Download Diagnosis and acute management of suspected nephrolithiasis in

Diagnosis and acute management
of suspected nephrolithiasis in
adults
•
Renal and ureteral stones are a common problem in primary
care practice .
• Patients may present with the classic symptoms of renal colic
and hematuria.
•
Others may be asymptomatic or have atypical symptoms such
as vague abdominal pain, acute abdominal or flank pain,
nausea, urinary urgency or frequency, difficulty urinating,
penile pain, or testicular pain.
ETIOLOGY
• Eighty percent of patients with nephrolithiasis form calcium
stones, most of which are composed primarily of calcium
oxalate or, less often, calcium phosphate
• The other main types include uric acid, struvite (magnesium
ammonium phosphate), and cystine stones.
• The same patient may have more than one type of stone
concurrently (eg, calcium oxalate and uric acid)
INDIVIDUAL CRYSTALLINE COMPONENTS
• Calcium oxalate — Calcium oxalate is the most common
component found in kidney stones (approximately 70 to 80
percent). Calcium oxalate can be found in monohydrate and
dihydrate forms.
• Calcium oxalate can also be present in combination with uric
acid or calcium phosphate.
• Urinary risk factors for calcium oxalate crystal formation are
lower urine volume, higher urine calcium excretion, higher
urine oxalate excretion, and lower urine citrate excretion.
•
Calcium oxalate crystals are pH insensitive in the physiologic
pH range of 5 to 8.
• Calcium phosphate — Calcium phosphate is found in
approximately 15 percent of kidney stones and can be present
in combination with calcium oxalate or struvite.
• because of differences in solubility due to urine pH, calcium
phosphate is not found mixed with uric acid.
• The two forms of calcium phosphate include apatite,, or
brushite; the frequency of apatite is much greater than
brushite.
• Urinary risk factors for calcium phosphate crystal formation
are lower urine volume, higher urine calcium excretion, lower
urine citrate excretion, higher urinary pH, and likely higher
urine phosphate excretion.
•
In contrast to calcium oxalate crystals, calcium phosphate
crystals are pH sensitive, forming in "alkaline" urine (usually
pH 6.5 or higher).
In general, calcium phosphate stones are associated with the
same risk factors as calcium oxalate stones (other than
hyperoxaluria)
• Uric acid — Uric acid is present in approximately 8
percent of analyzed stones, sometimes in combination with
calcium oxalate.
• The urinary risk factors for uric acid crystal formation are
lower urine volume, higher urine uric acid excretion, and most
importantly, lower urinary pH. Uric acid crystals are pH
sensitive, forming in "acidic" urine (usually pH 5.5 or lower).
• Struvite — Struvite is the crystal name for stones that form
only in the presence of urease-producing bacteria (eg, Proteus
mirabilis) .
• Other names for this crystal type include "triple phosphate"
(because the phosphate is in the triple-negative form) and
magnesium ammonium phosphate carbonate apatite.
• Struvite is found in approximately 1 percent of analyzed
stones and is much more common in women than in men
(due to the higher risk of urinary tract infections in women).
•
If a preexisting calcium-containing kidney stone is
subsequently infected with a urease-producing bacterium, the
stone analysis may report that the composition of the stone
includes calcium oxalate or calcium phosphate in addition to
struvite.
• Because urease splits urea into one carbon dioxide molecule
and two ammonia molecules, the net reaction often leads to a
urine pH outside of the physiologic range (8.5 or 9).
•
Other than the presence of urease, there are no other
urinary risk factors for struvite crystal formation
•
Struvite stones only form in patients with a chronic upper UTI
due to a urease-producing organism such as Proteus or
Klebsiella.
• The stone may grow rapidly over a period of weeks to months
and, if not adequately treated, can develop into a staghorn or
branched calculus involving the entire renal collecting system
• Cystine stones — Cystine stones only develop in patients
with cystinuria (an autosomal recessive disorder) due to the
poor solubility of cystine in the urine.
• The diagnosis of cystinuria is made by identification of the
pathognomonic hexagonal cystine crystals on urinalysis
(which can be seen in the initial urinalysis in about 25 percent
of patients; and by measurement of a urinary cystine
concentration of greater than 250 mg/liter
Other crystal types — Rare crystal types include:
●Triamterene
●Acyclovir
●Indinavir
• Risk factors — The risk of nephrolithiasis is influenced by
urine composition, which can be affected by certain diseases
and patient habits.
