomiting.

As the stone travels through the ureter, the pain moves from the flank
to the lower abdomen, down to the groin, and eventually to the scrotal
or labial areas.

Associated irritative bladder symptoms are common when the stone is

located in the distal or intramural ureter.

Patients with large renal stones known as staghorn calculi, shown below, are
often relatively asymptomatic.
o

Complete staghorn calculus that fills the collecting system of the

kidney (no intravenous contrast material in this patient). Although
many staghorn calculi are struvite (related to infection with ureasesplitting bacteria), the density of this stone suggests that it may be
metabolic in origin and is likely composed of calcium oxalate.
Percutaneous nephrostolithotomy or perhaps even open surgical
nephrolithotomy is required to remove this stone.
[ CLOSE WINDOW ]

Complete staghorn calculus that fills the collecting system of the

kidney (no intravenous contrast material in this patient). Although
many staghorn calculi are struvite (related to infection with ureasesplitting bacteria), the density of this stone suggests that it may be
metabolic in origin and is likely composed of calcium oxalate.
Percutaneous nephrostolithotomy or perhaps even open surgical
nephrolithotomy is required to remove this stone.

Staghorn refers to the presence of a branched kidney stone occupying

the renal pelvis and at least one calyceal system. Such calculi usually
manifest as infection and hematuria rather than as acute pain.

Asymptomatic bilateral obstruction, which is uncommon, manifests as

symptoms of renal failure.

Important historical features are as follows:

Duration, characteristics, and location of pain

History of urinary calculi

Prior complications related to stone manipulation

Urinary tract infections

Loss of renal function

Family history of calculi

Solitary or transplanted kidney

Chemical composition of previously passed stones

Physical

Dramatic costovertebral angle tenderness is common; this pain can move to

the upper or lower abdominal quadrant as a ureteral stone migrates distally.

Peritoneal signs are usually absentan important consideration in

distinguishing renal colic from other sources of flank or abdominal pain.

Findings should correlate with the reports of pain, so that complicating factors
(eg, urinary extravasation, abscess formation) can be detected.

Beyond this, the specific location of tenderness does not always correlate
with the exact location of the stone, although the calculus is often in the
general area of maximum discomfort.

Causes

Most research on the etiology and prevention of urinary tract stone disease
has been directed toward the role of elevated urinary levels of calcium,
oxalate, and uric acid in stone formation, as well as reduced urinary citrate
levels.

Hypercalciuria is the most common metabolic abnormality. Some cases of

hypercalciuria are related to increased intestinal absorption of calcium
(associated with excess dietary calcium and/or overactive calcium absorption
mechanisms), some are related to excess resorption of calcium from bone (ie,
hyperparathyroidism), and some are related to an inability of the renal
tubules to properly reclaim calcium in the glomerular filtrate (renal-leak
hypercalciuria).

Magnesium and especially citrate are important inhibitors of stone formation

in the urinary tract. Decreased levels of these in the urine predispose to stone
formation.

A low fluid intake, with a subsequent low volume of urine production,

produces high concentrations of stone-forming solutes in the urine. This is an
important, if not the most important, environmental factor in kidney stone
formation.

The exact nature of the tubular damage or dysfunction that leads to stone
formation has not been characterized.

The most common findings on 24-hour urine studies include hypercalciuria,

hyperoxaluria, hyperuricosuria, hypocitraturia, and low urinary volume. Other
factors, such as high urinary sodium and low urinary magnesium
concentrations, may also play a role. To identify these risk factors, a 24-hour
urine profile, including appropriate serum tests of renal function, uric acid,
and calcium, is needed. Such testing is available from various commercial
laboratories. A finding of hypercalcemia should prompt follow-up with an
intact parathyroid hormone study to evaluate for primary and secondary
hyperparathyroidism.

1. See Also
1. Nephrolithiasis
2. Nephrolithiasis Risk Factors
2. Epidemiology
1. Represents 75-90% of Nephrolithiasis
3. Evaluation: General
1. Do not perform evaluation during hospitalization
2. Single Stone episodes with no residual stones
1. Serum Calcium
2. Consider 24 hour urine
1. Urine volume

2. Urine Calcium
3. Recurrent, Residual or Family History of stones
1. Urine Volume
2. Conside Creatinine Clearance
3. Urine Calcium (Hypercalciuria >300 mg/day)
4. Urine Sodium
5. Urine Uric Acid (Hyperuricosuria >750 mg/day)
6. Urine Oxalate (Hyperoxaluria >40 mg/day)
7. Urine Citrate (Hypocitraturia <320 mg/day)
4. Evaluation: Stone Type
1. Mixed Calcium Oxalate and Phosphate (See above)
1. Hypercalciuria (50%)
2. Low urine volume (30-50%)
3. Hyperoxaluria (20-30%)
4. Hypocitraturia (20-30%)
5. Hyperuricosuria (20%)
2. Pure Calcium Phosphate Stones (uncommon)
1. Causes
1. Distal Renal Tubular Acidosis
2. Primary Hyperparathyroidism
3. Excessive alkalinization
4. Sarcoidosis
2. Obtain Serum Electrolytes
1. Hyperkalemia

