Pathophysiology

Urinary calculi may remain within the renal parenchyma or renal pelvis or be passed into the ureter and
bladder. During passage, calculi may irritate the ureter and may become lodged, obstructing urine flow
and causing hydroureter and sometimes hydronephrosis. Common areas of lodgment include the
ureteropelvic junction, the distal ureter (at the level of the iliac vessels), and the ureterovesical junction.
Larger calculi are more likely to become lodged. Typically, a calculus must have a diameter > 5 mm to
become lodged. Calculi 5 mm are likely to pass spontaneously.
Even partial obstruction causes decreased glomerular filtration, which may persist briefly after the
calculus has passed. With hydronephrosis and elevated glomerular pressure, renal blood flow declines,
further worsening renal function. Generally, however, in the absence of infection, permanent renal
dysfunction occurs only after about 28 days of complete obstruction.
Secondary infection can occur with long-standing obstruction, but most patients with Ca-containing calculi
do not have infected urine.

Symptoms and Signs

Even large calculi remaining in the renal parenchyma or renal pelvis are usually asymptomatic unless
they cause obstruction and/or infection. Severe pain, often accompanied by nausea and vomiting, usually
occurs when calculi pass into the ureter, cause obstruction, or both. Sometimes gross hematuria also
occurs.
Pain (renal colic) is of variable intensity but is typically excruciating and intermittent, often occurs
cyclically, and lasts 20 to 60 min. Nausea and vomiting are common. Pain in the flank or kidney area that
radiates across the abdomen suggests upper ureteral or renal pelvic obstruction. Pain that radiates along
the course of the ureter into the genital region suggests lower ureteral obstruction. Suprapubic pain along
with urinary urgency and frequency suggests a distal ureteral, ureterovesical, or bladder calculus.
On examination, patients may be in obvious extreme discomfort, often ashen and diaphoretic. Patients
with renal colic may be unable to lie still and may pace, writhe, or constantly shift position. The abdomen
may be somewhat tender on the affected side as palpation increases pressure in the already-distended
kidney, but peritoneal signs (guarding, rebound, rigidity) are lacking.
For some patients, the first symptom is hematuria or either gravel or a calculus in the urine. Other patients
may have symptoms of a UTI, such as fever, dysuria, or cloudy or foul-smelling urine.

Diagnosis

Clinical differential diagnosis

Urinalysis

Imaging

Determination of calculus composition

The symptoms and signs suggest the diagnosis. With peritonitis (eg, due to appendicitis, ectopic
pregnancy, or pelvic inflammatory disease), pain is usually constant, and patients lie still because
movement worsens pain; patients often also have rebound tenderness or rigidity. Cholecystitis may cause
colicky pain, usually in the epigastrium or right upper quadrant, often with Murphy sign. Bowel obstruction
may cause colicky abdominal pain and vomiting, but the pain is usually bilateral and not located primarily
in the flank or along the ureter. Pancreatitis may cause upper abdominal pain and vomiting, but the pain is
usually constant, may be bilateral, and is usually not along the flank or ureter. With most of these
disorders, urinary symptoms are uncommon and other symptoms may suggest which organ system is
actually involved (eg, vaginal discharge or bleeding in pelvic disorders among females). Dissecting aortic
aneurysm must be considered, particularly in the elderly, because, if a renal artery is affected, it can
cause hematuria, pain that radiates along a ureteral distribution, or both. Other considerations in the
general evaluation of acute abdominal pain are discussed elsewhere (see Evaluation).

Pearls & Pitfalls

Giving fluid (oral or IV) does not

speed the passage of urinary calculi.

