Metabolic workup & medical management of urolithiasis

Metabolic workup & Medical
management of Urolithiasis

GOALS OF M.E.
Why?
• The main goal of metabolic evaluation is
to prevent recurrent stone formation in high-
risk stone producers,
to prevent further growth of any existing
stones, &
to prevent extrarenal complications in
associated systemic disorders.

CHARACTERISTICS
It should be
• simple to perform,
• economically viable,
• provide information that can be applied
toward a selective, rational therapy of stone
disease.

Selection of Patients
for Metabolic Evaluation
• First-time “stone formers”-50% risk of recurrence within
subsequent 10 years.
• Stone clinic effect: “single stone formers” placed on a
conservative program of high fluid intake alone or combined
with avoidance of dietary excess revealed a low incidence of
recurrent stone disease.
• Decision to thoroughly investigate a first-time stone former
should ideally be shared by the physician and the patient.

Contd...
• Formation of a first stone may be the harbinger of a
more severe underlying systemic disorder such as
renal tubular acidosis, bone disease, or
hypercalcemia due to hyperparathyroidism.
• In such patients, metabolic evaluation is justified
solely to make the correct diagnosis in order to
prevent extrarenal complications.

TIMING
When?
• At least 1 month after stone passage or stone
removal, allowing the patient to return to
their normal routine.

Indications for a Metabolic Stone
Evaluation
Who ?
• Recurrent stone formers
• Strong family history of stones
• Intestinal disease (particularly chronic diarrhea)
• Pathologic skeletal fractures
• Osteoporosis
• History of urinary tract infection with calculi
• Personal history of gout
• Infirm health (unable to tolerate repeat stone episodes)
• Solitary kidney
• Anatomic abnormalities
• Renal insufficiency
• Stones composed of cystine, uric acid, struvite
• Children

Abbreviated Protocol for Low-Risk,
Single Stone Formers
History
• Underlying predisposing conditions
• Medications(calcium, vitamin C, vitamin D, acetazolamide, steroids)
• Dietary excesses, inadequate fluid intake or excessive fluid loss
Multichannel blood screen
• Basic metabolic panel (sodium, potassium, chloride, carbon dioxide, blood urea nitrogen,
creatinine)
• Calcium
• Intact parathyroid hormone
• Uric acid
Urine
• Urinalysis
pH > 7.5: infection lithiasis
pH < 5.5: uric acid lithiasis
Sediment for crystalluria
• Urine culture
Urea-splitting organisms: suggestive of infection lithiasis
• Qualitative cystine

Contd...
Radiography
• Radiopaque stones: calcium oxalate, calcium phosphate,
magnesium ammonium phosphate (struvite), cystine
• Radiolucent stones: uric acid, xanthine, triamterene
Intravenous pyelography: radiolucent stones, anatomic
abnormalities
Stone analysis

CRYSTAL MORPHOLOGY
Scanning electron
micrographs of various
urinary crystals.
• A, Ca P Apatite(Amorphous)
• B, Struvite (Rectangular,Coffin-
lid)
• C, Ca oxalate dihydrate
(Envelope,tetrahedral)
• D, Ca oxalate
monohydrate(Hourglass)
• E, Cystine(Hexagonal)
• F, Ammonium acid
urate.(amorphous shards)
• G, Brushite(Needle-shaped)

Extensive Diagnostic Evaluation
• Should be performed in patients with recurrent
nephrolithiasis, and stone formers at increased risk
for further stone formation.
• To identify underlying physiologic derangements.
• Pt. to discontinue any medication that interferes with
metabolism of calcium, uric acid, or oxalate.
(vitamin D, calcium supplements, antacids, diuretics,
acetazolamide, & vitamin C) & any current
medication for stone treatment (thiazides,
phosphate, allopurinol, or magnesium).

Contd...
• It involves two outpatient visits.Three 24-hour urine
samples are collected.
• First two 24-hour specimens: on random diet,
reflective of their usual dietary intake.
• Third 24-hour sample: after 1 week, on a calcium-,
sodium-, & oxalate-restricted diet.