• For calcium oxalate stones, urinary risk factors include
hypercalciuria, hyperoxaluria, hypocitraturia, and dietary
risk factors such as a low calcium intake, high oxalate intake,
high animal protein intake, high sodium intake, or low fluid
intake
• Increased intake of Vitamin C has been associated with a
higher risk of stones in men
There are numerous other factors potentially associated with an
increased risk of stone formation:
●A history of prior nephrolithiasis. The rate of stone recurrence
is 10 to 30 percent at three to five years among patients with
idiopathic calcium oxalate stones
Patients with a family history of stones have an increased risk of
nephrolithiasis.
The risk of stones increases in individuals with enhanced enteric
oxalate absorption (eg, gastric bypass procedures, bariatric
surgery, short bowel syndrome).
Less common causes include frequent upper UTI (eg, as a result
of spinal cord injuries) and use of medications that may
crystallize in the urine such as indinavir, acyclovir, sulfadiazine,
and triamterene
Nephrolithiasis has also been reported in children receiving
prolonged ceftriaxone therapy
• Stone disease is approximately twofold higher in patients
with hypertension
• Additional potential risk factors include diabetes, obesity,
gout, and excessive physical exercise (including marathon
running), which may increase crystalluria and possibly the
risk of stones in predisposed individuals
• Low fluid intake is associated with increased stone risk. The
type of fluid taken in may be important, although data are
sometimes conflicting
• CLINICAL MANIFESTATIONS — Patients may
occasionally be diagnosed with asymptomatic nephrolithiasis
when a radiologic imaging study of the abdomen is performed
for other purposes or when surveillance imaging is done in
those with a prior history of stones.
• The asymptomatic phase is more likely to persist in those who
have never had a clinical episode of renal colic.
• EVALUATION — All patients presenting with their first stone
should undergo a focused history, radiologic imaging, and at
least a limited laboratory evaluation.
• There is general agreement that a complete metabolic
evaluation, in addition to the basic laboratory testing, is
indicated in all patients with multiple stones at first
presentation, in patients with a strong family history of
stones, and in individuals with active stone disease, which is
defined as recurrent stone formation, enlargement of existing
stones, or the recurrent passage of gravel.
• Focused history — The purpose of the focused history is to
identify stone risk factors, such as a family history of stone
disease and certain dietary habits
Summarized briefly, adverse dietary habits include:
●Low fluid intake or a high fluid loss (eg, from sweating or
gastrointestinal losses), which leads to a lower urine output
and, therefore, a higher concentration of lithogenic factors.
●Higher animal protein diet, which can lead to hypercalciuria,
hyperuricosuria, hypocitraturia, and elevated urinary acid
excretion
●Higher salt diet, which increases urinary calcium excretion.
●Increased intake of higher oxalate-containing foods, particularly
spinach. The exact contribution of dietary oxalate to urinary
oxalate is controversial and likely varies considerably from
person to person.
●Lower calcium intake, which acts by increasing the absorption
and subsequent excretion of oxalate due to decreased calcium
oxalate complex formation within the intestinal lumen .
●Excessive vitamin C and D supplementation.
• In addition, certain medications can occasionally crystallize in
the urine and lead to stone formation. Examples include,
sulfadiazine, and triamterene
•
Radiologic testing — The diagnosis of nephrolithiasis is
initially suspected by the clinical presentation. Helical noncontrast CT or ultrasonography can be used initially to
visualize and confirm the presence of a stone.
• Women who could potentially be pregnant should undergo a
urine pregnancy test before a CT scan is performed.
• It is important to appreciate that ureteral dilatation without a
stone on radiologic examination could represent recent
passage of a stone.
●Non-contrast helical CT
CT is more sensitive than ultrasonography and therefore more
likely to visualize a stone, if present. However, CT is also
associated with radiation exposure, and cumulative doses of
radiation may be high in patients who have recurrent
nephrolithiasis and need frequent imaging.
• Laboratory testing — There is disagreement whether a
complete metabolic evaluation should be performed after the
first stone. Limited data suggest that single stone formers
have similar metabolic abnormalities as patients with
recurrent nephrolithiasis
• However, there are data suggesting that a comprehensive
medical evaluation is not cost-effective for patients who have
only formed one stone
• Three options have been proposed for laboratory evaluation
after a first stone: a limited evaluation, a complete metabolic
evaluation similar to patients with multiple stones or active
stone disease, or a targeted approach
• Limited evaluation
The limited evaluation should include routine blood
chemistries. At least one repeated measurement of serum
calcium should be performed in patients whose first value is
high-normal since most patients with urolithiasis due to
primary hyperparathyroidism, have values between 10.2 and
11 mg/dL .Other findings that may be important include a low
serum phosphorus and a low serum bicarbonate
concentration, the latter being suggestive of distal renal
tubular acidosis or chronic diarrhea.
• Complete metabolic evaluation — Other clinicians
recommend a complete evaluation after the first stone
because of the potentially high rate of recurrence ,potential
morbidity from recurrent stones.
