Optimum Nutrition for Kidney Stone Disease

Ita P. Heilberg and David S. Goldfarb

We summarize the data regarding the associations of individual dietary components with kidney stones and the effects on 24-
hour urinary profiles. The therapeutic recommendations for stone prevention that result from these studies are applied where
possible to stones of specific composition. Idiopathic calcium oxalate stone-formers are advised to reduce ingestion of animal
protein, oxalate, and sodium while maintaining intake of 800 to 1200 mg of calcium and increasing consumption of citrate and
potassium. There are few data regarding dietary therapy of calcium phosphate stones. Whether the inhibitory effect of citrate
sufficiently counteracts increasing urine pH to justify more intake of potassium and citrate is not clear. Reduction of sodium
intake to decrease urinary calcium excretion would also be expected to decrease calcium phosphate stone recurrence. Con-
versely, the most important urine variable in the causation of uric acid stones is low urine pH, linked to insulin resistance as
a component of obesity and the metabolic syndrome. The mainstay of therapy is weight loss and urinary alkalinization provided
by a more vegetarian diet. Reduction in animal protein intake will reduce purine ingestion and uric acid excretion. For cystine
stones, restriction of animal protein is associated with reduction in intake of the cystine precursor methionine as well as cys-
tine. Reduction of urine sodium results in less urine cystine. Ingestion of vegetables high in organic anion content, such as cit-
rate and malate, should be associated with higher urine pH and fewer stones because the amino acid cystine is soluble in more
alkaline urine. Because of their infectious origin, diet has no definitive role for struvite stones except for avoiding urinary alka-
linization, which may worsen their development.
Published by Elsevier Inc. on behalf of the National Kidney Foundation, Inc.
Key Words: Calcium, Citrate, Oxalate, Protein, Nephrolithiasis

I ntroduction thiasis patients.2 Although higher dietary calcium intake

may augment intestinal absorption of calcium and cause
Many data of various sorts, from epidemiology to increased urinary calcium excretion,3 the net effect of cal-
urine chemistry, demonstrate that diet is an important cium restriction on risk of stones in patients with IH is not
contributor to the prevalence of kidney stones. Al- established. Support for dietary calcium restriction has
though many other variables, such as genetics, contrib-
waned as doubts about efficacy, clinical trial evidence,
ute, the composition of urine is largely determined by
and concerns about bone health have supervened. Cal-
diet composition. Therefore, treatment of stone recur-
cium absorption is higher in IH cases at all levels of cal-
rence with dietary modification is appealing to patients cium intake, reflecting an increase in active calcium
and physicians because it is also relatively inexpensive transport by the intestine. When challenged by an ex-
and safe. Nevertheless, the long-term adherence of pa- tremely low calcium diet, patients with IH excrete more
tients to diet and the effectiveness of diet are sup- calcium in the urine than was ingested, suggesting that
ported more by short-term metabolic studies and some of the urine calcium must derive from bone.4 In-
epidemiological observations than by randomized con- creased urinary calcium excretion on a low-calcium diet
trolled trials (RCTs). Comparisons of diet with pharma- in genetic hypercalciuric stone-forming rats also indi-
cologic therapy have not been made so that their cates an increase in bone resorption or a defect in kidney
relative efficacy and the ability of patients to adhere calcium reabsorption.5,6 In patients with IH, decreased
to these regimens is unknown. Given these uncer- bone mineral density, high bone resorption, and
tainties, it is not possible to stress enough the impor- reduced bone formation are also commonly observed.7-9
tance of increasing fluid intake to increase urine
volume and reduce the concentrations of stone-
forming salts, a therapy of proven effectiveness.1
In the present review, we summarize the data regard- From the Nephrology Division, Universidade Federal de S~ao Paulo, S~ao
ing individual dietary components thought to be causa- Paulo, Brazil; and Nephrology Division, New York University Langone Medi-
tive in the pathophysiology of kidney stones. The cal Center, New York, NY, and Nephrology Section, New York Harbor VA
Health Care System, New York, NY.
therapeutic recommendations for stone prevention that I.P.H. reports nothing to disclose. D.S.G. Takeda and Keryx: He has served
result are based on stone type (Table 1) and 24-hour uri- as a consultant to Quintiles. He has received honoraria from Amgen, Reata, and
nary profile (Table 2). Hospira. He has served as a site principal investigator for clinical trials. He has
received research funding from the National Institute of Diabetes and Digestive
and Kidney Disease and the Office of Rare Diseases Research.
Calcium Address correspondence to David S. Goldfarb, Department of Nephrology,
Oversaturation of urine with calcium is one of the most New York VA Medical Center, 423 E 23rd St./111G, New York, NY 10010.
E-mail: [email protected]
important risk factors for calcium nephrolithiasis. Idio- Published by Elsevier Inc. on behalf of the National Kidney Foundation, Inc.
pathic hypercalciuria (IH) represents a complex, primary 1548-5595/$36.00
metabolic alteration in at least half of calcium nephroli- http://dx.doi.org/10.1053/j.ackd.2012.12.001

