Clinical Presentation

Symptoms may vary and depend on the location and size of the kidney stones or
calculi within the urinary collecting system. In general, symptoms may include
acute renal or ureteral colic, hematuria (microscopic or gross blood in the urine,
urinary tract infection, or vague abdominal or flank pain. ! thorough history and
physical e"amination, along with selected laboratory and radiologic studies, are
essential to making the correct diagnosis. Small nonobstructing stones or #silent
stones# located in the calyces of the kidney are sometimes found incidentally on
"$rays or may be present with asymptomatic hematuria. Such stones often pass
without causing pain or discomfort.
Kidney Stone Symptoms
Stones in the kidneys can become lodged at the %unction of the kidney and ureter
(ureteropelvic %unction, resulting in acute ureteral obstruction with severe
intermittent colicky flank pain. Pain can be localized at the costovertebral angle.
&ematuria may be present intermittently or persistently and it may be microscopic
or gross.
Ureteral Stone Symptoms
Stones that can pass into the ureter may produce ureteral colic, which is an
acute, sharp, spasm$like pain located in the flank. &ematuria may be present.
Stones moving down the ureter to the pelvic brim and iliac vessels will produce
spasms with intermittent, sharp, colicky pain radiating to the lateral flank and
around the umbilical region.
!s a stone passes through the distal ureter, near the bladder, the pain remains
sharp but with a wa"ing and waning 'uality. (elief is offered when the spasm
subsides or the pain may intensify and radiate to the groin, testicles, or labia.
)ausea, vomiting, diaphoresis, tachycardia, and tachypnea may be present and
patients are typically uncomfortable.
Bladder Stone Symptoms
*nce a stone enters the bladder, dysuria, urgency, and frequency may be the
only symptoms e"perienced. Immediate relief of symptoms occurs once the stone
passes out of the bladder.
Kidney Stone Complications
*ccasionally, stones can in%ure the kidneys by causing infection, resulting in
fever, chills, and loss of appetite or urinary obstruction. If a +,I accompanies the
urinary obstruction, pyelonephritis or urosepsis can occur. If stones are bilateral,
they can cause renal scarring and damage, resulting in acute or chronic renal
failure.
Pathophysiology of )ephrolithiasis
!ny factor that reduces urinary flow or causes obstruction, which results in
urinary stasis or reduces urine volume through dehydration and inade'uate fluid
intake, increases the risk of developing kidney stones. -ow urinary flow is the
most common abnormality, and most important factor to correct with kidney
stones. It is important for health practitioners to concentrate on interventions for
correcting low urinary volume in an effort to prevent recurrent stone disease
(.unver / Preminger, 01123 Pak, Sakhaee, Crowther, / 4rinkley, 2561.
Contributing Factors of Nephrolithiasis
Sex. .ales tend to have a three times higher incidence of kidney stones than
females. 7omen typically e"crete more citrate and less calcium than men, which
may partially e"plain the higher incidence of stone disease in men ()ational
Institutes of &ealth 8)I&9, 2556$011:.
thnic Bac!ground. Stones are rare in )ative !mericans, !fricans, !merican
4lacks, and Israelis (.enon / (esnick, 0110.
Family "istory. Patients with a family history of stone formation may produce
e"cess amounts of a mucoprotein in the kidney or bladder allowing crystallites to
be deposited and trapped forming calculi or stones. ,wenty$five percent of stone$
formers have a family history of urolithiasis. ;amilial etiologies include absorptive
hypercalciuria, cystinuria, renal tubular acidosis, and primary hypero"aluria
(.unver / Preminger, 0112.