Fast and Calcium Load Test:
• discriminate b/w various forms of hypercalciuria.
• no longer performed by most clinicians.
• essential if plan to place a patient with absorptive
hypercalciuria on a calcium binding resin.
 Normal fasting urinary calcium < 0.11 mg/dL GF
 Normal postload urinary calcium < 0.2 mg calcium/mg
creatinine

Calcium Load Test.
• After 7 days of a low-calcium, low-sodium diet,
patients fast for 12 hours from 9 PM.
 Distilled water is provided at 9 PM and midnight.
At 7 AM the next day, patients completely empty
the bladder and discard the urine.
They drink an additional 600 mL of distilledwater.
Urine is collected from 7 to
9AM.Thisisthefastingsample.

At 9 AM, 1 g of calcium mixed in a liquid
synthetic meal is given orally.
Urine is collected from 9 AM to 1 PM. This is
the postload sample. Both urine samples are
analyzed for calcium, creatinine, and cAMP .
cAMP measurements are used as an indirect
estimate of parathyroid function because
most PTH assays are insensitive to rapid
changes in serum calcium.

Simplified Metabolic Evaluation
• All patients: basic metabolic screening, searching for
systemic disorders.
• High-risk stone patients: more extensive metabolic
evaluation based on two 24-hour urine samples.
• Cornerstone of these simplified protocols- development
of a urine preservation method that allows collection of
urine without refrigeration.
• Urinary constituents most commonly assayed: calcium,
oxalate, citrate, total volume, sodium, magnesium,
potassium, pH, uric acid, and sulfate.
• Commercially available urine analysis packages.

STONE ANALYSIS TO DETERMINE METABOLIC
ABNORMALITIES
• Most stones are a mixture of more than one component,
relative ratios or predominance of any particular molecule
has predictive value.
• Ca apatite & mixed Ca oxalate-Ca apatite stones: RTA & 1°
hyperparathyroidism
• Pure & Mixed Uric acid stones: Gouty diathesis
• Brushite stones: RTA
• Infection stones: Infection
• Cystine stones: Cystinuria
• Pure uric acid, pure infection & pure cystine stones- start
treatment; no further testing required.

IMAGING IN DETERMINING STONE
COMPOSITION
• Radiologic imaging is mainly used for
determination of the presence or absence of
calculi, renal anatomy, and associated findings
(i.e., hydronephrosis).
• Thus diagnostic imaging plays a crucial role in
the surgical planning and follow-up of patients
with nephrolithiasis.

IMAGING IN DETERMINING STONE
COMPOSITION
• Hounsfield unit (HU)measurement to
determine stone composition- significant
variation for diff.stone types.
• DECT technology: to distinguish b/w uric acid,
Ca phosphate & Ca oxalate calculi.
HU ratios
DECT Slope algorithm
DECT attenuation values.

Composition Hounsfield units
Calcium oxalate dihydrate 1800-2500
Calcium oxalate monohydrate 500-1800
Magnesium phosphate 1500
Struvite 800-1500
Cysteine 700-1200
Uric acid 100-700

ECONOMICS OF METABOLIC
EVALUATION
• Routine performance of a comprehensive
metabolic evaluation may not be economically
sound if applied to all stone patients.
• Many first-time stone formers may not benefit
economically from a metabolic evaluation unless
initial screening puts them in a high-risk category.
• Recurrent stone formers are best treated with a
metabolic evaluation and directed medical
therapy.

CONSERVATIVE MEDICAL M/M
1.Fluid recommendations
2.Dietary recommendations
3.Obesity

1. Fluid recommendations
VOLUME:
• Forced increase in fluid intake
to achieve atleast a urine
output of 2L.
• Two effects:
1.Mechanical diuresis that
ensues may prevent urinary
stagnation & formation of
symptomatic calculi.
2.Creation of dilute urine alters
supersaturation of stone
components.

Contd...
WATER HARDNESS:
• Although water
hardness can alter
urinary parameters, it
does not play a
significant role in
recurrence risk.

Contd...
CARBONATED BEVERAGES:
• Carbonated water offers increased protection
against recurrent stone formation, by increasing
urinary citrate levels.
• Soda flavored with phosphoric acid may increase
stone risk, whereas those with citric acid may
decrease risk.
• Caffeine intake may increase the risk of stone
recurrence in calcium stone formers by increasing
the excretion of calcium.

Contd...
CITRUS JUICES:
• Citrus juices
(particularly lemon and
orange juices) may be a
useful adjunct to stone
prevention.

2. Dietary Recommendations
PROTEIN RESTRICTION:
• Incidence of renal stones is higher with increased
animal protein intake.
• Protein intake increases urinary calcium, oxalate, &
uric acid excretion and probability of stone
formation even in normal subjects.
• Diets high in fruits and vegetables impart a
significantly reduced risk of stone formation than
diets high in animal protein.