Patients suspected of having a calculus causing colic require urinalysis and usually an imaging study. If a
calculus is confirmed, evaluation of the underlying disorder, including calculus composition testing, is
required.
Urinalysis:
Macroscopic or microscopic hematuria is common, but urine may be normal despite multiple calculi.
Pyuria with or without bacteria may be present. Pyuria suggests infection, particularly if combined with
suggestive clinical findings, such as foul-smelling urine or a fever. A calculus and various crystalline
substances may be present in the sediment. If so, further testing is usually necessary because the
composition of the calculus and crystals cannot be determined conclusively by microscopy. The only
exception is when typical hexagonal crystals of cystine are found in a concentrated, acidified specimen,
confirming cystinuria.

Imaging tests:

Noncontrast helical CT is the initial imaging study. This study can detect the location of a calculus as well
as the degree of obstruction. Moreover, helical CT may also reveal another cause of the pain (eg, aortic
aneurysm). For patients who have recurrent calculi, cumulative radiation exposure from multiple CT scans
is a concern. For patients with typical symptoms, ultrasonography or plain abdominal x-rays can usually
confirm presence of a calculus with minimal or no radiation exposure. MRI may not identify calculi.

Although most urinary calculi are demonstrable on plain x-ray, neither their presence nor their absence
obviates the need for more definitive imaging, so this study can be avoided except in some patients with
suspected recurrent calculi. Both renal ultrasonography and excretory urography (previously called
intravenous urography) can identify calculi and hydronephrosis. However, ultrasonography is less
sensitive for small or ureteral calculi in patients without hydronephrosis, and excretory urography is time
consuming and exposes the patient to the risk of IV contrast agents. These studies are generally used
when helical CT is unavailable.

Identifying the cause:

The calculus is obtained by straining the urine (or, if necessary, during operative removal) and sent to the
laboratory for stone analysis. Some calculi are brought in by patients. Urine specimens that show
microscopic crystals are sent for crystallography.

In patients with a single Ca calculus and no additional risk factors for calculi, evaluation to exclude
hyperparathyroidism is sufficient. Evaluation entails urinalysis and determination of plasma Ca
concentration on 2 separate occasions. Predisposing factors, such as recurrent calculi, a diet high in
animal protein, or use of vitamin C or D supplements, should be sought.

Patients with a strong family history of calculi, conditions that might predispose to calculi formation (eg,
sarcoidosis, bone metastases, multiple myeloma), or conditions that would make it difficult to treat calculi
(eg, solitary kidney, urinary tract anomalies) require evaluation for all possible causative disorders and
risk factors. This evaluation should include serum electrolytes, uric acid, and Ca on 2 separate occasions.
Follow-up determination of parathyroid hormone levels is done if necessary. Urine tests should include

routine urinalysis and 2 separate 24-h urine collections to determine urine volume, pH, and excretion of
Ca, uric acid, citrate, oxalate, Na, and creatinine.

Treatment

Analgesia

Facilitate calculus passage (eg, with -receptor blockers such as tamsulosin

)

For persistent or infection-causing calculi, complete removal using primarily endoscopic

techniques

Analgesia:
Renal colic may be relieved with opioids, such as morphine

and, for a rapid onset,fentanyl

. Ketorolac

30 mg IV is rapidly effective and nonsedating. Vomiting usually resolves as pain decreases, but
persistent vomiting can be treated with an antiemetic (eg, ondansetron

10 mg IV).

Facilitating calculus passage:

Although increasing fluids (either oral or IV) has traditionally been recommended, fluid administration has
not been proven to speed the passage of calculi. Patients with calculi < 1 cm in diameter who have no
infection or obstruction, whose pain is controlled with analgesics, and who can tolerate liquids can be
treated at home with analgesics and -receptor blockers (eg, tamsulosin

0.4 mg po once/day) to facilitate calculus passage. Calculi that have not passed within 6 to 8 wk typically
require removal. In patients with infection and obstruction, initial treatment is relief of obstruction with a
ureteral catheter and treatment of the infection followed by removal of calculi as soon as possible.

Calculus removal:
The technique used for removal depends on the location and size of the calculus. Techniques include
shock wave lithotripsy and, to ensure complete removal or for larger calculi, endoscopic techniques.
Endoscopic techniques may involve rigid or flexible endoscopes and may involve direct-vision removal
(basketing), fragmentation with some sort of lithotripsy device (eg, pneumatic, ultrasonic, laser), or both.