#edical "istory. Past medical history may provide vital information about the
underlying etiology of a stone<s formation (see ,able 2 . ! positive medical
history of skeletal fracture(s and peptic ulcer disease suggests a diagnosis of
primary hyperparathyroidism. Intestinal disease, which may include chronic
diarrheal states, ileal disease, or prior intestinal resection, may be a
predisposition to enteric hypero"aluria or hypocitraturia. ,his may result in
calcium o"alate nephrolithiasis because of dehydration and chemical imbalances
(see ;igure 2. Irritable bowel disease or intestinal surgery may prevent the
normal absorption of fat from the intestines and alter the manner in which the
intestines process calcium or o"alate. ,his may also lead to calculi or stone
formation. Patients with gout may form either uric acid stones (see ;igure 0 or
calcium o"alate stones. Patients with a history of urinary tract infections (+,Is
may be prone to infection nephrolithiasis caused by urea$splitting bacteria
(.unver / Preminger, 0112. Cystinuria is a homozygous recessive disease
leading to stone formation. (enal tubular acidosis is a familial disorder that
causes kidney stones in most patients who have this disorder.
(=nlarge Image
Figure $.
Calcium *"alate Stone
(=nlarge Image
Figure %.
+ric !cid Stone
&ietary "abits. ;luid restriction or dehydration may cause kidney stone
formation. >ietary intake that is high in sodium, o"alate, fat, protein, sugar,
unrefined carbohydrates, and ascorbic acid (vitamin C has been linked to stone
formation. -ow intake of citrus fruits can result in hypocitraturia, which may
increase an individual<s risk for developing stones.
n'ironmental Factors. ;luid intake consisting of drinking water high in
minerals may contribute to kidney stone development. !nother contributing factor
may be related to geographical variables such as tropical climates ()I&, 2556$
011:. Stone formation is greater in mountainous, high$desert areas that are
found in the +nited States, 4ritish Isles, Scandinavia, .editerranean, )orthern
India, Pakistan, )orthern !ustralia, Central =urope, .alayan Peninsula, and
China (.enon / (esnick, 0110. !ffluent societies have a higher rate of small
upper tract stones whereas large struvite (infection stones occur more commonly
in developing countries (see ;igure ?. 4ladder stones are more common in
underserved countries and are likely related to dietary habits and malnutrition
(.enon / (esnick, 0110.
(=nlarge Image
Figure (.
Struvite Stone
#edications. .edications such as ephedrine, guaifenesin, thiazide, indinavir,
and allopurinol may be contributory factors in the development of calculi
(see Drug-Induced Nephrolithiasis.
)ccupations. *ccupations in which fluid intake is limited or restricted or those
associated with fluid loss may be at greater risk for stone development as a result
of decreased urinary volume.
*ther Causes of )ephrolithiasis
*o+ Urine ,olume
-ow urine output is defined as @ 2 literAday. ,he typical etiologies of
nephrolithiasis are low fluid intake and reduced urine volume. *ther possible
causes of low urine volume include chronic diarrheal syndromes that result in
large fluid loses from the gastrointestinal tract and fluid loss from perspiration, or
evaporation from lungs or e"posed tissue. Stone formation may be initiated by a
low urine output, providing a concentrated environment for substances such as
calcium, o"alate, uric acid, and cystine to begin crystallization.
No -athological &isturbance
In appro"imately ?:B of the stone$forming population, no identifiable risk factors
for stone formation can be found (-evy, !dams$&uet, / Pak, 255:. ,his group
includes individuals with normal serum calcium and P,&, normal fasting and
calcium load response, normal urine volumes, normal p&, calcium, o"alate, uric
acid, citrate, and magnesium levels in the presence of calcium nephrolithiasis.
&rug./nduced Nephrolithiasis
phedrine Calculi. =phedrine and its metabolites (norephedrine,
pseudoephedrine, and norpseudoephedrine are sympathomimetic agents that
have been used for the treatment of enuresis, myasthenia gravis, narcolepsy, and
rhinorrhea (Powell, &su, ,urk, / &ruska, 2556. In addition to numerous side
effects, ephedrine and its derivatives have been associated with the production of
urinary stones (4lau, 2556. ,he diagnosis of these calculi is similar to that of
other radiolucent calculi. ,wenty$four hour urine metabolic analyses can aid in
identifying ephedrine or its respective metabolites.