SODIUM RESTRICTION
• An important element of dietary prevention of recurrent
nephrolithiasis.
• A high sodium intake increases calcium excretion,
urinary pH and decreases citrate excretion. Net effect-
increased propensity for crystallization of calcium salts
in urine.
• Animal protein restriction, moderate calcium ingestion,
& a reduced-sodium diet decreases stone episodes by
roughly 50%.
• Calcium stone formers who ingest large quantities of
daily salt are more likely to suffer from decreased bone
mineral density

DIETARY CALCIUM:
• Evidence supports maintenance of a moderate
calcium intake in calcareous nephrolithiasis.
• Dietary calcium restriction may subsequently
increase oxalate absorption, thereby raising Ca
oxalate supersaturation.
• "Safe" Calcium supplementation: Time & Type
Time- to be taken with meals.
Ca citrate- "Stone friendly" Ca supplement.

Vit D supplementation
• Vitamin D repletion is
likely safe for stone
formers; however, 24-
hour urine calcium
should be monitored
during vitamin D
therapy.

Bisphosphates
• Bisphosphonates
combined with thiazide
diuretics appear to
reduce hypercalciuria
while protecting the
bone.

• Avoidance of excess dietary oxalate is reasonable &
intuitive..
OXALATE AVOIDANCE:

Vitamin C limited dose
• Vitamin C in large
doses may increase
the risk for stone
recurrence.
• Doses should
probably be limited
to 2 g/day.

3. Obesity
• Increased BMI, larger
waist size, & weight
gain correlate with an
increased risk of stone
episodes.
• More pronounced for
women.

Contd...
METABOLIC SYNDROME:
• Hypertension, Hypertriglyceridemia, Glucose
intolerance & Central obesity.
• Obesity & Insulin resistance → impaired
ammonium excretion→ Low urinary pH→
Increased incidence of uric acid stone
formation.

Contd...
IMPACT OF WEIGHT-LOSS DIETS:
• a low-carbohydrate, high-protien diet
delivers a marked acid load to kidney,
increases risk for stone formation & bone loss.

Contd...
IMPACT OF BARIATRIC SURGERY:
• Bariatric surgery may significantly increase
the overall risk of stone formation.
• Jejunoileal bypass(before) & Roux-en-Y
gastric bypass(now) both increase oxalate
nephropathy & nephrolithiasis.

Conservative Management Summary
• It is anticipated that with these conservative
measures alone, a significant number of patients
may be able to normalize their urinary risk factors
for stone formation.
• Thus only these conservative measures may be
necessary to keep their stone disease under
control.
• After 3 to 4 months on conservative
management, patients should be re-evaluated
using either standard laboratory assays or an
automated urinalysis package

• If the patient’s metabolic or environmental
abnormalities have been corrected, the
conservative therapy can be continued and
the patient followed every 6 to 12 months
with repeat 24-hour urine testing as indicated.
• If, however, a metabolic defect persists, a
more selective medical therapy may be
instituted.

SELECTIVE MEDICAL M/M
• Selective treatment program would be more
effective and safe than “random” therapy.

I.Calcium-Based Calculi
HYPERCALCIURIA(>200mg/day):
• Absorptive Hypercalciuria(AH): an increased amount
of Ca absorbed by intestinal tract.
 AH type1- increased urinary excretion of calcium
on both fasting & loading specimens.
 AH type2- elevated urinary Ca on regular diet,
normalises on fasting.
a low iPTH due to suppression from a constant
abundance of available serum Ca.

Rx: Absorptive Hypercalciuria
AH type1:
• Thiazides(1st choice)+Pot.citrate +dietary
restriction.(drug holiday in long-term therapy)
• Thiazides do not treat underlying cause of AH but
reduce urinary calcium & manage its symptoms.
• MoA: Thiazides directly stimulate calcium resorption
in distal nephron while promoting sodium
excretion.
• S/E: Potassium wasting, muscle cramps,
hyperuricosuria, intracellular acidosis,
hypocitraturia

Contd...
• Sodium cellulose phosphate (SCP) effectively
decreases absorption of intestinal Ca but
abandoned due to GI intolerance & side
effects.
• S/E: GI distress, hypomagnesemia,
hyperoxaluria, PTH stimulation.