Advances in Chronic Kidney Disease, Vol 20, No 2 (March), 2013: pp 165-174 165
166 Heilberg and Goldfarb

Finally, Worcester and colleagues demonstrated a greater The protective effect of increased dietary calcium to
decrease in kidney calcium reabsorption in IH stone- reduce stone recurrence was tested in an RCT that com-
formers after meals.10 Therefore, most individuals with pared the effect of a diet containing 1200 mg of calcium
IH appear to have a more generalized systemic abnor- per day (30 mmol/day), but reduced amounts of animal
mality in calcium homeostasis in which simultaneous protein (52 g/day) and salt (50 mmol/day), with a lower
dysregulation of calcium transport in the intestine, kid- calcium diet (400 mg/day ¼ 10 mmol/day) in 120 hy-
ney, and bone takes place. Attempts to classify hypercal- percalciuric men with recurrent calcium oxalate
ciuria on the basis of pathophysiology have not been stones.19 Both groups were counseled to reduce oxalate
shown to lead to superior therapeutic efficacy and are intake. Urinary calcium levels presented a marked and
not recommended in clinical practice.11,12 significant decrease in both groups, whereas urinary ox-
Large prospective observational studies show that low alate excretion was significantly decreased in the partic-
calcium intake is associated with a 34% higher risk of kid- ipants assigned to the higher calcium diet and
ney stones in young men,13 with similar findings in youn- nonsignificantly increased in the low-calcium diet
ger14 and older women.15 The inverse association group. The higher calcium intake was associated with
between dietary calcium and incident kidney stones has a 49% lower unadjusted relative risk of recurrence of
been ascribed to a secondary increase in urinary oxalate, stone disease at 5 years. Because dietary sodium and an-
which results from hyperabsorption of free oxalate dur- imal protein may contribute to the causation of calcium
ing low calcium intake. This then leads to reduction of stones,20 this trial, although suggestive, did not directly
the formation of insoluble, nonabsorbable calcium oxa- address the independent role of dietary calcium in the
late complexes in the intesti- pathogenesis of kidney
nal lumen. When the CLINICAL SUMMARY
stones.21 No such study
relation between diet and has been performed in
kidney stones in the Health  Idiopathic calcium oxalate stone-formers are advised to re- women.
Professionals Follow-Up duce ingestion of animal protein, oxalate, and sodium In conclusion, the consen-
Study was re-evaluated af- while maintaining intake of 800 to 1200 mg of calcium sus is that dietary calcium
ter 14 years of follow-up, and increasing consumption of citrate and potassium. restriction is no longer
the inverse association be-  Reduction of sodium intake to decrease urinary calcium considered appropriate ther-
tween dietary calcium and excretion would also be expected to decrease calcium apy for hypercalciuria be-
the risk of kidney stone for- phosphate stone recurrence. cause there is no evidence
