Mini-review

Dietary treatment of nephrolithiasis

Antonio Nouvenne defined acquired diseases such as cystinuria, congenital hy-

Tiziana Meschi peroxaluria, primary hyperparathyroidism, renal tubular acido-
Angela Guerra sis, infections or anatomical alterations of the urinary tract (sec-
Franca Allegri ondary nephrolithiasis), all conditions in which diet plays a mar-
ginal role. In the majority of cases stone disease strikes other-
Beatrice Prati
wise healthy people (idiopathic nephrolithiasis) and appears to
Loris Borghi be closely correlated to life style and diet (5).
Although only few well conducted randomized-control trials
Department of Clinical Sciences, University of Parma, Parma, have been performed so far, large cohort studies, such as the
Italy Nurses’ Health Study (6, 7) and the Health Professionals Fol-
low-up Study (8, 9), have provided, together with various ex-
Address for correspondence: perimental studies, evidence which is consistent enough to
Loris Borghi, M.D., Ph.D. state that appropriate dietary manipulations can successfully
Department of Clinical Sciences, University of Parma prevent both the first appearance and the recurrences of idio-
Via A. Gramsci 14, 43100 Parma pathic nephrolithiasis. Hence, it is extremely important that not
Ph. +39 0521 703374 just the specialist, but the general practitioner also should be
Fax +39 0521 985468 fully aware of the primary role of diet in the management of this
E-mail: loris.borghi@unipr.it condition.
In 90% of cases of idiopathic nephrolithiasis, the stones are
made of calcium oxalate, often associated with variable traces
Summary of calcium phosphate and, occasionally, uric acid; in 10% they
are made of pure uric acid (10). Nutrition has a direct impact on
The prevalence of idiopathic nephrolithiasis is increasing in the mechanisms involved in the genesis of urinary calculi (11).
rich countries. Dietary manipulation could contribute to the The first step in the genesis of a kidney stone is the formation
prevention of both its first appearance and the recurrence of of crystal nuclei. This event occurs when the concentration of a
the disease. The target of dietary treatment is to decrease the salt exceed the solubility limit (supersaturation). Sometimes
“urinary lithogenic risk factors” such as low urine volume, hy- this is also accompanied by a deficit in the protective sub-
percalciuria, hyperoxaluria, hyperuricosuria, hyperphospha- stances known as crystallization inhibitors, e.g. citrate and
turia, hypocitraturia, hypomagnesuria and excessively alka- magnesium. By the term “urinary stone risk factors” (12), we
line or acid urinary pH. Due to the lack of randomized con- refer to a series of conditions which, all together, either pro-
trolled trials focused on this problem, there is not ample evi- mote or prevent the crystallization of a salt.
dence to confidently recommend dietary changes. Despite For calcium oxalate stones, the most widely recognized urinary
this, numerous recent and past experiences support modifica- stone risk factors are low urine volume (< 2 L/day), hypercal-
tion of diet as having a primary role in the prevention of ciuria (> 250 mg/day [6.25 mmol]), hyperoxaluria (> 45 mg/day
nephrolithiasis. In particular, it is recommended to limit ani-
[0.5 mmol]), hyperuricosuria (> 700 mg/day [0.24 mmol]),
mal protein and salt intake, to consume milk and derivatives
hypocitraturia (< 320 mg/day [1.7 mmol]), and hypomagnesuria
in amounts corresponding to calcium intake of about 1200
(< 60 mg/day [2.5 mmol])
mg/day and to assume fiber (40 g/day), vegetables and fruit
daily avoiding foods with high oxalate content. Furthermore,
For calcium phosphate stones, important factors are hyper-
vitamin C intake not exceeding 1500 mg/day plays a protective phosphaturia (> 1100 mg/day [35.6 mmol]) and an excessively
role as well as avoiding vitamin B6 deficiency and abstaining, alkaline urine pH (> 7.0) along with low urine volume, hypercal-
if possible, from vitamin D supplements. Lastly, it is recom- ciuria and hypocitraturia.
mended to drink enough water to bring the urinary volume up For uric acid stones, favoring factors are low urine volume, hy-
to at least 2 L/day and, as much as possible, to use fresh or peruricosuria and an excessively acid urine pH (< 5.5).
frozen products rather than prepacked or precooked foods The existence of a genetic substratum in idiopathic stone dis-
which are often too rich in sodium chloride. ease cannot be overlooked (13), but diet undoubtedly has a di-
rect effect on all of the above urinary stone risk factors as well
KEY WORDS: nephrolithiasis, diet, prevention. as on the subsequent pathogenic steps.