For symptomatic calculi < 1 cm in diameter in the renal pelvis or proximal ureter, shock wave lithotripsy is
a reasonable first option for therapy. For larger calculi or if shock wave lithotripsy is unsuccessful,
ureteroscopy (done in a retrograde fashion) with holmium laser lithotripsy is usually used. Sometimes
removal is possible using an endoscope inserted anterograde through the kidney.

For midureteral calculi, ureteroscopy with holmium laser lithotripsy is usually the treatment of choice.
Shock wave lithotripsy is an alternative.

For distal ureteral calculi, endoscopic techniques, such as direct removal and use of intracorporeal
lithotripsy (eg, pneumatic, electrohydraulic, laser), are considered by many to be the procedures of
choice. Shock wave lithotripsy can also be used.

Calculus dissolution:
Uric acid calculi in the upper or lower urinary tract occasionally may be dissolved by prolonged
alkalinization of the urine with K citrate 20 mEq po bid to tid, but chemical dissolution of calcium calculi is
not possible and of cystine calculi is difficult.

Prevention
In a patient who has passed a first Ca calculus, the likelihood of forming a 2nd calculus is about 15% at 1
yr, 40% at 5 yr, and 80% at 10 yr. Drinking large amounts of fluids8 to 10 ten-ounce (300-milliliter)
glasses a dayis recommended for prevention of all stones. Recovery and analysis of the calculus,
measurement of calculus-forming substances in the urine, and the clinical history are needed to plan
other prophylactic measures.
In < 3% of patients, no metabolic abnormality is found. These patients seemingly cannot tolerate normal
amounts of calculus-forming salts in their urine without crystallization. Thiazide diuretics, K citrate, and
increased fluid intake may reduce their calculus production rate.
For hypercalciuria, patients may receive thiazide diuretics (eg, chlorthalidone

25 mg po once/day or indapamide

1.25 mg po once/day) to lower urine Ca excretion and thus prevent urinary supersaturation with Ca
oxalate. Patients are encouraged to increase their fluid intake to 3 L/day. A diet that is low in Na and
high in K is recommended. Even with a high K intake, supplementation with K citrate is recommended to
prevent hypokalemia. Restriction of dietary animal protein is also recommended.
For patients with hypocitruria, K citrate (20 mEq po bid) enhances citrate excretion. A normal Ca intake
(eg, 1000 mg or about 2 to 3 dairy servings per day) is recommended, and Ca restriction is avoided. Oral
orthophosphate has not been thoroughly studied.
Hyperoxaluria prevention varies. Patients with small-bowel disease can be treated with a combination of
high fluid intake, Ca loading (usually in the form of Ca citrate 400 mg po bid with meals),cholestyramine

, and a low-oxalate, low-fat diet. Hyperoxaluria may respond to pyridoxine 5 to 500 mg po once/day,
possibly by increasing transaminase activity, because this activity is responsible for the conversion of
glyoxylate, the immediate oxalate precursor, to glycine.
In hyperuricosuria, intake of animal protein should be reduced. If the diet cannot be changed,allopurinol

300 mg each morning lowers uric acid production. For uric acid calculi, the urine pH must be increased to
between 6 and 6.5 by giving an oral alkalinizing drug that contains K (eg, K citrate 20 mEq bid) along with
increased fluid intake.
Infection with urea-splitting bacteria requires culture-specific antibiotics and complete removal of all
calculi. If eradication of infection is impossible, long-term suppressive therapy (eg, with nitrofurantoin

) may be necessary. In addition, acetohydroxamic acid

can be used to reduce the recurrence of struvite calculi.

To prevent recurrent cystine calculi, urinary cystine levels must be reduced to < 250 mg cystine/L of
urine. Any combination of increasing urine volume along with reducing cystine excretion (eg, with mercaptopropionylglycine or penicillamine

) should reduce the urinary cystine concentration.