mation was limited to men  The most important urine variable in the causation of uric that lower calcium intake pre-
younger than 60 years.16 Al- acid stones is low urine pH, which is linked to insulin vents stones and because of
though the cause of this age- resistance as a component of obesity and the metabolic the threat of bone dem-
syndrome.
specific difference remains ineralization.7,22 Instead, a
unclear, vitamin D defi-  The mainstay of therapy for uric acid stones is weight loss moderate increase in cal-
ciency and a diminished and urinary alkalinization provided by a more vegetarian cium intake (800–1200 mg,
diet.
ability to absorb dietary cal- approximately 3-4 servings
cium, more prevalent in of dairy per day) by subjects
older people, might account with low calcium intake
for this observation. More available luminal calcium appears appropriate, whereas those with moderate
would then result in more oxalate being bound in poorly calcium intake can continue that practice.
absorbable complexes so that additional dietary calcium
would not have further effect. In contrast, supplemental
Oxalate
calcium is associated with a slight but significantly higher
risk of incident stones in older but not younger Urinary oxalate derives from dietary sources and endog-
women.15,17 The inconsistent findings regarding the enous metabolism, with the relative proportions contrib-
effect of dietary versus supplemental calcium might be uted by each source varying among individuals.23 In
due to different timing of ingestion of the latter. metabolic studies with controlled oxalate intake, as ex-
Ingestion of supplements without food may lead to pected, urinary oxalate excretion increases as dietary ox-
increased calcium absorption and urinary excretion alate intake increases.24 The mean contribution of dietary
with little or no effect on the absorption and excretion oxalate to urinary oxalate excretion ranged from approx-
of oxalate. Therefore, calcium supplements should be imately 24 to 42% on a 10- to 50-mg/day diet. When the
administered as calcium citrate and preferentially taken calcium content was also reduced from 1002 mg to 391
with, or shortly after, meals by stone-forming individ- mg, the dietary contribution of oxalate further increased
uals.18 It is also possible that dairy products (the major to 53%. This finding further emphasizes that oxalate ab-
source of dietary calcium) may contain other inhibitory sorption is also highly dependent on calcium intake.25,26
factors. The proportion of oxalate absorbed from an oral load, as
 Table 1. Dietary Recommendations According to Stone Type
Stone Type Nutrient Intake Recommendation
Calcium Calcium Oxalate Sodium* Potassium† Animal Protein Citrate Fructose Fluids
 Idiopathic calcium oxalate 800-1200 mg Avoid oxalate-rich foods Reduce to ,100 mEq Increase to .120 mEq Reduce to ,1.2 g/kg Increase Reduce Increase
 Calcium phosphate 800-1200 mg Reduce to ,100 mEq ? Reduce to ,1.2 g/kg ? Increase
Uric acid Increase Reduce (also purines) Increase Increase
Cystine Reduce to 100 mEq Increase Reduce to ,1.2 g/kg Increase Increase
Struvite 800-1200 mg Reduce to ,100 mEq Increase

