Medical Management of Renal

calculi
Dr Jigen Gohel
 Conservative therapy
• Selective medical therapy
• Preventive therapy
 Selective medical therapy- Drug list
• Sodium cellulose phosphate
• Orthophosphate
• Thiazide
• Allopurinol
• Potassium citrate
• Α-mercaptopropionylglycine (Tiopronin [Thiola])
• Captopril
• D-penicillamine
• Acetohydroxamic acid
 Sodium cellulose phosphate
• MOA :
Binds calcium and inhibits calcium absorption
• USE :
Absorptive hypercalciuria
• DOSE :
10-15 g/day divided with meals
• SIDE EFFECT :
GI distress, hypomagnesaemia, hyperoxaluria, PTH
stimulation
• CURRENT STATUS :
 Sodium cellulose phosphate
Decrease No change Mild
increase

Urinary Urinary Urinary

calcium citrate phosphours

Brushite Urinary uric Urinary

saturation acid oxalate
 Thiazide
• MOA : directly stimulate calcium resorption in the distal
nephron AND promoting excretion of sodium.
• DOSE
– HYDROCHLOROTHIAZIDE : 25MG BD
– CHLORTHALIDONE : 25-50 MG OD
– INDAPAMIDE : 2.5 MG OD
• SIDE EFFECT :
– Potassium wasting,
– muscle cramps,
– hyperuricosuria,
– intracellular acidosis,
–
 Thiazide

Moderate mild Mild Mild

decrease decrease increase/mil increase/No
d decrease change

Urinary calcium Urinary citrate Urinary oxalate Urinary phosphurus

Calcium oxalate Urinary uric acid

saturation

Brushite saturation
 orthophosphate
• MOA :
– Renal : impaire renal tubular reabsorption of calcium and
– Intenstine : binding calcium in the intestinal tract
• Dose : 0.5 g PO tid
• Side effect :
– GI distress,
– hypomagnesemia,
– hyperoxaluria,
– PTH stimulation
– soft tissue calcification
• contraindicated in nephrolithiasis complicated by UTI
 orthosphosphate
Mild decrease No change Marked Mild increase
increase

Urianry Urinary uric Urinary Urinary

calcium acid phosphorus oxalate
Calcium Urinary citrate
oxalate
saturation Brushite
saturation
 Allopurinol

• MOA : block xanthine oxidase to convert xanthine

to uric acid
• Dose : 300 mg PO daily
• Side effect : Rash, myalgia
 Allopurinol
Urinary uric acid Urinary calcium
Urinary phosphorus
Urinary oxalate
Urinary citrate
Calcium oxalate Saturation
Brushite saturation