2. Serum Bicarbonate increased

3. Hyperchloremia
5. Evaluation: Specific Populations
1. Hmong patients more commonly have increased Uric Acid
2. African americans rarely form calcium stones
1. Evaluate if Hypercalciuria and Hypercalcemia
2. Underlying causes
1. Sarcoidosis
2. Primary Hyperparathyroidism
6. Management
1. See Nephrolithiasis
2. Increase fluid increase >2.5 Liters per day
3. Hypercalcemia
1. Evaluate for Hyperparathyroidism
4. Normocalcemia and uncomplicated calcium stone disease
1. Normocalciuria
1. Potassium Citrate (Urocit-K) 20 meq PO tid
2. Hypercalciuria (>250 mg/day)
1. Increase Dietary Calcium >1000 mg/day
1. Take calcium only with meals
2. Take calcium as food not calcium supplement
2. Follow low sodium diet (<150 meq/day)
3. Decrease dietary meat intake
4. Avoid Loop Diuretics (e.g. Lasix)

5. Medications: Thiazide Diuretic with potassium

1. Hydrochlorothiazide 25 to 50 mg PO daily and
2. Potassium supplement
1. Normocitraturia:
1. Potassium chloride
2. Hypocitraturia:
1. Potassium citrate 20 meq PO tid
5. Hyperoxaluria
1. Mild Hyperoxalauria (40-60 mg/day)
1. Normal Dietary Calcium
2. Low Oxalate Diet
3. Decrease Ascorbic acid <1-2 grams/day
2. Enteric Hyperoxaluria (60-80 mg/day)
1. Calcium Supplements with meals
2. Low Fat Diet
3. Trial of Cholestyramine 2-4 grams per meal
3. Primary Hyperoxaluria (>80 mg/day)
1. Trial Pyridoxine (Vitamin B6)
2. Monitor Renal Function frequently
3. Referral to Hepatology
7. Prognosis
1. Recurrence risk within 2 years: 35%
Calcium nephrolithiasis (C1855801)
Concepts

Finding (T033)

Calcium
nephrolithiasis

English

OMIM
Derived from
the NIH UMLS
(Unified Medical
Language
System)

Sources

Cystine CalculiAka: Cystine Stone, Cystine Nephrolithiasis,

Cystinuria

Advertisement
1. See Also
1. Nephrolithiasis
2. Pathophysiology
1. Disorder of dibasic amino acid transport
2. Results in decreased renal cystine resorption
3. Cystine dissolves poorly at normal Urine pH
1. Calculi form at cystine concentration >250
mg/day
4. Autosomal recessive inheritance
1. Only homozygote patients form cystine stones
3. Types
1. Pure cystine stones
2. Mixed cystine and calcium oxalate
4. Management

1. General
1. Diuresis: reduce cystine <300 mg/L
2. Urine Alkalinization: pH >7.5
2. Protocol
1. Tiopronin (Thiola) and
2. Increase fluid intake to maximize urine output
3. Other management
1. Penecillamine
2. Chemolysis (Tham-E, Acetylcysteine)
3. Extracorporeal Shock Wave Lithotripsy (ESWL)
Cystinuria (C0010691)
An inherited disorder due to defective reabsorption of
CYSTINE and other BASIC AMINO ACIDS by the PROXIMAL
Definitio RENAL TUBULES. This form of aminoaciduria is
n (MSH) characterized by the abnormally high urinary levels of
cystine; LYSINE; ARGININE; and ORNITHINE. Mutations
involve the amino acid transport protein gene SLC3A1.
inherited abnormality of renal tubular transport of dibasic
Definitio
amino acids leading to massive urinary excretion of
n (CSP)
cystine, lysine, arginine, and ornithine.
Concepts Disease or Syndrome (T047)
ICD9

270.0

MSH

D003555

English

CSNU, CSNU - Cystinuria, Cystinuria, Cystinurias

Spanish cistinuria
Parent
Amino Acid Metabolism, Inborn Errors (C0002514), Renal
Concepts Tubular Transport, Inborn Errors (C0035091), Urinary
Calculi (C0042018), Renal Aminoacidurias (C0002534),
Amino acid transport disorder (C0268641), Specific renal

tubule transport defect (C0403495)

Sources

AOD, COSTAR, CSP, DXP, LCH, MSH, MTHICD9, NDFRT,

OMIM, SCTSPA, SNOMEDCT
Derived from the NIH UMLS (Unified Medical Language System)

Kidney stones
Definition

A kidney stone is a solid mass made up of tiny crystals. One or more stones can be in the kidney
or ureter at the same time.
See also: Cystinuria
Alternative Names

Renal calculi; Nephrolithiasis; Stones - kidney

Causes

Kidney stones can form when urine contains too much of certain substances. These substances
can create small crystals that become stones.
The biggest risk factor for kidney stones is dehydration.
Kidney stones may not produce symptoms until they begin to move down the tubes (ureters)
through which urine empties into the bladder. When this happens, the stones can block the flow
of urine out of the kidneys. This causes swelling of the kidney or kidneys, causing pain. The pain
is usually severe.
Kidney stones are common. A person who has had kidney stones often gets them again in the
future. Kidney stones often occur in premature infants.
Some types of stones tend to run in families. Certain kinds of stones can occur with bowel
disease, ileal bypass for obesity, or renal tubule defects.
There are different types of kidney stones. The exact cause depends on the type of stone.