0uaifenesin Calculi. Cuaifenesin is a widely used e"pectorant that has been
recently associated with nephrolithiasis. Cuaifenesin calculi are radiolucent and
present in patients who ingest this medication in e"cess. ,wenty$four hour urine
metabolic analysis can aid in the identification of guaifenesin or b$0$
metho"ypheno"y$lactic acid.
/ndina'ir Calculi. Indinavir sulfate (Cri"ivan
D
is currently one of the most
fre'uently used protease inhibitors used against human immunodeficiency virus,
the virus that causes !I>S. ,he incidence of calculi in patients taking indinavir
ranges from ?B to 01B (Schwartz, Schenkman, !rmenakas, / Stoller, 2555.
Indinavir calculi are radiolucent when they are pure, and are radiopa'ue when
they contain calcium.
1anthine Calculi. ,hese stones occur due to a rare hereditary condition with
"anthine o"idase deficiency (see ;igure E. ,he deficiency in this enzyme results
in decreased levels of serum and urinary uric acid. !cidic urine causes crystal
precipitation, resulting in stone formation (4ernier, 011:. ,hese stones are also
seen in patients treated with iatrogenic inhibition of "anthine o"idase with
"anthine o"idase inhibitors for hyperuricosuria such as allopurinol.
(=nlarge Image
Figure 2.
Fanthine Stone
>iagnosis of Gidney Stones
+rolithiasis can mimic other etiologies of visceral pain. It is imperative to consider
causes of surgical abdomens such as appendicitis, cholecystitis, peptic ulcer,
pancreatitis, ectopic pregnancy, and dissecting aneurysm in patients who present
with abdominal pain. Initial assessment includes a thorough history and physical
e"amination, basic serum and urine chemistries, and a radiologic imaging study.
;irst$time stone formers may benefit from a more detailed laboratory evaluation
to identify causal factors for stone formation. .ultiple or recurrent stone$formers
(metabolically active stone formers re'uire a more comprehensive laboratory
evaluation ()I&, 2556$011:.
.etabolic =valuation
,he primary ob%ective of a diagnostic evaluation of nephrolithiasis should be to
efficiently and economically identify the particular physiological defect present in
the patient to enable the selection of specific and rational therapy. ,he evaluation
should be able to identify the metabolic disorders responsible for recurrent stone
disease, including cystinuria, distal renal tubular acidosis, enteric hypero"aluria,
gouty diathesis, and primary hyperparathyroidism.
! detailed history and physical e"amination are imperative for both first$time
stone$formers and recurrent stone$formers. Past medical history emphasis
should include information about previous +,Is, diet and fluid intake, medications
including vitamin intake, bowel disease, gout, renal disease, bone or parathyroid
disease, and bowel surgery.
;irst$time stone$formers may undergo an abbreviated diagnostic evaluation such
as stone analysis, urinalysis, culture and sensitivity, and a comprehensive
metabolic panel, which includes serum calcium, uric acid, and phosphorus.
(ecurrent stone$formers and first$time stone$formers are at risk for recurrence.
4oth will benefit from an e"tensive diagnostic evaluation such as stone analysis,
urinalysis, culture and sensitivity, comprehensive metabolic panel, which includes
serum calcium, uric acid, and phosphorus, parathyroid hormone level, and 0E$
hour urine collections (random and after being on a special diet. Patients at risk
include children, middle$aged white males with a family history of stones, and
patients with intestinal disease (chronic diarrheal or malabsorptive states, gout,
nephrocalcinosis, osteoporosis, pathologic skeletal fractures, or urinary tract
infection. Stones composed of cystine, struvite, or uric acid should undergo a
complete metabolic workup (Preminger, Peterson, Peters, / Pak, 256:.
Urine 3ssessment
+rinalysis with urine culture and sensitivity are mandatory tests. (eports may
reveal microscopic or gross hematuria and pyuria with or without infection.
Increase or decrease in urine p& and the presence of crystals may give clues to
whether the stone is alkaline or acidic. ! cyanide nitroprusside test will screen for
suspected cystinuria.