Practice Essentials
Nephrolithiasis specifically refers to calculi in the kidneys, but renal calculi and ureteral calculi
(ureterolithiasis) are often discussed in conjunction. The majority of renal calculi contain calcium. The pain
generated by renal colic is primarily caused by dilation, stretching, and spasm because of the acute
ureteral obstruction.

Essential update: Clinical prediction rule created for estimating risk of kidney stones
Moore and colleagues derived and validated an objective clinical prediction rule for uncomplicated
ureteral stones that uses 5 patient factorssex, timing, origin (ie, race), nausea, and erythrocytes
(STONE)to create a score between 0 and 13 (the STONE score). Patients with a high STONE score
are very likely to have a kidney stone and very unlikely to have an important disorder other than a kidney
stone as a cause of their symptoms, and thus may be able to avoid a CT scan or be evaluated with a
reduced-dose scan.[1]
The factors most predictive of ureteral stones were male sex, short duration of pain, non-black race, the
presence of nausea or vomiting, and microscopic hematuria. In the derivation and validation cohorts,
ureteral stones were found in 8.3% and 9.2%, respectively, of low probability (STONE score 0-5) patients,
51.6% and 51.3% of moderate probability (score 6-9) patients, and 89.6% and 88.6% of high probability
(score 10-13) patients.[1]
CT scans revealed acutely important alternative causes of symptoms on CT scan in 2.9% and 3.7% of the
derivation and validation cohorts overall. In the high score group, however, only 0.3% of the derivation
cohort and 1.6% of the validation cohort had acutely important alternative findings. [1]

Signs and symptoms

The classic presentation for a patient with acute renal colic is the sudden onset of severe pain originating
in the flank and radiating inferiorly and anteriorly; at least 50% of patients will also have nausea and
vomiting. Patients with urinary calculi may report pain, infection, or hematuria. Patients with small,
nonobstructing stones or those with staghorn calculi may be asymptomatic or experience moderate and
easily controlled symptoms.
The location and characteristics of pain in nephrolithiasis include the following:

Stones obstructing ureteropelvic junction: Mild to severe deep flank pain without radiation to the
groin; irritative voiding symptoms (eg, frequency, dysuria); suprapubic pain, urinary frequency/urgency,
dysuria, stranguria, bowel symptoms
Stones within ureter: Abrupt, severe, colicky pain in the flank and ipsilateral lower abdomen;
radiation to testicles or vulvar area; intense nausea with or without vomiting
Upper ureteral stones: Radiate to flank or lumbar areas

Midureteral calculi: Radiate anteriorly and caudally

Distal ureteral stones: Radiate into groin or testicle (men) or labia majora (women)
Stones passed into bladder: Mostly asymptomatic; rarely, positional urinary retention
See Clinical Presentation for more detail.

Diagnosis
The diagnosis of nephrolithiasis is often made on the basis of clinical symptoms alone, although
confirmatory tests are usually performed.
Examination in patients with nephrolithiasis includes the following findings:

Dramatic costovertebral angle tenderness; pain can move to upper/lower abdominal quadrant
with migration of ureteral stone
Generally unremarkable abdominal evaluation: Possibly hypoactive bowel sounds; usually
absence of peritoneal signs; possibly painful testicles but normal-appearing
Constant body positional movements (eg, writhing, pacing)
Tachycardia
Hypertension
Microscopic hematuria
Testing
The European Association of Urology recommends the following laboratory tests in all patients with an
acute stone episode[2] :

Urinary sediment/dipstick test: To demonstrate blood cells, with a test for bacteriuria (nitrite) and
urine culture in case of a positive reaction
Serum creatinine level: To measure renal function
Other laboratory tests that may be helpful include the following:

CBC with differential in febrile patients

Serum electrolyte assessment in vomiting patients (eg, sodium, potassium, calcium, PTH,
phosphorus)
Serum and urinary pH level: May provide insight regarding patients renal function and type of
calculus (eg, calcium oxalate, uric acid, cystine), respectively
Microscopic urinalysis
24-Hour urine profile
Imaging studies
The following imaging studies are used in the evaluation of nephrolithiasis:

Noncontrast abdominopelvic CT scan: The imaging modality of choice for assessment of urinary
tract disease, especially acute renal colic
Renal ultrasonography: To determine presence of a renal stone and the presence of
hydronephrosis or ureteral dilation; used alone or in combination with plain abdominal radiography

Plain abdominal radiograph (flat plate or KUB): To assess total stone burden, as well as size,
shape, composition, location of urinary calculi; often used in conjunction with renal ultrasonography or
CT scanning
IVP (urography) (historically, the criterion standard): For clear visualization of entire urinary
system, identification of specific problematic stone among many pelvic calcifications, demonstration of
affected and contralateral kidney function
Plain renal tomography: For monitoring a difficult-to-observe stone after therapy, clarifying stones
not clearly detected or identified with other studies, finding small renal calculi, and determining number
of renal calculi present before instituting a stone-prevention program
Retrograde pyelography: Most precise imaging method for determining the anatomy of the ureter
and renal pelvis; for making definitive diagnosis of any ureteral calculus
Nuclear renal scanning: To objectively measure differential renal function, especially in a dilated
system for which the degree of obstruction is in question; reasonable study in pregnant patients, in
whom radiation exposure must be limited
See Workup for more detail.

Management
Supportive care and pharmacotherapy
Medical treatment of nephrolithiasis involves supportive care and administration of agents, such as the
following:

IV hydration
Nonnarcotic analgesics (eg, APAP)
PO/IV narcotic analgesics (eg, codeine, butorphanol, morphine sulfate, oxycodone/APAP,
hydrocodone/APAP, meperidine, nalbuphine)
NSAIDS (eg, ketorolac, ketorolac intranasal, ibuprofen)
Uricosuric agents (eg, allopurinol)
Antiemetics (eg, metoclopramide)
Antidiuretics (eg, DDAVP)
Antibiotics (eg, ampicillin, gentamicin, ticarcillin/clavulanic acid, ciprofloxacin, levofloxacin,
ofloxacin)
Alkalinizing agents (eg, potassium citrate, sodium bicarbonate): For uric acid and cysteine calculi
Corticosteroids (eg, prednisone, prednisolone)
Calcium channel blockers (eg, nifedipine)
Alpha blockers (eg, tamsulosin, terazosin)
Surgical option
Stones that are 7 mm and larger are unlikely to pass spontaneously and require some type of surgical
procedure, such as the following:

Stent placement
Percutaneous nephrostomy
Extracorporeal shockwave lithotripsy
Ureteroscopy
Percutaneous nephrostolithotomy
Open nephrostomy

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

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 resulting calculi give rise to
symptoms when they become impacted within the ureter as they pass toward the urinary bladder.

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. Supersaturation of
the urine is likely the underlying cause of uric and cystine stones, but calcium-based stones
(especially calcium oxalate stones) may have a more complex etiology.

The second phenomenon, 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 (which are always composed of calcium phosphate). Evan et al recently proposed this
model based on evidence accumulating from several laboratories. [4]

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.

Development of renal colic pain and renal damage

The colicky-type pain known as renal colic usually begins in the upper lateral midback over the
costovertebral angle and occasionally subcostally. It radiates inferiorly and anteriorly toward the
groin. The pain generated by renal colic is primarily caused by the dilation, stretching, and spasm
caused by the acute ureteral obstruction. (When a severe but chronic obstruction develops, as in
some types of cancer, it is usually painless.)

In the ureter, an increase in proximal peristalsis through activation of intrinsic

ureteral pacemakers may contribute to the perception of pain. Muscle spasm, increased proximal
peristalsis, local inflammation, irritation, and edema at the site of obstruction may contribute to the
development of pain through chemoreceptor activation and stretching of submucosal free nerve
endings.