Empty box indicates that nutrient intake is not considered relevant; ? indicates unclear if dietary modification is beneficial or adverse.
*100 mEq Na corresponds to 2.3 g Na, about 6 g NaCl.
†120 mEq K corresponds to 4.7 g K.

Optimum Nutrition for Stone Disease

Table 2. Dietary Recommendations According to the Level of 24-h Urinary Excretion
Level of 24 h Urinary Parameters Nutrient Intake Recommendation
Calcium Oxalate Sodium Potassium Animal Protein Citrate Fructose Fluids
High calcium 800-1200 mg Avoid oxalate-rich foods Reduce Increase Reduce Increase Reduce Increase
High oxalate 800-1200 mg or more Reduce Reduce ? Reduce Increase Reduce Increase
High sodium 800-1200 mg Reduce Increase Reduce Increase Increase
High uric acid 800-1200 mg Reduce Increase Reduce (also purines) Increase Reduce Increase
Low pH 800-1200 mg Adequate Increase Reduce Increase Reduce Increase
Low citrate 800-1200 mg Reduce Increase Reduce Increase Reduce

Empty box indicates that nutrient intake is not considered relevant; ? indicates unclear if dietary modification is beneficial or adverse.

167
168 Heilberg and Goldfarb

measured by radiolabeled oxalate ingestion in calcium Protein

stone-formers, is higher than in nonstone-formers: 9.2
versus 6.8%.27 On the basis of these studies, it is possible The nutrient that clearly has universal effects on most of
that dietary oxalate restriction might be most efficacious the urinary parameters involved in stone formation is an-
imal protein (meat, fish, poultry, eggs; dairy products are
if prescribed for those with hyperoxaluria and hyper-
not included).20 The combination of a low-calcium diet
absorption, although this test has not been used pros-
with a high-animal-protein diet is particularly harmful
pectively in this manner to selectively prescribe an
because it also induces negative calcium balance.22
oxalate-restricted diet. The method of food preparation
and local agricultural variables may contribute to varia- High animal protein intake, a source of purines, contrib-
tion in oxalate content, but questions remain about utes to hyperuricosuria, a risk factor for calcium stones.37
what proportion of dietary oxalate is soluble and bio- The accompanying acid load leads to hypocitraturia
available versus insoluble.28 Fat malabsorption is also re- because of reduced tubular citrate reabsorption.38,39 The
effect of dietary protein on urinary oxalate is
sponsible for increased intestinal oxalate absorption in
controversial, with some studies showing an increase40-42
many conditions in which reducing dietary fat might be
whereas others report no change.43 Increased protein
considered.29-31
intake on a controlled oxalate diet increased urinary
In epidemiological studies in 3 cohorts of men and
women, oxalate intake assessed by food frequency ques- glycolate but did not affect total daily oxalate excretion
tionnaires (FFQs) surprisingly did not differ between in normal subjects, suggesting that endogenous oxalate
stone-formers and nonstone-formers. The relative risks synthesis was not increased.44
for stones in participants were 1.22 for men, 1.21 for older Finally, the effect of dietary protein on urinary excre-
tion of calcium is clear and well established. Animal
women, and not significant for younger women, compar-
protein-induced hypercalciuria occurs from more bone
ing the highest versus the lowest quintiles of dietary ox-
resorption and lower tubular calcium reabsorption. The
alate intake.32 Overall, the effect was small. In addition,