Calcium stones are most common. They occur more often in men than in
women, and usually appear between ages 20 - 30. They are likely to come
back. Calcium can combine with other substances, such as oxalate (the most
common substance), phosphate, or carbonate to form the stone. Oxalate is
present in certain foods. Diseases of the small intestine increase the risk of
forming calcium oxalate stones.

Cystine stones can form in people who have cystinuria. This disorder runs in
families and affects both men and women.

Struvite stones are mostly found in women who have a urinary tract infection.
These stones can grow very large and can block the kidney, ureter, or
bladder.

Uric acid stones are more common in men than in women. They can occur
with gout or chemotherapy.

Other substances also can form stones.

Symptoms

The main symptom is severe pain that starts suddenly and may go away suddenly:

Pain may be felt in the belly area or side of the back

Pain may move to groin area (groin pain) or testicles (testicle pain)

Other symptoms can include:

Abnormal urine color

Blood in the urine

Chills

Fever

Nausea

Vomiting

Exams and Tests

Pain can be severe enough to need narcotic pain relievers. The belly area (abdomen) or back
might feel tender to the touch.
Tests for kidney stones include:

Analysis of the stone to show what type of stone it is

Uric acid level

Urinalysis to see crystals and red blood cells in urine

Stones or a blockage of the ureter can be seen on:

Abdominal CT scan

Abdominal/kidney MRI

Abdominal x-rays

Intravenous pyelogram (IVP)

Kidney ultrasound

Retrograde pyelogram

Tests may show high levels of calcium, oxylate, or uric acid in the urine or blood.
Treatment

The goal of treatment is to relieve symptoms and prevent further symptoms. (Kidney stones that
are small enough usually pass on their own.) Treatment varies depending on the type of stone
and how severe the symptoms are. People with severe symptoms might need to be hospitalized.
When the stone passes, the urine should be strained and the stone saved and tested to determine
the type.
Drink at least 6 - 8 glasses of water per day to produce a large amount of urine. Some people
might need to get fluids through a vein (intravenous).
Pain relievers can help control the pain of passing the stones (renal colic). For severe pain, you
may need to take narcotic pain killers or nonsteroidal anti-inflammatory drugs (NSAIDS) such as
ibuprofen.
Depending on the type of stone, your doctor may prescribe medicine to decrease stone formation
or help break down and remove the material that is causing the stone. Medications can include:

Allopurinol (for uric acid stones)

Antibiotics (for struvite stones)

Diuretics

Phosphate solutions

Sodium bicarbonate or sodium citrate (which make the urine more alkaline)

Surgery is usually needed if:

The stone is too large to pass on its own

The stone is growing

The stone is blocking urine flow and causing an infection or kidney damage

Today, most treatments are much less invasive than in the past.

Extracorporeal shock-wave lithotripsy is used to remove stones slightly

smaller than a half an inch that are located near the kidney. This method uses
ultrasonic waves or shock waves to break up stones. Then, the stones leave
the body in the urine.

Percutaneous nephrolithotomy is used for large stones in or near the kidney,

or when the kidneys or surrounding areas are incorrectly formed. The stone is
removed with an endoscope that is inserted into the kidney through a small
opening.

Ureteroscopy may be used for stones in the lower urinary tract.

Standard open surgery (nephrolithotomy) may be needed if other methods do

not work or are not possible.

Outlook (Prognosis)

Kidney stones are painful but usually can be removed from the body without causing permanent
damage. They tend to return, especially if the cause is not found and treated.
Possible Complications

Decrease or loss of function in the affected kidney

Kidney damage, scarring

Obstruction of the ureter (acute unilateral obstructive uropathy)

Recurrence of stones

Urinary tract infection

When to Contact a Medical Professional

Call your health care provider if you have symptoms of a kidney stone.
Also call if symptoms return, urination becomes painful, urine output decreases, or other new
symptoms develop.

Prevention

If you have a history of stones, drink plenty of fluids (6 - 8 glasses of water per day) to produce
enough urine. Depending on the type of stone, you might need to take medications or other
measures to prevent the stones from returning.
You may need to change your diet to prevent some types of stones from coming back.
References

Cameron MA, Sakhaee K. Uric acid nephrolithiasis. Urol Clin North Am. 2007;34(3):335-346.
Chandhoke PS. Evaluation of the recurrent stone former. Urol Clin North Am. 2007; 34(3):315322.
Finkielstein VA. Strategies for preventing calcium oxalate stones. CMAJ. 2006;174(10):14071409.
Pietrow PK, Preminger GM. Evaluation and medical management of urinary lithiasis. In: Wein
AJ, ed. Campbell-Walsh Urology. 9th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 43.