,wo 0E$hour urine collections should be performed evaluating calcium, sodium,
phosphorus, magnesium, o"alate, uric acid, citrate, sulfate, creatinine, p&, and
total volume. ,he first 0E$hour urine should be a random specimen. ,he second
0E$hour urine should be obtained after the patient has been on a sodium, o"alate,
and calcium$restricted diet.
Serum 3ssessment
Complete blood count (C4C may reveal an elevated white blood count (74C
suggesting urinary systemic infection, or depressed red blood cell count
suggesting a chronic disease state or severe ongoing hematuria. Serum
electrolytes, 4+), creatinine, calcium, uric acid, and phosphorus assess current
renal function, dehydration, and the metabolic risk of future stone formation. !n
elevation in P,& level will confirm a diagnosis of hyperparathyroidism.
4adiologic 3ssessment
/ntra'enous -yelography 5/,-6. Intravenous pyelography (urography has long
been considered the primary diagnostic study of choice for identifying urinary
tract calculi. ,he IHP provides anatomical and functional information, identifies
the precise size and location of a stone, the presence and severity of the
obstruction, and renal or ureteral abnormalities. ;or these reasons, the IHP has
been among the most important diagnostic tests that may enable successful
management decisions.
Computed 7omography 5C76 Scan
C, scan (with and without contrast is believed to be the best radiographic
e"amination for acute renal colic as it creates images of the urinary tract and
shows delayed penetration of intravenous contrast through the obstructed kidney.
,he delayed penetration of the contrast through an obstructed kidney is the
hallmark of acute urinary obstruction. ,he C, findings indicative of acute urinary
obstruction secondary to a stone would include renal enlargement,
hydronephrosis, ureteral dilatation, perinephric stranding, and periureteral edema
(Gatz, -ane, / Sommer, 255I3 Smith, Herga, >alrymple, .cCarthy, (osenfield,
255I. *ther conditions that can mimic ureteral colic can be identified as well as
anatomic abnormalities and obstruction. ;or many reasons, the C, scan is
considered superior to an IHP in detecting both renal and ureteral calculi, and is
routinely performed on most patients in which a diagnosis of urolithiasis is
suspected (Smith, Herga, >alrymple, .cCarthy, / (osenfield, 255I.
4adionuclide /maging
(enal scan is considered the gold standard for assessing renal function,
especially in the setting of recurrent or long$standing nephrolithiasis. It is
noninvasive, does not re'uire any special preparation or bowel preparation,
e"poses the patient to minimal radiation, and is nearly free of allergic
complications.
-lain 1.4ays
Plain abdominal F$rays entailing a flat plate radiograph of kidney, ureter, and
bladder (G+4 will identify renal stones that are radiopa'ue (>epartment of the
)avy 4ureau of .edicine and Surgery, 011E. !bdominal F$rays are helpful in
documenting the number, size, and location of stones in the urinary tract and the
radiopacity may provide information on the type of stones present. Plain
abdominal films can be useful in identifying nephrocalcinosis, suggestive of
hyperparathyroidism, primary hypero"aluria, renal tubular acidosis, or
sarcoidosis.
4enal Ultrasound
+ltrasonography can be used as a screening tool for hydronephrosis or stones
within the kidney or renal pelvis. ! renal ultrasound can also determine the
amount of renal parenchyma present in an obstructed kidney, in addition to the
presence of stones. ,he ultrasound can be used in combination with plain
abdominal radiograph to determine hydronephrosis or ureteral dilation (7olf,
011E. ,his may be helpful in assessment during pregnancy (see ,able E .
.edical .anagement
=ffective kidney stone prevention is dependent on the stone type and
identification of risk factors for stone formation (see,able : / ,able I . !n
individualized treatment plan incorporating dietary changes, supplements, and
medications can be developed to help prevent the formation of new stones.
Certain conservative recommendations should be made for all patients
regardless of the underlying etiology of their stone disease. Patients should be
instructed to increase their fluid intake in order to maintain a urine output of at
least 0,111 mlAday. Patients should also limit their dietary o"alate and sodium
intake, thereby decreasing the urinary e"cretion of o"alate and calcium. !
restriction of animal proteins is encouraged for patients with #purine gluttony# and
hyperuricosuria.