Introduction The role of water and other fluids

Like other “well-being diseases” such as obesity, hypertension, The urine volume plays a huge role on the saturation of litho-
atherosclerosis, myocardial infarction and type 2 diabetes, genic salts. We used the computer program Equil (14) to simu-
nephrolithiasis is progressively on the increase in rich countries late the changes of the relative saturation for calcium oxalate,
(1, 2), being now a very common condition affecting in the USA calcium phosphate and uric acid when the urine volume in-
10% of the population (3) with an economic burden of about 2 creases from 0.5 to 3.0 L/day, while keeping constant all the
billion dollars per annum (4). other urinary parameters involved in the calculation of satura-
Only in extremely rare cases it is a result of hereditary or well- tion point. By this way, we saw that with diuresis below 1 L/day,

Clinical Cases in Mineral and Bone Metabolism 2008; 5(2): 135-141 135
A. Nouvenne et al.

even the urine of a normal subject reaches extremely high su- forming stones (8,9) a response not shared by the females of
persaturation levels, certainly high enough to promote sponta- the Nurses’ Health Study (6). Indeed, in younger women, ani-
neous crystallization of the lithogenic salts. If, on the other mal proteins exerted, if anything, a moderately protective ac-
hand, the volume is maintained over 2.5 L/day, the urine be- tion (7). However, in a nation-wide survey in the UK (32), vege-
comes undersaturated for calcium phosphate and uric acid and tarians showed a prevalence of urinary stone formation about
only slightly supersaturated for calcium oxalate, making spon- half that found in a sample taken from the general population
taneous crystallization impossible. Given that, in the context of matched for age, sex and social class.
these physiological variations in diuresis, ion excretion is large- As to the urinary stone risk factors, most studies found that ani-
ly independent of urine volume, this example simulates very mal proteins (meat, fish and poultry) have an unfavorable effect
closely what actually happens when water intake is high. because they increase calciuria, uricuria, and phosphaturia,
It could be argued that the increase in urine volume would di- while reducing citrate and urine pH (33). It has been estimated
lute the crystallization inhibitors, and thus offset its positive ef- that in normal subjects for every 25 g increase in dietary animal
fects on lithogenic salts. However, observations made on both protein, urinary calcium rises 32 mg (34). When overweight
normal subjects and idiopathic calcium stone formers dispel subjects (35) increased their habitual protein intake, from about
this argument because (a) the level of supersaturation required 90 g/day to approximately 170 g/day of largely animal proteins
to cause spontaneous calcium oxalate nucleation in diluted (Atkins diet) for 6 weeks, their calciuria rose by about 90
urine is greater than that required in the non diluted urine of the mg/day (2.25 mmol), uricuria by about 130 mg/day (1.3 mmol),
same subjects (15); (b) the oxalate amount one has to add to phosphaturia by about 620 mg/day (20.2 mmol), while their cit-
the diluted urine to produce calcium oxalate crystallization in raturia decreased by about 180 mg/day (0.9 mmol) and the
vitro is higher than that required in non diluted urine (16), and urine pH from 6.09 to 5.67. Some studies have reported that
(c) the inhibitory power of the macromolecules extracted from animal proteins also produce an increase in oxaluria (36). With
non diluted urine is not quantitatively different from that of the urine volumes kept unchanged, the final outcome of a high ani-
macromolecules extracted from non diluted urine (16). Finally, mal protein intake is an increase in supersaturation for both
studies in progress in our laboratory in both normal subjects calcium oxalate and uric acid. Even more relevant is the fact
and calcium stone formers show that the number and quantity that, at parity of animal protein load, these urinary effects seem
of calcium oxalate crystals and crystalline aggregates pro- more marked in stone formers, as though these subjects had a
duced with an oxalate load in vitro are markedly lower in dilut- sort of genetic hypersensitivity towards such foods (37).
ed urine than in non diluted urine. The mechanisms by which animal proteins produce these ef-
Increased urine volume might exert its antilithogenic effect also fects are only partially understood. The increases in uricuria
by reducing the transit time of renal intratubular fluids, thereby and phosphaturia are directly related to the high purine and
favoring the expulsion of the crystals (17) and inhibiting the for- phosphorus content of animal proteins. The increase in calci-
mation of Randall’s plaques (18). uria and the reduction in citraturia and urine pH are mainly at-
By converse, low urine volume is a lithogenic risk factor (19), tributed to the high content of sulphurated amino acids (methio-
as shown by cohort studies in which subjects consuming less nine and cysteine) which, by producing high quantities of hidro-
than 1.5 liters of fluid per day had about a 50% increase in inci- genions, cause a metabolic shift towards a state of subclinical
dence of kidney stone as compared to those consuming over acidosis (38). The mechanism of the increased oxaluria is less
2.5 L of fluid per day (6-9). clear. According to a widely quoted view, the oxalate precur-
Two trials are to be quoted about the beneficial effects of wa- sors present in animal proteins, such as the amino acids tyro-
ter. The first (20) showed that the incidence of kidney stones in sine, tryptophan, phenylalanine and hydroxyproline, cause an
a community living in warm climate and that had been educat- increase in endogenous oxalate production (39).
ed to drink more water was ten times lower than that detected It is important to point out that the vegetable proteins produce
in a matched community that had not been educated to do so; urinary effects different from those of the animal proteins. An
the second (21), a randomized-controlled study, showed that experiment was carried out on normal subjects in which 75
the calcium stone formers who increased their water intake in g/day of exclusively animal proteins were first replaced by an
order to increase their urine volume, from approx. 1 to approx. equal quantity of mixed ovo-vegetable proteins, then by exclu-
2 liters per day, during 5 years had a recurrence rate of 12 % sively vegetable proteins (40). The data show that with an ex-
as compared to 27% who had not changed their water intake. clusively vegetarian intake the urine contains less calcium, less
Whilst there is no doubt that the quantity of water consumed is phosphorus, more oxalate, more citrate and fewer acids. These
important for both the primary and secondary prevention (re- differences may be explained by the different content of
currences) of stone formation, it is still controversial whether purines, oxalates, sulfates and fibers. On the whole, these data
hard waters, i.e. rich in calcium and other minerals, are as ef- clearly indicate that vegetable proteins have a much lower lith-
fective as light waters (22). ogenic potential, particularly with regard to uric acid stone dis-
As to the fluids other than water, some reports (23-31) suggest ease.
that coffee, tea, beer, wine, orange juice, lemon juice and Only two randomized-controlled trials have been carried out to
blackcurrant juice can reduce the risk of stone formation, while evaluate the hypothesis that a reduction in animal proteins
grapefruit juice, apple juice, soda and cola drinks increase it. could prevent recurrences in idiopathic calcium stone disease.
In conclusion, the evidence currently available shows that a One showed that after a period of over 4 years the group treat-
water intake sufficient to increase urine volume to at least 2 ed with low animal protein and high fiber diet had a higher re-
liters/day exerts an antilithogenic effect. Some fluid such as or- currence rate (12/50 = 24%) than the control group (2/49 = 4%)
ange juice or lemon juice might elicit some additional benefits. treated with high fluid and a usual calcium intake (41). It should
be, however, pointed out that this trial had several major limita-
tions: a) the water intake in the control group was higher; b)
The role of proteins compliance with the low protein diet was actually very poor; c)
there may have been differences between the two groups as
As regards the effect of animal proteins, the findings from co- regards the intake of dietary calcium and fiber, both of which
hort studies are conflicting. The male subjects from the Health influence stone formation.
Professionals Follow-up Study, whose intake of animal proteins The other trial compared a low calcium diet (i.e., free of milk
exceeded 75 g/day (upper quintile) had the highest risk of and dairy products) with a low-animal protein, low-salt and nor-