The term "renal colic" is actually a misnomer, because this pain tends to remain constant,
whereas intestinal or biliary colic is usually somewhat intermittent and often comes in waves. The
pattern of the pain depends on the individuals pain threshold and perception and on the speed
and degree of the changes in hydrostatic pressure within the proximal ureter and renal pelvis.
Ureteral peristalsis, stone migration, and tilting or twisting of the stone with subsequent
intermittent obstructions may cause exacerbation or renewal of the renal colic pain.

The severity of the pain depends on the degree and site of the obstruction, not on the size of the
stone. A patient can often point to the site of maximum tenderness, which is likely to be the site of
the ureteral obstruction (see the image below).

Nephrolithiasis: acute renal colic. Distribution of renal and ureteral pain.

A stone moving down the ureter and causing only intermittent obstruction actually may be more
painful than a stone that is motionless. A constant obstruction, even if high grade, allows for
various autoregulatory mechanisms and reflexes, interstitial renal edema, and pyelolymphatic and
pyelovenous backflow to help diminish the renal pelvic hydrostatic pressure, which gradually
helps reduce the pain.

The interstitial renal edema produced stretches the renal capsule, enlarges the kidney (ie,
nephromegaly), and increases renal lymphatic drainage. (Increased capillary permeability
facilitates this edema.) It may also reduce the radiographic density of the affected kidneys
parenchyma when viewed on a noncontrast CT scan.

Distention of the renal pelvis initially stimulates ureteral hyperperistalsis, but this diminishes after
24 hours, as does renal blood flow. Peak hydrostatic renal pelvis pressure is attained within 2-5
hours after a complete obstruction.

Within the first 90 minutes of a complete ureteral obstruction, afferent preglomerular arteriolar
vasodilation occurs, which temporarily increases renal blood flow. Between 90 minutes and 5
hours after the obstruction, renal blood flow starts to decrease while intraureteral pressure
continues to rise. By 5 hours after a complete obstruction, both renal blood flow and intraluminal
ureteral pressure decrease on the affected side.

Renal blood flow decreases to approximately 50% of normal baseline levels after 72 hours, to
30% after 1 week, to 20% after 2 weeks, and to 12% after 8 weeks. By this point, intraureteral
pressures have returned to normal, but the proximal ureteral dilation remains and ureteral
peristalsis is minimal.

Interstitial edema of the affected kidney actually enhances fluid reabsorption, which helps to
increase the renal lymphatic drainage to establish a new, relatively stable, equilibrium. At the
same time, renal blood flow increases in the contralateral kidney as renal function decreases in
the obstructed unit.

In summary, by 24 hours after a complete ureteral obstruction, the renal pelvic hydrostatic
pressure has dropped because of (1) a reduction in ureteral peristalsis; (2) decreased renal
arterial vascular flow, which causes a corresponding drop in urine production on the affected side;
and (3) interstitial renal edema, which leads to a marked increase in renal lymphatic drainage.

Additionally, as the ureter proximal to the stone distends, some urine can sometimes flow around
the obstruction, relieving the proximal hydrostatic pressure and establishing a stable, relatively
painless equilibrium. These factors explain why severe renal colic pain typically lasts less than 24
hours in the absence of any infection or stone movement.

Whether calyceal stones cause pain continues to be controversial. In general, in the absence of
infection, how a renal stone causes pain remains unclear, unless the stone also causes
obstruction. Arguably, proving that a calyceal stone is causing an obstruction can be difficult.
However, a stone trapped in a calyx plausibly could block the outflow tract from that calyx,
causing an obstruction and subsequent pain.

Experimental studies in animals have suggested that renal damage may begin within 24 hours of
a complete obstruction and that permanent kidney deterioration starts within 5-14 days. Whereas
some practitioners wait several months for a stone to pass in an asymptomatic patient, others
argue that permanent damage is occurring as long as intervention is delayed.