presence of nonresorbable calcium sulfate in the tubular
no trial of oxalate lowering with stone formation as the
outcome has been performed. Newer data on food lumen consequent to sulfate production from oxidation
oxalate content would be important in the design of of excessive sulfur-containing amino acids may also con-
an RCT (see https://regepi.bwh.harvard.edu/health/ tribute.45,46 In addition, acidosis has an effect on calcium
Oxalate/files). Therefore, the efficacy of restricting die- absorption by TRPV5 channels and their expression in
the distal tubule, leading to increased urine calcium
tary oxalate intake for stone prevention remains un-
excretion.47 However, a very recent study concluded
proven, except for special conditions such as bariatric
that hypercalciuria associated with high dietary protein
surgery.29,33 It is possible that increasing calcium intake,
intake was not due to the acid load.48
especially if low, is a more useful means of reducing
urine oxalate excretion than reducing oxalate intake Epidemiological data reveal a positive association be-
alone.19 tween animal protein consumption and new kidney
Another variable of uncertain significance in deter- stone formation in men but not women.13,15,17 The risk
mining the importance of dietary oxalate is colonization associated with animal protein intake varied with body
mass index (BMI) only in men with a BMI of less than
with Oxalobacter formigenes, an obligate oxalate-
25 kg/m2.16 The lack of association in overweight men re-
degrading anaerobe in the normal intestinal micro-
mains unexplained.
biome. Its presence in the colon is associated with lesser
Short-term dietary protein restriction (0.8 g/kg/day)
urine oxalate excretion.34 The organism may also be ca-
pable of stimulating oxalate secretion from the host’s for 2 weeks significantly reduced urinary excretion of cal-
blood to the intestinal lumen, thereby offering another cium, phosphate, hydroxyproline, uric acid, and oxalate
mechanism of reducing the host’s urine oxalate load.35 and increased citrate excretion in patients with nephroli-
Other intestinal commensals such as Enterococcus faeca- thiasis.41 Patients with recurrent nephrolithiasis may be
more sensitive to the calciuric action of protein.49 Despite
lis, Eubacterium lentum, and some lactic acid bacteria
poor adherence to a 4-month period of low animal pro-
present in various food products may also use oxalate
tein intake, 38.7% of stone-formers exhibited a reduction
as an energy source and lead to decreasing oxaluria.
in urine urea and calcium excretion. Significant correla-
Several studies have assessed the effects of oral admin-
istration of different probiotic preparations on oxaluria tions between urea and calcium outputs were detected
with variable results.34,36 However, individuals only among those with hypercalciuria.50
characterized by high oxalate absorption were most Few clinical trials have definitively evaluated the ef-
likely to experience clinically significant reductions in fect of animal protein restriction on calcium oxalate stone
formation. An RCT of a low-animal-protein, high-fiber
urinary oxalate in response to acute probiotic
diet was conducted in calcium oxalate stone-formers fol-
ingestion, which suggests that dietary oxalate plays
lowed regularly for up to 4.5 years with FFQs and urine
a key role as a determinant of urinary oxalate
chemistry measurements.51 The intervention group had
excretion in response to the use of probiotics.
 Optimum Nutrition for Stone Disease 169