"ypercalciuria 50eneral6
4esides treating underlying disease, management of hypercalciuria includesJ
-ow calcium diet (about E11 mg calcium.
>istilled water, if high calcium content in water supply
-imit vitamin C (@ 1.:gAday.
&igh sodium intake
,hiazide diuretics
Cellulose phosphate
*rthophosphate
3bsorpti'e "ypercalciuria 87ype /
,hiazides are commonly used for the management of absorptive hypercalciuria
,ype I as these medications stimulate calcium reabsorption in the distal nephron,
preventing formation of kidney stones by reducing the amount of calcium in the
urine. ,hiazides force a mandatory increase in urinary volume but can cause
electrolyte disorders. Side effects include decreased level of potassium, fre'uent
urination, se"ual dysfunction, and increased triglycerides.
-ess$common medications used for treatment include orthophosphate, sodium
cellulose phosphate, and urease inhibitors. *rthophosphate and sodium cellulose
phosphate reduce the absorption of calcium from the intestines thereby reducing
calcium in the urine. ,he urease inhibitors dissolve crystals and struvite kidney
stones and prevent formation of new crystals. Side effects can include a bad
taste in the mouth, diarrhea, and dyspepsia.
)either sodium cellulose phosphate nor thiazide corrects the basic, underlying
physiological defect in absorptive hypercalciuria. Sodium cellulose phosphate
should be used in patients with severe absorptive hypercalciuria ,ype I (urinary
calcium K ?:1 mgAday or in those resistant to or intolerant of thiazide therapy. In
patients with absorptive hypercalciuria ,ype I, who may be at risk for bone
disease (for e"ample, growing children and post$menopausal women, or who
presently have bone loss, thiazide may be the medication of first choice. Sodium
cellulose phosphate may be substituted for short$term therapy when thiazide
action is decreased.
Potassium supplementation (+rocit$G
D
, Polycitra$G
D
crystalor syrup should be
added when using thiazide therapy to prevent hypokalemia and decrease urinary
citrate e"cretion. ! typical treatment program might include chlorthalidone 0:
mgAday. Potassium citrate 2: to 01 m=' twiceAday should be provided with both
of these diuretics. Side effects include abdominal discomfort, nausea, and
vomiting.
3bsorpti'e "ypercalciuria 8 7ype //
In absorptive hypercalciuria ,ype II, specific drug therapy may not be necessary
since the physiologic defect is not as severe as in absorptive hypercalciuria ,ype
I. .any patients show disdain for drinking fluids and e"creting concentrated urine.
! low intake of calcium (E11$I11 mgAday and a high intake of fluids (sufficient to
achieve a minimum urine output of K 0 litersAday would be acceptable treatment.
)ormal urine calcium e"cretion would be restored by dietary calcium restriction
alone, and the increase in urine volume would help reduce urinary saturation of
calcium o"alate.
4enal "ypercalciuria
,hiazides are indicated for the treatment of renal hypercalciuria. ,his diuretic can
correct the renal leak of calcium by augmenting calcium reabsorption in the distal
tubule and by causing e"tracellular volume depletion and stimulating pro"imal
tubular reabsorption of calcium.
"yperoxaluria
*ral administration of large amounts of calcium (1.0: g to 2.1 g four timesAday or
magnesium has been recommended for controlling enteric hypero"aluria. ! high
fluid intake is recommended to assure ade'uate urine volume in patients with
enteric hypero"aluria. Calcium citrate may theoretically have a role in the
management of enteric hypero"aluria. ,his treatment may lower urinary o"alate
by binding o"alate in the intestinal tract. Calcium citrate may also raise the
urinary citrate level and p&. Side effects are constipation, gas, and increased
calcium leak. Cholestyramine is also another method used to treat calcium
o"alate stones. Cholestyramine binds to bile in the intestines which limits the
amount of o"alate absorbed from the intestines, therefore less o"alate is e"creted
in the urine. Side effects include constipation, abdominal pain, gas, and
heartburn.