Based on personal experience and anecdotal cases, the author recommends waiting no longer
than 4 weeks for a stone to pass spontaneously before considering intervention. Convincing
asymptomatic patients of the need for surgical intervention may be difficult in the absence of a
clear consensus in the urological community about the length of time to wait before surgical stone
removal, fragmentation, or bypass.

If only a partial obstruction is present, the same changes occur, but to a lesser degree and over a
longer period. Proximal ureteric and renal pelvic hydrostatic pressures tend to remain elevated
longer, and ureteral peristalsis does not diminish as quickly. If the increased pressure is sufficient
to establish a reasonable flow beyond the obstructing stone, glomerular filtration and renal blood
flow approximates reference range baseline levels, although pain may be ongoing.

What are the risk factors for forming kidney stones?

For unknown reasons, the number of people in the United States with kidney stones has been
increasing over the past 20 years. Caucasians are more prone to develop kidney stones than
African Americans. Although stones occur more frequently in men, the number of women who
get them has been increasing over the past 10 years, causing the ratio to change. If a person
forms a stone, there is a 50 percent chance they will develop another stone.

Scientists do not always know what makes stones form. While certain foods may promote
stones in susceptible people, researchers do not believe that eating specific items will cause
stones in people who are not vulnerable. Yet factors such as a family or personal history of
kidney stones and other urinary infections or diseases have a definite connection to this
problem. Climate and water intake may also play a role in stone formation.

One of the main reasons stones forms is the loss of body fluids or being (dehydrated). When
one does not consume enough fluids during the day, the urine can become concentrated and
darker. This increases the chance that crystals can form from materials within the urine,

because there is less fluid available to dissolve them. Stone formers should maintain 2 liters of
urine output every day. Also, a family history of stones, especially in a first-degree relatives
(parent or sibling), dramatically increases the probability of having stones.

Diet can also affect the probability of stone formation. A high-protein diet can cause the acid
content in the body to increase. This decreases the amount of urinary citrate, a "good"
chemical that helps prevent stones. As a result, stones are more likely to form. A high-salt diet
is another risk factor, as an increased amount of sodium passing into the urine can also pull
calcium along with it. The net result is an increased calcium level in the urine, which increases
the probability for stones. Intake of oxalate-rich foods such as leafy green vegetables, nuts,
tea or chocolate may also worsen the situation.

Certain bowel conditions can also increase the risk such as chronic diarrhea, Crohns disease,
and gastric bypass surgery. Obesity is also an independent risk factor for stone formation.

Although most stone formers do not have a medical condition that directly leads to their stone
development, conditions do exist that place patients at high risk for stone formation. For
example, stones can form because of obstruction to urinary passage like in prostate
enlargement or stricture disease. Stone formation has also been linked to hyperarathyrodism,
an endocrine disorder that results in more calcium in your urine. Susceptibility can also be
raised if you are among the people with rare hereditary disorders such as cystinuria(formation
of cystine stones in the kidneys, ureter, and bladder or primary hyperoxaluria (excessive
urinary excretion of oxalate). Development of kidney stones is due to the excess of the amino
acid, cystine or the oxalate in your urine.

Another condition that can cause stones to form is absorptive hypercalciuria, a surplus of
calcium in the urine that occurs when the body absorbs too much from food. Another condition
that results in a high level of calcium in the urine is resorptive hypercalciuria where the kidney
leaks calcium into the urine. The high levels result in calcium oxalate or phosphate crystals
forming in the kidneys or urinary tract. Similarly, hyperuricosuria, excess uric acid tied to gout
or the excessive consumption of protein-rich products, may also trigger kidney stones.

Consumption of calcium pills by a person who is at risk to form stones, certain diuretics or
calcium-based antacids may increase the risk of forming stones by increasing the amount of
calcium in the urine. Calcium oxalate stones may also form in people who have chronic
inflammation of the bowel or who have had an intestinal bypass operation or ostomy. This is
because of loss of more water from the body as well as absorption of oxalate from the
intestine.