an increase in the relative risk of recurrent stones, leading weight, BMI, urinary calcium, citrate, and uric acid excre-
the authors to conclude that the diet had no advantage tion; and duration of stone disease, a multiple regression
over advice to increase fluid intake alone. Measurement analysis showed that a high NaCl intake was the single
of urea excretion suggested that the intervention group variable that was most predictive of risk of low bone den-
had difficulty adhering to the diet. On the other hand, sity. No RCTs addressing sodium restriction as a sole
in the trial of Borghi and colleagues the reduction of die- therapy have been performed. Nevertheless, in the RCT
tary protein as prescribed was confirmed by a lower uri- by Borghi and colleagues the reduction in sodium intake
nary urea and sulfate and might have been partly accompanying higher calcium intake may have been im-
responsible for the reduction of stone recurrence by de- portant to reduce calciuria.19
creasing oxalate and calcium excretion.19 Finally, a more
recent 4-year randomized trial of low-animal-protein
Citrate and Potassium
compared with high-fiber diets revealed no change in
urinary calcium levels and recurrence rates despite a sig- The primary mechanisms of action of urine citrate are to
nificant decrease in 24-hour urinary sulfate in the low- increase the solubility of stone-forming calcium salts and
protein group.52 Again, there was imperfect adherence, inhibit calcium oxalate crystal growth. Modulation of cit-
so that the effectiveness of protein restriction in clinical rate excretion in the kidney is influenced by multiple fac-
practice may either be considered not definitively tested tors, but systemic acid-base variables have the strongest
or as a manipulation not likely to find more enthusiastic effect.58 Whereas acid loads and acidosis increase kidney
adherents. tubule reabsorption of citrate, alkali loads and alkalosis
Despite well described effects of increased animal pro- reduce it, hence increasing urinary citrate excretion. In
tein to increase stone risk as assessed by adverse changes addition, the systemic alkalinization that occurs with cit-
in urine chemistry, no protein-restricted diet has been rate supplementation reduces calcium excretion. This ef-
shown to reduce stone recurrence rates except one that fect is also important in increasing urine pH, reducing the
included higher calcium intake and restricted sodium in- risk of uric acid and cystine-based calculi. However, com-
take. Given the difficulty that modern, Western popula- pliance with potassium citrate preparations can be diffi-
tions have with protein restriction, the importance of cult, especially in the older population, because of
such a dietary prescription has not been demonstrated gastrointestinal side effects. Substitution of increased an-
but might be worthwhile for patients with high protein imal protein intake with high intake of fruits and vegeta-
intake suggested by history or by 24-hour urine results. bles among stone-formers is associated with increased
urine pH and volume (because of the water content of
fruits and vegetables) and increases of 68% in urinary cit-
Sodium
rate and potassium with concomitant reductions in am-
High sodium intake and a subsequent decrease in proxi- monium excretion.59 Citrus fruits such as oranges,
mal sodium reabsorption reduce kidney tubular calcium lemons, limes, and some tangerines are natural sources
reabsorption. The effect of sodium intake on increasing of dietary citrate and may be a nonpharmacological, die-
calcium excretion is well established. Every 100-mEq in- tary alternative therapy to potassium citrate supplemen-
crease in daily dietary sodium leads to an approximate tation for the management of hypocitraturia or uric acid
25- to 40-mg increase in urinary calcium excretion per and cystine stones.
day.53 In kidney stone-forming subjects, daily urinary cal- Numerous short-term studies of urinary chemistry
cium excretion varied directly with moderate changes in measures have demonstrated that urinary citrate levels
dietary sodium intake.54,55 increased after consumption of either grapefruit60,61
Although epidemiological studies revealed a positive, or orange juice61-63 or lemonade64-67 whereas a few
independent association between sodium consumption yielded no improvements in citraturia with
and new kidney stone formation in women,13,17 the lemonade.63,68 Citrate in orange and grapefruit juices is
interpretation of the results may be limited by the complexed mainly by potassium, thus also increasing
inaccuracy of the assessment of sodium intake by urinary pH. However, citrate in lemon juice, with high
semiquantitative FFQs. Recently, a cross-sectional study citric acid content, is largely accompanied by protons,
aimed at delineating associations between dietary and hence not conferring the alkalinizing load that orange
urinary factors with 24-hour urinary calcium excretion juice provides.63 Nevertheless, some citraturic effect of
found that participants in the highest quartiles of urinary oral citric acid may be attributed to some of the absorbed
sodium excreted 37 mg/day more urinary calcium than citrate escaping liver oxidation and degradation.69 Be-
participants in the lowest quartile.56 The adverse effects cause any organic anion that causes a systemic alkalosis
of a high sodium chloride (NaCl) intake (assessed by increases citrate excretion, malate may also increase uri-
24-hour sodium excretion) on calcium excretion and nary citrate.70 The significant caloric load that accom-
bone loss have also been reported in stone-formers.57 Af- panies the ingestion of large volumes of orange juice is
ter adjustment for calcium and protein intakes; age, a major concern that is not shared by freshly squeezed
170 Heilberg and Goldfarb