Contd...
• Thiazides- limited long-term effectiveness in
AH type1.
Other hypocalciuric agents:
• Indapamide(OD dose)
• Amiloride + thiazide(K.Cit not needed)
• Triamterene(Risk of triamterene stones)

Contd...
AH type2:
• No specific drug Rx needed.
• Moderate Ca intake(400 to 600 mg/day) &
high fluid intake(sufficient to achieve a
minimum urine output of >2 L/day).
• Avoidance of excessive sodium intake further
decrease hypercalciuria.

Contd...
Orthophosphate:
• MoA- inhibit 1,25-(OH)2vitamin D synthesis;
reduces urinary Ca by binding Ca in intestinal
tract.
• Has a role when other methods are
ineffective.
• S/E: GI upset,soft tissue calcification.

Contd...
Dietary Bran:
• Rice bran binds intestinal Ca & increases
urinary pyrophosphate.
• Thiazide + bran superior to bran alone.

Contd...
• Renal Hypercalciuria: due to a wasting of
calcium by functioning nephron.
• constant loss of Ca from distal tubules.
• hypercalciuria during all phases of fasting,
loading, or restriction of dietary calcium.
• mild elevation of iPTH.

Rx:Renal Hypercalciuria
• Thiazides(Rx of choice) + Pot.citrate(correct
hypokalemia, increase urinary citrate)
• Thiazides correct renal leak of Ca by augmenting
calcium reabsorption in distal tubule and by causing
ECV depletion and stimulating proximal tubular
reabsorption of Ca.
• Correction of 2° hyperparathyroidism restores
normal serum 1,25-dihydroxyvitamin D
concentration & intestinal Ca absorption.
• Sustained correction for upto 10 yrs.

• Potassium citrate supplementation (40 to 60
mEq/day) is advised, because this medication
has been shown to be effective in averting
hypokalemia and increasing urinary citrate,
when administered to patients with calcium
nephrolithiasis taking thiazide

Contd...
• Resorptive Hyperclaciuria
(1°hyperparathyroidism): overproduction of
PTH from dominant adenoma or diffuse
hyperplasia.
• Hypercalcemia,hypercalciuria in all phases, &
raised iPTH.

Rx: 1°hyperparathyroidism
• Parathyroidectomy: resection of dominant
adenoma or all four glands.
• No established medical Rx.
• Orthophosphates used only when Sx cannot
be undertaken.

Contd...
• HYPERURICOSURIC CA OXALATE
NEPHROLITHIASIS (HUCN): (>800mg/day)
• Hyperuricosuria + pH> 5.5.
• Causes: increased dietary purine intake, Gout,
MPD/LPD,MM, neoplastic states, pernicious
anemia, 2°polycythemia, Hbpathies,
thalassemia etc.

Rx: HUCN
• Decreased dietary protein intake.
• Allopurinol decreases uric acid production by
inhibiting Xanthine oxidase( which converts
xanthine to uric acid).
• Potassium citrate alters the urinary milieu in
hyperuricosuria by decreasing
supersaturation of uric acid & calcium
oxalate.

Contd...
HYPEROXALURIA: (>40mg/day)
• Enteric Hyperoxaluria: fat malabsorption results in
saponification of fatty acids with divalent cations
such as Ca and Mg, thereby reducing Ca oxalate
complexation and increasing the pool of available
oxalate for reabsorption.
• Diarrhoea,dehydration,HCO3
- losses.
• A/w chronic diarrheal syndrome, small bowel
resection, jejunoilleal bypass, intrinsic disease.

Rx: Enteric Hyperoxaluria
• Oxalate-restricted diet.
• High fluid intake (to ensure adequate urine volume).
• Anti-diarrhoeal agent.
• Probiotics & gut flora correction (O.formigenes).
• Pot.Citrate (correct hypokalemia, metabolic acidosis,
increase urinary citrate).
• Oral Ca citrate or Mg gluconate(ileal disease)
• Cholestyramine(binds bile salts in bowel lumen).
• Replace dietary fat with MCT(correct
malabsorption).

• Primary Hyperoxaluria: rare AR disorder of
glyoxylate metabolism, normal glyoxylate to glycine
conversion is prevented, preferential oxidative
conversion to oxalate.
• Two types; PH1 & PH2.
Contd...

Rx: Primary Hyperoxaluria
• Present during childhood with early stone
formation, tissue deposition of oxalate
(oxalosis), & renal failure due to
nephrocalcinosis.
• Death before age 20 in untreated patients
• Early Dx & Combined liver-kidney transplant.