"yperuricosuria
!llopurinol (?11 mgAday is the drug of choice in patients with hyperuricosuric
calcium o"alate nephrolithiasis (with or without hyperuricemia because of its
ability to reduce uric acid synthesis and lower urinary uric acid by inhibition of the
enzyme "anthine o"idase. ,he usual dose is ?11 mgAday3 however, the dosage
should be reduced in patients with renal insufficiency. Side effects are rash,
diarrhea, and increased liver enzymes.
Potassium citrate represents an alternative to allopurinol in the treatment of this
condition. +se of potassium citrate in hyperuricosuric calcium o"alate
nephrolithiasis is warranted since citrate has an inhibitory activity with respect to
calcium o"alate (and calcium phosphate crystallization, aggregation, and
agglomeration. Potassium citrate (?1 to I1 m='Aday in divided doses may
reduce the urinary saturation of calcium o"alate.
"ypocitraturia
;or patients with hypocitraturic calcium o"alate nephrolithiasis, treatment with
potassium citrate can restore normal urinary citrate, thus lowering urinary
saturation of calcium and inhibiting crystallization of calcium salts.
&istal 4enal 7ubular 3cidosis
Potassium citrate therapy is able to correct metabolic acidosis and hypokalemia
found in patients with distal (,!. It will also restore normal urinary citrate levels,
although large doses (up to 201 m='Aday may be re'uired for severe acidosis.
Since urinary p& is generally elevated in patients with (,!, the overall rise in
urinary p& is small. Citrate is a significant urinary calcium stone inhibitor that
retards crystallization of calcium o"alate and calcium phosphate. Potassium
citrate binds to calcium in the urine, preventing formation of crystals and raising
the urinary citrate level and p&. It will effectively alkalinize the urine, which makes
it useful in the treatment, dissolution, and prevention of uric acid stones. +rinary
p& should be monitored periodically during citrate therapy because of e"cessive
alkalinization. Side effects are mucous loose stools and minor CI complaints.
Sodium citrate and citric acids are other alkalizing agents used to prevent kidney
stones by inhibiting stone formation through alkalization.
Chronic &iarrheal States
Patients with chronic diarrhea fre'uently have hypocitraturia due to bicarbonate
loss from the intestinal tract. Potassium citrate therapy can significantly reduce
the stone formation rate in these patients. ,he dose of potassium citrate is
dependent on the severity of hypocitraturia in these patients. ,he dosage ranges
from I1 to 201 m='Aday in three to four divided doses.
0outy &iathesis
,he ma%or ob%ective in the management of gouty diathesis is to increase the
urinary p& above :.:, preferably to a level between p& I.1 and I.:. Potassium
citrate is the drug of choice in managing patients with gouty diathesis. Potassium
citrate is an ade'uate alkalinizing agent, capable of maintaining urinary p& at
appro"imately I.: at a dose of ?1 to I1 m=' per day in two divided doses.
Cystinuria
,he ob%ective for treatment of cystinuria is to reduce the urinary concentration of
cystine to a level below its solubility limit (011$0:1 mgAliter. ,he initial treatment
program includes a high fluid intake and oral administration of soluble alkali
(potassium citrate at a dose sufficient to maintain the urinary p& at I.: to L.1.
7hen this conservative program is ineffective, d$penicillamine or alpha$
mercaptopropionylglycine (2,111 to 0,111 mgAday in divided doses has been
used. Potassium citrate is absorbed to prevent uric acid stones as it binds to
calcium in urine, preventing formation of crystals. Sodium bicarbonate makes the
urine less acidic, which makes uric acid or cystine kidney stone formation less
likely. Possible side effects include increased formation of calcium$type stones,
fluid retention, and sodium in blood. +rinary p& should be monitored periodically
during citrate therapy because e"cessive alkalinization may occur, which can
increase the risk of calcium phosphate precipitation and stones. Side effects are
mucous loose stools and minor CI complaints. Sodium citrate and citric acid are
other alkalizing agents used to prevent kidney stones by inhibiting stone
formation through alkalization.