lemon/lime juices that can be sweetened with artificial lime juice from either fresh fruit or concentrates provided
sweeteners, thereby minimizing increased calciuria asso- more citric acid per liter than ready-to-consume grape-
ciated with fructose ingestion71 or perhaps other carbo- fruit or orange juice.82 In the nonjuice category of tested
hydrates.72 An additional benefit of citrus juice is the beverages, only lemonade-flavored Crystal Light pre-
requisite increase in overall fluid consumption, thus in- sented a high concentration of citrate.81 However, con-
creasing daily urine volume and reducing urine supersat- sumption of diet orange soda to provide 60 mEq of
uration. Noncitrus fruits such as pineapple and cranberry citrate would have to be in excess of 2 L/day or more
may also be rich in citrate. However, the effect of cran- than 9 8-oz glasses per day.83 Finally, pH is an important
berry extracts on urine citrate excretion is variable and determinant of alkali load in beverages containing or-
it may increase oxalate excretion73 (as also observed for ganic anions such as citrate. The carboxyl groups of cit-
orange juice63), probably because of the presence of a cer- rate will have no effect on urine pH if protonated, but if
tain amount of oxalate or conversion of ascorbic acid to accompanied by other cations such as potassium or so-
oxalate in vivo.74 Fresh tomato juice is also reported to dium, they will serve as net base. Commercial oral rehy-
contain a considerable amount of citrate.75 Finally, vari- dration solutions that contain a higher pH and more
ous melons—noncitrus alkaline fruits rich in potassium, citrate content led to an increase in citraturia and urinary
citrate, and malate—yield increases in urinary citrate ex- pH.84 However, these sports drinks may contain too
cretion similar to those provided by orange, hence repre- many calories and fructose to be preferred beverages
senting another dietary alternative for the treatment of for stone prevention. The amount of vitamin C added
hypocitraturic stone-formers.76 to juices is also a concern because of its conversion to ox-
Despite the evidence of increased urinary citrate in- alate, although the amount is not high if compared with
duced by citrus juice consumption, observational studies vitamin C supplements.74
do not show a reduction of the risk for stone formation
associated with orange juice. For reasons yet un-
Other Beverages
explained, stone risk increased up to 44% for each
240-mL serving of grapefruit juice consumed daily in A prospective controlled study showed that increasing
men and women.77,78 In one observational study, the water intake to achieve a urinary volume of approxi-
risk of stones increased by 35% with apple juice mately 2.5 L/day was associated with reduced stone re-
consumption77 despite its effect to increase urinary cit- currence.1 Although the exact daily amount of fluids
rate excretion.61 needed by stone-formers remains uncertain, advice on
On the other hand, observational studies show that how much to drink to form at least 30 mL/kg of body
higher potassium intake is inversely associated with inci- weight of urine per day can be recommended. Achieving
dent kidney stones in men and older women, with the ex- 2.5 to 3 L per day may be optimal.
ception of younger women.13,15,17 The effect of higher Although there is general agreement on the need to in-
potassium intake would mostly relate to the cation crease urinary volume in stone-formers, controversy ex-
being accompanied by an organic anion, such as citrate ists regarding the effect of water hardness on kidney
and malate, representing an alkaline load. However, stone incidence.85 The magnesium and bicarbonate con-
potassium deficiency stimulates proximal tubular tent of some mineral waters may result in favorable
citrate reabsorption so that potassium intake per se changes in urinary pH, magnesium and citrate excretion,
might reduce stone risk regardless of the accompanying inhibitors of calcium oxalate stone formation, counterbal-
anion. Martini and colleagues have observed ancing increased calcium excretion.86,87 The risk of uric
a significant correlation between urinary potassium and acid precipitation may also decrease with bicarbonate-
citrate.54 Patients whose self-assigned diets more closely containing water intake. However, increased risk of cal-
resembled the Dietary Approaches to Stop Hypertension cium phosphate stone formation may be observed.88
(DASH)-style diet, which is rich in fruits and vegetables, Observational studies have found that caffeinated or
had a marked decrease in kidney stone risk.79 In a cross- decaffeinated coffee and tea reduce the risk of stone for-
sectional study of a large cohort of persons with and mation77,89 despite caffeine’s effect to increase urine
without nephrolithiasis, multivariate-adjusted 24-hour calcium excretion.90 Alcohol in general, and beer specifi-
urinary citrate excretion was 16% greater in those exhib- cally, are consistently associated with protection against
iting the highest quintile of scores for diets resembling stone prevalence,1,2,75 possibly because of the inhibition
the DASH diet.80 Higher urine potassium and pH were of antidiuretic hormone secretion, leading to decreased
also significantly associated with higher DASH score in urinary concentration.77,78,89 Beer was once said to
all cohorts, confirming the benefits of the alkali and contain sizeable oxalate content, but current methods
high potassium content of such diet. do not confirm that supposition. However, beer may
In 2 recent studies, quantitative analysis of citric acid contain purines and contribute to hyperuricosuria.
in commercially available fruit juice products and bever- Although observational studies have not shown an
ages was performed with variable results.81,82 Lemon and adverse effect of cola consumption on stone
 Optimum Nutrition for Stone Disease 171