Marked No change
decrease
 Potassium citrate

• DOSE : 20 mEq PO bid-tid

• Side effect : GI upset, hyperkalemia
 Potassium citrate

Moderate Mild No change Marked

decrease decrease increase
Calcium Urinary Urinary Urinary
oxalate calcium phosphor citrate
saturation Urinary uric
acidus
Urinary
oxalate
 D-Penicillamine
• MOA :increase cystine solubility in urine by
formation of a more soluble mixed-disulfide
bond with cystine
• DOSE : 250 mg PO daily (titrated to effect)
• SIDE EFFECT :
– Nephrotic syndrome
– dermatitis
– Pancytopenia
 α-Mercaptopropionyl glycine
• MOA : increase cystine solubility in urine by
formation of a more soluble mixed-disulfide
bond with cystine
• DOSE : 100 mg PO bid (titrated to effect)
• SIDE EFFECT : Rash, asthenia, rheumatologic
complaints, GI distress, mental status changes
 Captopril
• MOA : increase cystine solubility in urine by
formation of a more soluble mixed-disulfide
bond with cystine
• DOSE : 25 mg PO tid
• SIDE EFFECT : Rash, cough, hypotension
 Acetohydroxamic acid
• MOA : urease inhibitor, may • SIDE EFFECT :
reduce the urinary saturation – Thromboembolic
of struvite and therefore phenomena,
retard stone formation – tremor,
– headache,
– palpitations,
• DOSE : 100 mg PO bid
– edema,
(titrated to effect – GI distress,
– loss of taste,
– rash,
– alopecia,
– anemia,
 Absorptive Hypercalciuria 1
• No treatment is capable of correcting the basic abnormality
of absorptive hypercalciuria I
• Not considered a selective therapy because it do not
decrease intestinal calcium absorption
• Widely used to treat absorptive hypercalciuria, because of
its hypocalciuric action and the high cost and inconvenience
of alternative therapy
• Dietary moderation of calcium and oxalate, Combined with
thiazide and potassium citrate :
– controlled hypercalciuria, while preventing cx of osteopenia
commonly associated with absorptive hypercalciuria
• If thiazides lose their hypocalciuric action
(after long-term treatment), a
• Stop for short period than resume .
• potassium citrate and dietary alterations
continue during this period.
• Orthophosphates can be used when other
methods are ineffective
 Absorptive Hypercalciuria Type II
• No specific drug treatment
• Moderate calcium intake (400 to 600 mg/day)
– Restore normocalciuria
• High fluid intake (sufficient to achieve a
minimum urine output > 2 L/day)
– To reduce urinary saturation of calcium oxalate
• Avoidance of excessive sodium intake
– Decrease hypercalciuria and stone formation
 Renal Hypercalciuria
• Thiazides are first-line therapy
• Augmenting calcium reabsorption in the distal
tubule and by causing extracellular volume
depletion and stimulating proximal tubular
reabsorption of calcium.
– hydrochlorothiazide 25 mg twice per day,
– chlorthalidone 25 to 50 mg/day, or
– indapamide 2.5 mg/day.
• Potassium citrate supplementation (40 to 60
mEq/day)
 Primary Hyperparathyroidism
• Parathyroidectomy is treatment of choice
• No medical treatment for the nephrolithiasis
• Orthophosphates used only when parathyroid
surgery cannot be undertaken.
• Estrogen is useful in reducing serum and
urinary calcium in postmenopausal women
with primary hyperparathyroidism
Hyperuricosuric Calcium Oxalate Nephrolithiasis

• two pharmacologic approaches

• The first involves decreasing the production of
uric acid.
– Allopurinol (300 mg/day)
– Block xanthine oxidase to convert xanthine to uric
acid lead to decrease in serum uric acid will ultimately
lead to a decrease in urinary uric acid as well.
– Allopurinol cause dietary purine overindulgence so
helpful if patients are unable or unwilling to comply
with dietary purine restriction.
Hyperuricosuric Calcium Oxalate Nephrolithiasis

• restoration of normal urinary uric acid include an

increase in the urinary limit of metastability of
calcium oxalate so spontaneous nucleation of
calcium oxalate is slowed (inhibition of
monosodium urate–induced stimulation of calcium
oxalate crystallization)
• Potassium citrate can effectively alter the urinary
milieu in patients with hyperuricosuria by
decreasing the supersaturation of uric acid and
calcium oxalate.
 Enteric Hyperoxaluria
• Fluid intake strongly encouraged to correct
dehydration.
• Dietary calcium bind intestinal oxalate and decrease
its absorption.
• Potassium citrate (60 to 120 mEq/day) correct
hypokalemia and metabolic acidosis. Avoid Slow-
release formulations of citrate
• probiotics and alteration of gut flora ---investigational
– to increase the degradation of oxalate, thereby
preventing intestinal absorption
 Primary hyperoxaluria
• Pyridoxine
– converted to pyridoxal phosphate, which is a
cofactor for AGT
– combined liver-kidney transplantation
idiopathic hyperoxaluria
• dietary counseling (low-oxalate diet)
• pyridoxine
 Hypocitraturic Calcium Oxalate Nephrolithiasis-Distal
Renal Tubular Acidosis,thiazide induced,idiopathic

• Potassium citrate
– sustained decline in the urinary saturation of
calcium oxalate (from reduction in urinary calcium
and in citrate complexation of calcium)
– inhibitory activity against the crystallization of
calcium oxalate and calcium phosphate is
augmented because of the direct action of citrate.
Hypomagnesuric Calcium Nephrolithiasis