Targeted approach — A third approach is to base the extent of
the laboratory evaluation upon an estimation of the risk for
new stone formation
A complete metabolic evaluation, as described below, would be
performed in patients at moderate to high risk for recurrent
disease. Patients at high risk for recurrent disease include:
●Middle-aged, white males with a family history of stones
●Patients with chronic diarrheal states and/or malabsorption,
pathologic skeletal fractures, osteoporosis, urinary tract
infection, and/or gout
●Patients with stones composed of cystine, uric acid, calcium
phosphate, or struvite
• THE COMPLETE METABOLIC EVALUATION — The metabolic
evaluation for nephrolithiasis consists of both blood and urine
testing, including at least two 24-hour urine collections.
• Blood tests — A routine chemistry profile should be obtained,
including measurement of serum calcium. Although usually
normal, the presence of a low serum bicarbonate
concentration raises the possibility of Type I RTA.
• Urinalysis — A careful urinalysis should be performed since
certain findings point toward a specific diagnosis. A urine pH
above 7 with phosphate crystals in the urine sediment is
suggestive of calcium phosphate or struvite calculi, while the
presence of hexagonal cystine crystals is diagnostic of
cystinuria.
• Although uric acid crystals and calcium oxalate crystals may
be seen in individuals without stone disease, the specific
crystal type in a patient with stone disease is likely to
represent the composition of the stone.
• 24-hour urine collections — At least two 24-hour urine
collections should be obtained while the patient maintains
their usual diet, fluid intake and physical activities given the
high variability of the urine values.
• If there is a substantial discrepancy between two results, a
third collection may be required.
• Urine collections should not be performed if there is evidence
of renal/ureteral obstruction or urinary tract infection from
existing calculi.
• The urine volume, pH, and excretion of calcium, uric acid,
citrate, oxalate, sodium, and creatinine (to assess the
completeness of the collection) should be measured.
• Twenty-four hour urine collections may not be helpful in
determining the cause of new onset stones in dialysis patients
A variety of definitions for "normal" are frequently used for each
of the urinary parameters:
●Calcium − less than 250 mg per day in women or less than 300
mg per day in men
●Uric acid − less than 750 mg per day in women or less than 800
mg per day in men
●Oxalate − less than 45 mg per day in both women and men
●Citrate − greater than or equal to 320 mg per day in both
women and men
• Number of collections — Because of daily variations in
dietary intake, which are occasionally large, some have
recommended that two to three 24-hour collections be
obtained.
• we recommend that a minimum of two collections be
performed as part of the initial evaluation
• Timing of collections — The urine collections should be
obtained in the outpatient setting when the patient is on
usual diet; values should not be measured in the hospital. It is
common practice to wait at least one to three months after a
stone event to obtain the collections .At the least, one should
wait until the patient has completely recovered from any
surgical interventions and make sure that the urine is not
infected or the collecting system obstructed.
• We generally suggest waiting one to two months after the
last stone episode since the patient may have temporarily
modified their diet.
• if a patient is a recurrent stone former, then it should be
made clear to the patient and the treating urologist that
a stone must be sent for analysis during the next stone
episode.
• If stone composition is unknown, then treatment
recommendations to prevent future stone episodes will
be influenced by the 24-hour urine results and the
clinical picture.
• Hypercalciuria — If the urine calcium is elevated, then
attempts to lower the urine calcium concentration should be
instituted (often a thiazide diuretic will be necessary).
• In addition, primary hyperparathyroidism, sarcoidosis, and
distal (type 1) renal tubular acidosis should also be considered
in the patient with increased urine calcium levels.
• Hypocitraturia — If the citrate is low, choosing
treatment is a more difficult decision. Supplementing
citrate intake (eg, potassium citrate) will increase urinary
citrate excretion. However, this will also raise the urinary
pH. If the predominant calcium salt is calcium phosphate,
which forms more readily in an alkaline urine,
supplementation with citrate may, in fact, accelerate the
rate of stone formation. In this case, the urine pH may be
a useful guide. If the urine pH is 6.5 or higher, the use of
citrate supplements should be used with great caution.
• Hyperoxaluria — If hyperoxaluria is present, a low oxalate
diet should be tried first. The primary foods to avoid are
spinach and nuts. The following site contains the oxalate value
for different foods:
• Even if the urine calcium is high, increasing dietary calcium or
adding an over the counter calcium citrate supplement with
meals should be considered in addition to a low oxalate diet if
the low oxalate diet alone is insufficient.