prevalence,78,91 colas have lower citrate content than

*Recommended Dietary Allowances (recommendation varies according to life stage and gender): adapted from Dietary Reference Intakes reports from the National Academy of

†For more information see https://regepi.bwh.harvard.edu/health/oxalate/files. Energy requirements for a normal, healthy individual with sedentary lifestyle: 25-30 kcal/kg/d, with
a percentage of total energy of 45-65% from carbohydrates, 20-35% from fat, and 10-15% from protein (50% of high biological value, as from meat, fish, poultry, eggs, milk, and soy).
in corn syrup
clear sodas and are variably associated with worsening

Fruits and vegetables, Fruits (citrus and High amounts

Fructose
of urine parameters, including an increase in oxalate
excretion, suggesting an increased tendency to form
calcium oxalate crystals at least in vitro.92

ND
Phytate

potassium-rich)
and vegetables
Phytate, or inositol hexaphosphate, inhibits calcium salt

Citrate

noncitrus
crystallization and stone growth in vitro.93 Phytate-rich
foods include beans, cereals, whole grains, and rice. In
fact, these foods also have significant oxalate content,

.4.7 g/d* (120 mEq K) ND

and it is possible that their phytate content mitigates their
oxalate-induced lithogenic potential.94 Although rela-

products, meats,
dried peas, dairy
tively nonabsorbable with less than 5% of ingested phy-

Potassium
tate appearing in the urine, increased dietary phytate
content is associated with increases in urine excretion

and nuts
such that a clinically meaningful result is possible.95
Western diets contain progressively less phytate because

Table 3. Dietary Recommendations for Adult Stone-Formers

of greater refinement of grains and rice, corresponding to

Nutrient Intake Recommendation

increased stone prevalence. In prospectively followed co-

Na, about 6 g NaCl)

salted meats, nuts,

phosphate added;
,2.3 g/d* (100 mEq

cold cuts; canned

horts of men and women, increased dietary phytate con-

Dairy products (milk, Spinach, beetroot, Processed foods to

products; use of
tent, as estimated by FFQs, has been variably associated

Sodium

which NaCl/
with reductions in stone risk.15 However, phytate intake

salt-shaker
benzoate/
was not associated with reduced stone risk in men in
a multivariate analysis.16

Calories and Fructose

potatoes, nuts†
Many observations and epidemiological studies link obe-
Oxalate

sity, weight gain, insulin resistance, metabolic syndrome,

,200 mg/d

and diabetes with increased prevalence of stones.96-98

Sciences, Institute of Medicine, Food and Nutrition Board (http://www.nap.edu).

Higher BMI is associated with lower urine pH99 and
a higher prevalence of uric acid stones.100 However, alka-
linization alone may fail in uric acid stone-formers be-
cheese, yogurt, etc.)

cause they appear to have increased net acid excretion

and lower urine pH at any level of urine sulfate excretion
1000-1200 mg/d*
Calcium

(a surrogate of animal protein intake) compared with

nonuric acid stone-formers.101 Because higher BMI is as-
sociated with higher urine oxalate excretion, calcium ox-
alate stones might also increase with obesity. Therefore,
weight loss might be associated with reduced stone prev-
alence of any composition. However, low-carbohydrate
Animal protein (meat,
poultry, fish, eggs,

diets rich in animal protein such as the Atkins diet reduce

and dairy [milk,
cheese, yogurt,

urine pH and citrate excretion while increasing uric acid

Protein
0.8-1.0 g/kg/d

excretion. Therefore, such diets are not recommended for

Abbreviation: ND, not determined.

stone-formers.45 Perhaps their negative effect could be

etc.])

overcome by ample potassium citrate supplementation.

We would instead recommend a low-calorie DASH
diet, also useful for diabetes and hypertension. Weight
Watchers and other more balanced plans might also yield
Main food sources

satisfactory results.79,102 Of note, stone-formers advised

Average daily

to decrease their intake of protein (or fat) should not in-

crease their consumption of fructose-rich foods (espe-
intake

cially high-fructose corn syrup). Fructose was

independently associated with an increased risk of inci-
dent kidney stones whereas nonfructose carbohydrates
172 Heilberg and Goldfarb

were not associated with increased risk in any cohort.71 Acknowledgments

On the other hand, short-term studies of varying, con- The authors appreciate insightful conversations with Alessan-
trolled fructose intake were not associated with changes dra Baxmann, PhD.
in urinary excretion of calcium, oxalate, or uric acid.103
Therefore, the mechanisms linking the epidemiologic References
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