• Magnesium oxide or magnesium hydroxide

• Correction of the hypocitraturia with
potassium citrate
• The use of magnesium limited by risk of
diarrhea.
 Gouty Diathesis
• Goal : to increase the urinary ph above ph 5.5,
preferably between 6.0 and 6.5
• Potassium citrate -(30 to60 meq/day in two or three
divided doses).
• avoid Alkalinizing the urine to a ph of > 7.0
– Danger of increasing the risk for calcium phosphate
stone formation.
• If the urinary uric acid excretion is elevated or
hyperuricemia exists, allopurinol (300mg/day)
should be added.
 cystinuria
• The object of treatment for cystinuria is to reduce
the urinary concentration of cystine to below its
solubility limit (200 to 300 mg/L)
• The initial treatment includes a high fluid intake to
attempt to produce to 3 liters of urine per day. This
help reduce the supersaturation of urine with respect
to cystine.
• Oral administration of soluble alkali (potassium
citrate) at a dose sufficient to raise the urinary ph to
6.5 to 7.0
 cystinuria
• This treatment strategy attempts to increase the
solubility of the filtered cystine to prevent crystal
formation.
• the pKa of cystine is 8.3, which creates two
problems. First, it is quite difficult to achieve a
urine pH this high, making excessive alkalinization
an unrealistic target.
• Second, raising the urine pH to these levels will put
the patient at risk for the formation of calcium
phosphate calculi
 cystinuria
• Restriction of dietary sodium because excess
dietary sodium can lead to increases in cystine
excretion
 cystinuria
• Next line of therapy involves agents that
increase cystine solubility in urine by
formation of a more soluble mixed-disulfide
bond (i.E.,Cystine to drug, rather than cystine
to cystine). These agents include
– Α-mercaptopropionylglycine
– (Tiopronin [thiola]),
– D-penicillamine (cuprimine), and
– Captopril.
 cystinuria
• Doses start at 250 mg/day and are titrated to
effect show minimal toxicity
• D-penicillamine side effects:
– nephritic syndrome, dermatitis, and pancytopenia
 cystinuria
• α-mercaptopropionylglycine (tiopronin [Thiola
– This agent also contains a sulfhydryl group that forms a
disulfide bond with cystine
• better tolerated than D-penicillamine
• Common side effects include asthenia, GI distress,
rash, joint aches, and mental status changes.
• Dosages start at 100 mg, BD and are titrated to
achieve urinary concentrations of cystine less than
250 mg/L urine.
• total daily doses as high as 1200.
 Infection Lithiasis
• Aggressive surgical approaches.
• AUA Guidelines Committee has strongly
recommended endoscopic-based therapy (i.e.,
percutaneous nephrolithotomy) as the first-
line therapy
 Infection Lithiasis
• Complete elimination of all infected stone material
is essential for the prevention of recurrent struvite
stone formation
• The medical management of infection calculi
centers on the prevention of recurrence, rather
than medical dissolution.
• Thus long-standing effective control of infection
with urea-splitting organisms should be achieved if
at all possible with improved bladder health,
adequate urinary drainage, and suppressive
antibiotics.
 Infection Lithiasis
• Residual calculi often harbor organisms and
endotoxin within their interstices
• Antibiotics should be tailored to the
predominant organism found on culture and
sensitivity screening
• Patients undergoing removal of presumed
struvite calculi should be covered with broad-
spectrum antibiotics that account for local
resistance
 Infection Lithiasis
• Recurrence of colonization is likely if residual fragments
remain within the collecting system.
• After surgical stone removal, residual fragments may be
dissolved with hemiacidrin irrigation (renacidin) under
very careful observation. Historically, use of this agent was
associated with significant toxicity and even death
• Therefore this agent should be employed only after UTI
and/or Colonization has been brought under control.
• Chemolysis with various agents is no longer routinely used
for the management of struvite calculi
 Infection Lithiasis
• Acetohydroxamic acid, a urease inhibitor, may
reduce the urinary saturation of struvite and
therefore retard stone formation

• When given at a dose of 250 mg three times

per day, prevent recurrence of new stones and
inhibit the growth of stones in patients with
chronic urea-splitting infections
 Infection Lithiasis
• SIDE EFFECT : 15% developed deep venous
thrombosis.
– Due to low-grade intravascular coagulation
• Requiring careful follow-up for signs of thrombosis.
• Other thromboembolic phenomena, tremor,
headache, palpitations, edema, gi distress, loss of
taste, rash, alopecia, anemia, and abdominal pain.
• Because of these concerns, this agent is frequently
reserved for patients deemed too ill for surgical
management.
 Infection Lithiasis
• Other acidifying agents
– Ammonium chloride, methenamine hippurate,
and ascorbic acid.