•
However, the amount of urinary oxalate that is derived from
the diet is quite variable; thus, if a patient adheres to a low
oxalate diet and the urine oxalate does not fall, then the
oxalate restriction can be removed
• Hyperuricosuria — If hyperuricosuria is present, lifestyle
modification with the aim of reducing uric acid production (ie,
decreased purine intake and weight loss) should be
implemented
• However, if the urine pH is 6.0 or higher, the high urine uric
acid may not be playing a role, as it will stay in solution.
• Low urine volume — If the urine volume is less than two
liters in 24 hours, then patients should increase their fluid
intake with the goal of producing at least two liters of urine
per day
• Fluid should be ingested throughout the day and at bedtime,
and the volume should be increased when sweat losses are
greater, such as at higher ambient temperatures and with
exercise.
• RADIOLOGIC MONITORING — Another management issue is
whether to monitor a stone former, usually with
ultrasonography, (KUB), or (CT), to determine if new stones
have formed or previous stones have increased in size
• Monitoring should be performed initially at one year and, if
negative, every two to four years thereafter, depending
upon the likelihood of recurrence.
• ACUTE THERAPY — Many patients with acute renal colic
can be managed conservatively with pain medication and
hydration until the stone passes
• Forced intravenous hydration does not seem to be more
effective in reducing the amount of pain medication required
or increasing stone passage compared with minimal
intravenous hydration
• Urgent urologic consultation is warranted in patients with
urosepsis, acute renal failure, anuria, and/or unyielding pain,
nausea, or vomiting
• The likelihood that ureteral stones will pass depends upon the
size and location of the stone; smaller and more distal stones
are more likely to pass without intervention
• Straining urine — Patients should be instructed to strain
their urine for several days and bring in any stone that passes
for analysis. This will enable the clinician to better plan
preventive therapy.
• Pain control — Patients can be managed at home if they are
able to take oral medications and fluids.
• Hospitalization is required for those who cannot tolerate oral
intake or who have uncontrollable pain or fever.
• NSAIDs and opioids — Both NSAIDs and opioids have
traditionally been used for pain control in patients with acute
renal colic. NSAIDs have the possible advantage of decreasing
ureteral smooth muscle tone, thereby directly treating the
mechanism by which pain is thought to occur (ureteral spasm)
• Prospective randomized controlled studies suggest that
NSAIDs are at least as effective as opiates
• NSAIDs should be stopped three days before anticipated
shock wave lithotripsy to minimize the risk of bleeding.
• Stone passage — Stone size is the major determinant of
the likelihood of spontaneous stone passage, although stone
location is also important
Most stones ≤5 mm in diameter pass spontaneously. For stones
larger than 4 mm in diameter, there is a progressive decrease
in the spontaneous passage rate, which is unlikely with stones
≥10 mm in diameter.
Proximal ureteral stones are also less likely to pass
spontaneously.
• Facilitating stone passage — Several different medical
interventions increase the passage rate of ureteral stones,
including antispasmodic agents, calcium channel blockers, and
alpha blockers
• Studies directly comparing nifedipine and tamsulosin have
reported similar rates of stone passage, although rates were
slightly higher with tamsulosin
A potential advantage of tamsulosin is somewhat faster stone
passage and fewer hospitalizations and procedures. Other
alpha blockers appear to be similarly effective
• International guidelines from the American Urological
Association and the European Association of Urology on the
management of ureteral calculi suggest that:
●"In a patient who has a newly diagnosed ureteral stone <10
mm and whose symptoms are controlled, observation with
periodic evaluation is an option for initial treatment.
Such patients may be offered an appropriate medical therapy to
facilitate stone passage during the observation period. "
• Based upon data suggesting faster stone passage with an
alpha blocker versus calcium channel blockers, we initiate
treatment with tamsulosin (0.4 mg once daily) for four weeks
to facilitate spontaneous stone passage in patients with
stones ≤10 mm in diameter. Patients are then re-imaged if
spontaneous passage has not occurred.
• Patients with stones larger than 10 mm in diameter, patients
with significant discomfort, those with significant
obstruction or who have not passed the stone after four to
six weeks should be referred to urology for potential
intervention.
• Current options for therapy of stones that do not pass include
shock wave lithotripsy (SWL), ureteroscopic lithotripsy with
electrohydraulic or laser probes, percutaneous
nephrolithotomy and laparoscopic stone removal.
•
Open surgical stone removal is rarely needed.
• SWL is the treatment of choice in 75 percent of patients and
works best for stones in the renal pelvis and upper ureter.
• For patients with larger renal calculi (eg, >1.5 cm), renal
stones of harder composition (eg, cystine or calcium oxalate
monohydrate) or stones in complex renal or ureteral locations
(eg, lower pole calyx or mid-ureter), SWL is only successful in
approximately 50 percent of cases.
•
In these settings, endoscopic stone fragmentation with a
percutaneous or ureteroscopic approach is preferred.
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