Contd...
HYPOCITRATURIC CA OXALATE NEPHROLITHIASIS:
(<550mg/day in F; <450mg/day in M)
• Distal RTA(Type1): Hypokalemic,hyperchloremic,non-AG
metabolic acidosis.
• Abnormal collecting duct function; inability to acidify urine
in systemic acidosis.(pH>5.5).
• Ca phosphate stones m.c.
• Two-thirds pts.adults-nephrolithiasis, nephrocalcinosis.
• Infants- Vomiting or diarrhoea, FTT & growth retardation.
• Children- Renal stones & metabolic bone disease.

Rx: Distal RTA Hypocitraturia
• Potassium citrate correct
the metabolic acidosis &
hypokalemia in distal
RTA.
• Large doses(up to 120
mEq/day) may be
required in severe
acidotic states.
• Target dose in children:
3-4mEq/kg/day in
divided doses.

Contd...
• Chronic Diarrhoeal states: Lab findings like
enteric hyperoxaluria; except for bowel
inflammation.
• moderate decreases in urinary citrate
excretion with associated low urine volumes.
• Rx: Pot.Citrate(60-120mEq in 3-4 doses;
liquid prepn preferred due to rapid intestinal
transit time).

Contd...
• Thiazide-Induced & Idiopathic
Hypocitraturia:
• Rx: Pot.citrate therapy.

Contd...
HYPOMAGNESURIC CALCIUM
NEPHROLITHIASIS: (<80mg/day)
• Low urinary Mg, hypocitraturia, & low urine
volume.
1.Chronic thiazide therapy.
2.IBD causing malabsorption.
3.Laxative abuse.

Rx: Hypomagnesuria
• Magnesium supplementation beneficial in
stone reduction.
• Use of magnesium limited by risk of diarrhea
(Mg oxide, hydroxide).
• Potassium-magnesium citrate(new)may
restore urinary magnesium and citrate levels
with minimal GI side effects.

II.Uric acid Calculi
• Uric acid: end product of purine metabolism.
• pKa- 5.35. At more acidic pH, undissociated uric
acid predominates & precipitates; at higher pH 6.5,
>90% uric acid is ionised & soluble.
• 3 main determinants: low urine pH, low urine
volume & hyperuricosuria.
• "Gouty diathesis” refers to a stone-forming
propensity characterized by low urine pH of
unknown etiology with or without associated gouty
arthritis.

Rx: Gouty Diathesis
• Major goal: to increase urinary pH>5.5,
preferably b/w 6.0 & 6.5.
• Alkalinisation to a pH>7.0 should be avoided
(increased risk of Ca phosphate stone
formation).
• Pot.citrate therapy.
• Allopurinol, if hyperuricemia or
hyperuricosuria present.

III. Cystinuria
• AR error of transepithelial transport involving
intestine & kidneys.
• Inability to reabsorb dibasic amino acids cystine,
ornithine, lysine, and arginine (COLA).
• Resultant accumulation of cystine causes
crystallization when concentrations rise above the
saturation point (roughly 250mg/L of urine)
• Young age presentation.

Contd...
Object: to reduce urinary concentration of cystine to
below its solubility limit(200 to 300 mg/L).
• High fluid intake to produce 2.5-3L/day of urine.
• Urinary alkalinisation by Pot.citrate.
• Restricted salt/sodium diet.
• Use of cystine binding agents (increase cystine
solubility in urine via formation of a more soluble
mixed-disulfide bond).

Contd...
1.α-mercaptopropionylglycine (Thiola,
Tiopronin)- m.c.used.
S/E: asthenia, GI distress, rash, joint aches, and
mental status changes.
2. D-penicillamine (Cuprimine)
S/E: Nephrotic syndrome, dermatitis,
pancytopenia
3. Captopril
S/E: rash,cough,hypotension.

IV. INFECTION CALCULI(STRUVITE)
• Form in alkaline(pH>7.2), infected urine with
urease producing bacteria in an ammonia-rich
environment.
• Women produce more infection calculi than men.
• Infection calculi most likely produce staghorn
stones.
• Symptoms of UTI may be present.

Rx: Struvite stones
• PCNL first-line therapy for managing
complex, renal staghorn calculi.
• Complete elimination of all infected stone
material essential for prevention of recurrent
struvite stone formation.
• Antibiotic prophylaxis.
• Hemiacridin irrigation for residual fragment
dissolution.