• Mixed struvite stone more likely associated

with metabolic abnormalities then pure
struvite calculi
 Ammonium Acid Urate Stones
RIS FACTORS
• Associated with laxative abuse
• ileostomy diversion
• morbidly obese,
• recurrent UTIs,
• recurrent uric acid stones
 Ammonium Acid Urate Stones
• Bowel disease is treated, if possible, while
standard recommendations of fluid intake,
oral calcium, alkalinization, and oxalate
reduction are made
 Ammonium Acid Urate Stones
• Those with a history of uric acid calculi are
also treated in a similar manner with
– increased fluid intake,
– protein and salt restriction,
– alkalinization with potassium citrate, and
– the possible use of allopurinol.
Miscellaneous and Drug-Induced Stones

• Calculi Formed From Drug

– Indinavir
– Ephedrine
– Triamterene
– Magnesium trisilicate antacids (silicates)
– Trimethoprim-sulfamethoxazole
Miscellaneous and Drug-Induced Stones

• Calculi Provoked by Drug

– Carbonic anhydrase inhibitors
– Topiramate
– Furosemide
– Vitamin C (excess)
– Vitamin D (excess)
– Laxatives
 Medical Management of Bladder Calculi

• Renacidin may prove beneficial in irrigating

indwelling suprapubic or urethral catheters
to decrease and prevent encrustation and
occlusion
• Twice-daily or thrice-daily irrigation with
0.25% or 0.5% acetic acid solution also serve
as 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 treated with loop diuretics should be

screened for the development of nephrocalcinosis
• Should be switch to thiazide diuretic

• Although switching to a thiazide diuretic may not

actively Cause the dissolution of calculi, it at least
removes the causative agent and allows the kidney an
opportunity to heal and clear the calcium deposits
 Children and Adolescents
• Appearance of urinary calculi during childhood should raise the
distinct possibility of an inherited

Genetic disorder, such as cystinuria, distal RTA, or primary

hyperoxaluria
• Metabolic evalution should be done

• The most important is urinary calcium-to-creatinine ratio. A

calculated urinary calcium-to-creatinine ratio above 0.2 has
been considered abnormal and frequently promptsintervention
 Children and Adolescents

• The medical management of nephrolithiasis and the

prevention of subsequent recurrences in children do
not differ 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.

Medical Management of Calculi during Pregnancy

• Pregnant women create a unique urinary environment

that is promote stone formation
• Although the amount of urinary calcium rises quite
notably ,this effect is offset by an accompanying increase
in urinary citrate.
• As a result, it is widely assumed that there is no net
increase or decrease in the risk for calculi formation
 Medical Management of Calculi during
Pregnancy
• As a result of these temporary physiologic changes, a
metabolic evaluation is not generally undertaken to
determine the cause of the stone disease until after the
woman has delivered and returned to her baseline state of
health.
• Patients with a history of stones should be strongly
encouraged to maintain high fluid intake. Dietary
recommendations should be reinforced.
 Medical Management of Calculi during
Pregnancy
• Radiation exposure to the fetus should be avidly avoided.
Therefore ultrasonography has become the first-line imaging
study to search for calculi during pregnancy.

• Although this modality provides adequate images of the

kidneys, it can be difficult to fully discern the ureters and their
contents.

• Additionally, hydronephrosis of pregnancy may be confused for

hydronephrosis from an obstructing calculus.
 Medical Management of Calculi during
Pregnancy

• A limited IVP may be obtained that consists of one

scout image followed by one plate taken approx.
30 minutes after the injection of contrast.

• Each plain film exposes the fetus to 0.1 to 0.2 rads,

well below the threshold of 1.2 rads, at which the
risk begins to increase.
 Medical Management of Calculi during
Pregnancy

• Radiation exposure should be particularly avoided

during the first trimester during the time of
organogenesis and the greatest fetal risk.

• Magnetic resonance imaging (MRI) has also been

reported for stone diagnosis in pregnant patients
 Medical Management of Calculi during
Pregnancy

• Approx. 66% to 85% of pregnant women with ureteral

colic spontaneously pass the calculi when treated
conservatively with hydration, analgesics, and, if
infected, antibiotics
• The goal of therapy for the remaining patients is to do
the least required to keep the kidney functioning, the
patient free from symptoms, and the urine uninfected
 Medical Management of Calculi during
Pregnancy
• Stents should be placed cystoscopically with
minimal radiographic or sonographic
monitoring.
 Preventive therapy
• Fluid Recommendations
• Dietary Recommendations
– Obesity
– Metabolic Syndrome
– Impact of Weight-Loss Diets
– Impact of Bariatric Surgery
– Role of Dietary Calcium
– Role of Vitamin D and Biphosphonates
– Oxalate Avoidance
 Fluid Recommendations