Stru'ite 5/nfection6 *ithiasis
!cetohydro"amic acid (!&! is a urease inhibitor that retards stone formation by
reducing the urinary saturation of struvite. 7hen administered at a dose of 0:1
mg three timesAday, it may prevent recurrence of new stones and inhibit the
growth of stones in patients with chronic urea$splitting infections. In addition, in a
limited number of patients, use of !&! has resulted in dissolution of e"isting
struvite calculi. Side effects that have developed are deep venous thrombosis,
headache, hemolytic anemia, and depression.
&rug./nduced Nephrolithiasis
phedrine Calculi. ,here are no limited studies that address the management of
these calculi. !s with other calculi, a urine output of at least two litersAday is
recommended.
0uaifenesin Calculi. !s with ephedrine calculi, there are no limited studies
regarding pharmacologic management of these calculi.
/ndina'ir Calculi. Initial measures in the management of these calculi should
focus on hydration and analgesia as well as drug discontinuation and substitution
with another protease inhibitor.
1anthine Calculi. ,he medical management of "anthine calculi is limited
because the solubility of these calculi is essentially invariable within physiologic
p& ranges. Currently the recommendation includes a fluid intake of at least three
litersAday. If significant 'uantities of other purines are present in the urine, then
urinary alkalization with potassium citrate in the range of I.1 to I.: is indicated to
prevent hypo"anthine or uric acid calculi.
Conclusion
With appropriate diagnosis and treatment of specific disorders resulting in nephrolithiasis,
a remission rate greater than 80% can be obtained (see Table 8 ). In patients with mild to
moderate severit of stone disease, virtuall total control of stone disease can be achieved
with a remission rate greater than !"% (#reminger, $arve, % #a&, '!8"). The need for
surgical stone removal ma be reduced dramaticall or eliminated with an effective
prophlactic program. (elective pharmacologic therap also has the advantage of
overcoming nonrenal complications and averting certain side effects that ma occur with
nonselective medical therap. It is clear that selective medical therap alone cannot
provide total control of stone disease. ) satisfactor response re*uires continued
dedicated compliance b patients to the recommended program and a commitment of the
phsician to provide long+term followup and care with the intention of improving *ualit
of life b eliminating the smptoms caused b urinar tract stones.
11 of 11
-re'ious -age
DD
'.
#hlebolith. ! phlebolith is a small local, usually rounded, calcification within
a vein. ,hese are very common in the veins of the lower part of thepelvis, and
they are generally of no clinical importance. 7hen located in the pelvis they
are sometimes difficult to differentiate from kidney stones in the ureters on F$
ray.
829
Phleboliths in the pelvic region are present in about EE.0B of people and are more
common in females (:1.2B than males (?L.?B. ,he amount of phleboliths
increases with age and they also appear more often on the left than on the right side
of the pelvic region.
809
Phleboliths outside the pelvic region appear in about 0B of the
population.
8?9
Phleboliths can be diagnostic for hemangiomas on ultrasound.
-hleboliths
>r >avid 4lackmore and >r ;rank Caillard et al.
-hleboliths are literally vein stones, and represent calcification within venous structures.
,hey are particularly common in the pelvis where they may mimic ureteric calculi, and are
also encountered fre'uently in venous malformations.
In the former situation, two signs are helpful in distinguishing a ureteric calculus from a
phlebolith J
2. comet$tail sign J favours a phlebolith
0. soft$tissue rim sign J favours a ureteric calculus
Phleboliths appear as focal calcifications, often with radiolucent centers (another helpful sign
if present to distinguish them from ureteric calculi. ,his appearance is attributed to
calcification peripherally within the vessel, and is fre'uently seen on abdominal radiographs
(IIB of phleboliths
0
. It can also be seen on C, provided thin sections are obtained (at
:mm thick slices radiolucent centers will be inapparent in 55B of phleboliths
0