Contd...
• Acetohydroxamic acid, a urease inhibitor, reduce
urinary saturation of struvite, & retard stone
formation.
• When given at a dose of 250 mg three times per day,
acetohydroxamic acid has been shown to prevent
recurrence of new stones and inhibit the growth of
stones in patients with chronic urea-splitting
infections
• S/E: Thromboembolic phenomena, tremor headache,
palpitations, edema, GI distress, loss of taste, rash,
alopecia, anemia, abdominal pain

Ammonium Acid Urate Stones
• Ammonium acid urate
calculi are infrequently
seen in industrialized
nations and are often
associated with laxative
abuse
• Medical treatment for
these calculi is
determined by the
underlying cause of the
stone.
• Those with laxative abuse
are strongly encouraged
to develop a healthier
bowel regimen.
• Those withchronic
infections are treated
much like those with
struvite calculi.

MISCELLANEOUS
MEDICAL M/M OF BLADDER CALCULI:
• Stone dissolution using Suby G or M solution:
beneficial in irrigating indwelling suprapubic or
urethral catheters to decrease and prevent
encrustation and occlusion.
• Twice-or thrice-daily irrigation with 0.25%-0.5%
acetic acid solution beneficial prophylaxis against
recurrent struvite calculi when catheters must be
left indwelling for long periods.
• Uric acid calculi may be dissolved by irrigation with
alkaline solutions

Neonatal Nephrolithiasis
• Neonates with furosemide-induced nephrolithiasis
present with hematuria, worsening renal function, and
calcific densities on ultrasonography or plain film
radiography.
• Nephrocalcinosis is often present on imaging studies.
• Cessation of furosemide diuresis is considered helpful
and standard therapy.
• There has been previous suggestion that treatment
with thiazide diuretics may actually promote the
resolution of this process and reverse the likely
parenchymal injury

Children and Adolescents
Nephrolithiasis
• The appearance of urinary calculi during
childhood should raise the distinct possibility of
an inherited genetic disorder, such as cystinuria,
distal RTA, or primary hyperoxaluria.
• The medical management of nephrolithiasis and
the prevention of subsequent recurrences in
children do not differ that dramatically from the
approaches undertaken for adults.
• All patients (and their parents) are counseled to
improve fluid intake.

• Dietary recommendations are similar to those
made for adults.
• It is important to emphasize that dietary calcium
is not to be avoided in this age group.
• Rather, calcium should be sought through the
ingestion of dairy and other natural sources
rather than with the use of supplements.
• Such sources will also bind dietary oxalate during
meals and may decrease calcium oxalate
supersaturation in the urine.

MEDICAL M/M OF CALCULI DURING
PREGNANCY:
• Due to temporary physiologic changes, a metabolic
evaluation is not undertaken to determine the cause of the
stone disease until delivery & return to baseline health status.
• Majority of ureteral calculi during pregnancy pass
spontaneously.
• Dx during pregnancy- USG or limited IVP.
• Rx- Hydration, analgesics & antibiotics. Stents, if required
exchange every 4-6 weeks.
• URSL with Holmium laser lithotripsy is safe.

MET(medical expulsion therapy) for
ureteral stones
• For stone < 5mm : no additional benefit with MET
• For stone 5-10mm , MET with alfa blocker is suggested when:
– No contraindication:
• Pain not controlled
• Septic
• Derange in RFT
• Hypotension
– Benefit: 29% more patient will pass their stone than control, less
colicky & analgesic requirement
– Risk: 5% drop out due to hypotension
• Ca channel blocker: only 9% more (not significant)
• CCB vs AARB: 20% improvement in SPR with alpha blockers
[MA Hollingsworth Lancet. 2006]
• Single use of corticosteroid is discouraged

• Proximal 25%, mid 45%, distal 70%
• Stones that have not passed in 2 months
are unlikely to do so
• Vast majority of trials were limited to
patients with distal ureteric stones
• Tamsulosin is most studied , but all alfa blockers
works well class effect (YILMAZ JU2005)
• MET using tamsulosin resulted in a $1132 cost
advantage over observation (Bensalah et al.
EJU 2008)
• MET in paed gp is not effective [Aydogdu JU2009]

Mechanis of Action
• Ureter SM relaxation
• Alpha-1 adrenergic receptor
anatagonist in ureter in
humans and animals
• Density of alpha1-
anatagonist significantly
higher than alpha2/ beta
• Prevalence of alpha1a
(subtype) in human
Inhibit basal tone,
peristaltic frequency
and ureteral
contraction
Decrease basal and micturating bladder neck pressure
Decrease intraureteric pressure
Increase fluid transport ability
Facilitate spontaneous expulsion of ureteric stone

Evaluation
• 1. A clinician should perform a screening
evaluation consisting of a detailed medical
and dietary history, serum chemistries and
urinalysis on a patient newly diagnosed with
kidney or ureteral stones.