• Volume
– Fluid intake atleast 2 liters
– Mechanical diuresis prevent urinary stagnation
and formation of symptomatic calculi
 Water Hardness

• water hardness can alter urinary parameters,

this factor ultimately appears to have little
effect on clinical outcome.
• water hardness should be a minor concern
with respect to stone formation.
 Carbonated Beverages

• carbonated water offers increased protection against

recurrent stone formation as compared to still water
• increased intake of soda can confer an increased risk
for subsequent stone recurrence.
• citrus-flavored sodas (orange flavored, lemon/lime
flavored) have been shown to have high citrate
content, which may aid in stone prevention
• significant increase in urinary volume and a decrease
in calcium oxalate saturation when these were
compared to the self-selected diets.
 Carbonated Beverages

• Daily servings of apple or grapefruit juice increased the

risk for stone events.
• Caffeine intake may increase the risk for stone
recurrence in calcium-stone formers by increasing the
excretion of calcium
– Caffeine increased urinary calcium/creatinine,
magnesium/creatinine, citrate/creatinine, and
sodium/creatinine, but not oxalate/creatinine in stone
formers.
• Supersaturation calculations increased,despite the
noted increases in the inhibitors citrate and magnesium
 Citrus Juices

• Lemonade and orange juice increased urinary volume as

well as increased urinary citrate excretion.
• Orange juice
– Increase in urinary ph (6.48 vs. 6.75 from 5.71)
– Urinary citrate (952 vs. 944 from 571 mg/day)
– Decreased urinary undissociated uric acid levels
– Increased the inhibitor activity (formation product) of brushite
(calcium phosphate).
– Increased urinary oxalate
– Did not alter calcium excretion,
• orange juice beneficial in the control of calcareous and
uric acid nephrolithiasis.
• Natural juices are highest in citrate and potassium
content
– Grapefruit juice (197.5 meq/L),
– Lemon and orange juice (145.48 and 144.57 meq/L)
• Amount of fluid rather than type of fluid important
• Drink at least 3000 ml/day to maintain a urine
output greater than 2500 ml/day.
 Dietary Recommendations

• Dietary changes are having an important

impact on renal stone disease.
• Alterations in diet and physical activity may
significantly reduce the incidence of recurrent
nephrolithiasis
 Protein Restriction

• Renal stones is higher in populations in which there is

an increased animal protein intake.
• Patients with stones more sensitive to dietary protein
loading than normal subjects.
• Protein intake increases urinary calcium, oxalate, and
uric acid excretion.
• Dietary protein restriction decrease in calcium,
phosphate, and oxalate.
• Risk for hypercalciuria and hyperuricosuria with a diet
high in animal protein ,carbohydrate, sodium, and
 Protein Restriction

• In hypercalciuric patients, protein restriction

resulted in decreased urinary uric acid and
increased urinary citrate.
• Low-protein, low-salt,moderate-calcium diet cause
reduction in stone events compared to those
patients on the low-calcium diet
• Diets high in fruits and vegetables impart a
significantly reduced risk for stone formation than
do those diets high in animal protein
 Protein Restriction
• Dietary Approaches To Stop Hypertension (DASH)
diet is associated with a lower risk for kidney stone
formation due to increase in urinary citrate and
urine volume.
– Rich in fruit and vegetables,
– Moderate in low-fat dairy products,
– Low in animal protein
• Increased intake of meat may exacerbate calcium
oxalate stone disease.
 Sodium Restriction

• Sodium restriction important element of dietary

prevention of recurrent nephrolithiasis
• Excess sodium ingestion as a cause of calcium stone
disease
• The high sodium intake significantly
– Increased calcium excretion,
– Increased urinary ph
– Decreased citrate excretion.
• On other end Patients with hypocitraturic calcium oxalate
stone formation may benefit from sodium
supplementation
 Obesity

• Obesity has been associated with

– Impaired carbohydrate tolerance
– Inappropriate calcium response to glucose ingestion.
– Increased urinary excretion of oxalate, sodium,uric acid,
calcium, and phosphorus, as well as lower ph
– excessive food consumption
• Hypercalciuria in meat eaters is due to increased body
Weight.
• Daily urinary oxalate excretion related to BMI
• Citrate and urinary volume did not correlate with BMI
 Obesity

• Increased BMI(>30), larger waist size, and weight

gain correlated with an increased risk for stone
episodes.
• The magnitude of the association is greater in
women than in men
• MC metabolic abnormalities among obese patients
– Gouty diathesis (54%),
– Hypocitraturia (54%),
– Hyperuricosuria (43%).
 Obesity

• Medical therapy and Dietary recommendations

reduce stone episodes for these patients.
 Metabolic Syndrome

• Metabolic syndrome consists of a cluster of

disease states—
– glucose intolerance,
– elevated blood pressure,
– dyslipidemia, and
– central obesity—that increase the risk for developing
type 2 diabetes and coronary vascular disease.
• increased risk for stone disease in patients with
metabolic syndrome
 Metabolic Syndrome
• MC stone composition are calcium oxalate,
uric acid
• Increased risk for stone disease in diabetics
– Lower urinary ph
– Impaired ammonium excretion lead to increased
incidence of uric acid stone formation
– Degree of insulin resistance was also inversely related
to urinary ph
 Impact of Weight-Loss Diets

• Dietary fads include the use of low-carbohydrate,

high-protein, high-fat diets (Atkin's Diet,South
Beach Diet, and Sugar Busters Diet) delivers a
marked acid load to the kidney, increases the risk
for stone formation, and may increase the risk for
bone loss.
• Diet high in fruits and vegetables and low in
animal protein, specifically the DASH diet, is
associated with a reduced risk for stone formation
 Impact of Bariatric Surgery

• Risk for oxalate nephropathy and nephrolithiasis in the

RYGB population
• Adjustable gastric banding found only to have low urine
volume but no hypocitraturia
• Restrictive bariatric surgery incurs a lower risk for
subsequent stone development than RYGB.
• Currently, the pathophysiology of bariatric surgery–
induced hyperoxaluria remains unclear
• Potential causes include alteration in intestinal flora (i.e.,
Oxalobacter formigenes), fat malabsorption, or a reduced
amount of oxalate secretion
 Role of Dietary Calcium
• Maintenance of a moderate calcium intake in
calcareous nephrolithiasis
• Significantly restrict calcium intake likely led to an
increase in available intestinal oxalate absorption,
thereby raising the supersaturation of calcium
oxalate.
• Moderate-calcium diet, combined with salt
restriction and moderation of animal protein had
half as many stone episodes.
 Role of Dietary Calcium
• Decreased incidence of nephrolithiasis in subjects
who had increased levels of dietary calcium.
• This protection did not remain for those who
received increased calcium intake from
supplements instead of from dietary sources (i.E.,
Dairy products).
 Role of Dietary Calcium
• Calcium supplement with a meal or combined calcium supplement and

estrogen therapy is not associated with a significant increased risk for

calcium oxalate stone formation in the majority of postmenopausal

osteoporotic patients

• Type of calcium supplementation

• Calcium citrate will significantly increase urinary calcium excretion and

urinary citrate excretion.

• The concomitant increase in citraturia potentially offsets the lithogenic

potential of calcium supplement–induced hypercalciuria and therefore

 Role of Vitamin D and Biphosphonates

• Monitoring of 24-hour urine calcium in patients

who undergo vitamin D repletion.
• Bisphosphonates are common treatment for
osteoporosis.
• The combination of alendronate and
hydrochlorothiazide had a significantly greater
effect on urinary calcium and bone density than
alendronate alone.
• Bisphosphonates are safe and possibly preventive
for patients with calcium nephrolithiasis.
 Oxalate Avoidance

• only 10% to 20% of urinary oxalate is usually derived

from dietary sources
• contribution of dietary oxalate increased when calcium
consumption decreased
• it is difficult to restrict its intake because oxalate is
ubiquitous and found in most vegetable matter.
• avoid large portions of foodstuffs that are rich in oxalate,
such as spinach, beets, chocolate, nuts, and tea.
• low-oxalate diet most useful in patients with enteric
hyperoxaluria, those with underlying bowel
abnormalities, or patients who have undergone gastric
bypass surgery
• Risk of vitamin C (ascorbic acid) ingestion and
the possibility of its conversion to oxalate with
subsequent urinary excretion.
• Associated with two-fold increased risk for
kidney stone formation
• Limiting intake to maximum daily dose of less
than 2 g.