• 2. Clinicians should obtain serum intact
parathyroid hormone (PTH) level as part of the
screening evaluation if primary
hyperparathyroidism is suspected.

• 3. When a stone is available, clinicians should
obtain a stone analysis at least once.

• 4. Clinicians should obtain or review available
imaging studies to quantify stone burden.

• 5. Clinicians should perform additional
metabolic testing in high-risk or interested
first-time stone formers and recurrent stone
formers.

• 6. Metabolic testing should consist of one or
two 24-hour urine collections obtained on a
random diet and analyzed at minimum for
total volume, pH, calcium, oxalate, uric acid,
citrate, sodium, potassium and creatinine.

• 7. Clinicians should not routinely perform “fast
and calcium load” testing to distinguish
among types of hypercalciuria.

Diet Therapies
• 8. Clinicians should recommend to all stone
formers a fluid intake that will achieve a urine
volume of at least 2.5 liters daily.

• 9. Clinicians should counsel patients with
calcium stones and relatively high urinary
calcium to limit sodium intake and consume
1,000-1,200 mg per day of dietary calcium.

calcium oxalate stones and relatively high
urinary oxalate to limit intake of oxalate-rich
foods and maintain normal calcium
consumption.

• 11. Clinicians should encourage patients with
calcium stones and relatively low urinary
citrate to increase their intake of fruits and
vegetables and limit non-dairy animal protein.

• 12. Clinicians should counsel patients with uric
acid stones or calcium stones and relatively
high urinary uric acid to limit intake of non-
dairy animal protein

cystine stones to limit sodium and protein
intake.

Pharmacologic Therapies
• 14. Clinicians should offer thiazide diuretics to
patients with high or relatively high urine
calcium and recurrent calcium stones.

• 15. Clinicians should offer potassium citrate
therapy to patients with recurrent calcium
stones and low or relatively low urinary
citrate.

• 16. Clinicians should offer allopurinol to
patients with recurrent calcium oxalate stones
who have hyperuricosuria and normal urinary
calcium.

• 17. Clinicians should offer thiazide diuretics
and/or potassium citrate to patients with
recurrent calcium stones in whom other
metabolic abnormalities are absent or have
been appropriately addressed and stone
formation persists.

• 18. Clinicians should offer potassium citrate to
patients with uric acid and cystine stones to
raise urinary pH to an optimal level.

• 19. Clinicians should not routinely offer
allopurinol as first-line therapy to patients
with uric acid stones.

• 20. Clinicians should offer cystine-binding thiol
drugs, such as alpha-
mercaptopropionylglycine (tiopronin), to
patients with cystine stones who are
unresponsive to dietary modifications and
urinary alkalinization, or have large recurrent
stone burdens.

• 21. Clinicians may offer acetohydroxamic acid
(AHA) to patients with residual or recurrent
struvite stones only after surgical options have
been exhausted.

Follow-up
• 22. Clinicians should obtain a single 24-hour
urine specimen for stone risk factors within six
months of the initiation of treatment to assess
response to dietary and/or medical therapy.

• 23. After the initial follow-up, clinicians should
obtain a single 24-hour urine specimen
annually or with greater frequency, depending
on stone activity, to assess patient adherence
and metabolic response.

• 24. Clinicians should obtain periodic blood
testing to assess for adverse effects in patients
on pharmacological therapy.

• 25. Clinicians should obtain a repeat stone
analysis, when available, especially in patients
not responding to treatment.

• 26. Clinicians should monitor patients with
struvite stones for reinfection with urease-
producing organisms and utilize strategies to
prevent such occurrences.

• 27. Clinicians should periodically obtain
follow-up imaging studies to assess for stone
growth or new stone formation based on
stone activity (plain abdominal imaging, renal
ultrasonography or low dose computed
tomography [CT]).

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