136 Clinical Cases in Mineral and Bone Metabolism 2008; 5(2): 135-141
Dietary treatment of nephrolithiasis

mal calcium diet (42). After 5 years, the recurrence risk in the drate consumption, insulin resistance, diabetes mellitus and
first group was higher (23/60 = 38%) than in the other group obesity, the overall results of these studies enables us to con-
(12/60 = 20%), but it should be pointed out that, in this experi- clude that excessive consumption of carbohydrates, especially
ment, it was not possible to distinguish the protective effect of simple ones, should be considered as a risk factor for renal
the low animal protein intake from that due to the higher calci- stones, even if no prospective randomized trials exist on the re-
um and lower salt intake. al possibility of preventing stone recurrences by imposing a
All in all, the aforementioned dietary studies favor the view that suitable low glucide, low calorie diet on patients with such char-
subjects at risk for calcium or uric acid stone disease should acteristics.
avoid consuming large quantities of animal proteins.

The role of fats

The role of carbohydrates
Some observations suggest that fats are also implicated in
An increased intake of sucrose was found associated with stone formation. These observations can be briefly summa-
stone risk in women (6, 7), but not in men (9). rized as follows: stone formers show a high prevalence of hy-
It is well-known that an acute load of glucose causes a tran- percholesterolemia (54); high-fat, high-cholesterol diets can in-
sient calciuria rise in normal subjects and to an even greater duce stone disease in laboratory animals (55); urinary lipids
degree in idiopathic calcium stone formers and their relatives play a role in the formation of crystals and stones (56); fat in-
(43). Some investigators have conjectured that this effect is take is correlated with oxalate excretion (57), this relationship
mediated by insulin reducing the tubular reabsorption of calci- being more evident with regard to the dietary content of arachi-
um (44), but others refute this theory because, after comparing donic acid (58).
a diet with a high carbohydrate content (60% carbohydrates Other investigators found high levels of arachidonic acid in the
and 25% fat) with an isocaloric high-fat diet (50% fat, 35% car- plasma and membranes of red blood cells of stone formers
bohydrates), they did not find any differences in calcium excre- (59), probably related to hypercalciuria through an alteration in
tion, despite the higher levels of insulin in the subjects on the transmembrane ionic transport and overproduction of
higher carbohydrate diet (45). However, the comparison be- prostaglandin E2. These data concur with the demonstration
tween diets with low (220 g), medium (450 g) and high (600 g) that ω-3 fatty acid supplementation, in the form of eicosapen-
carbohydrate content, but unvaried in the content of proteins, taenoic acid (EPA) or fish oil, can reduce levels of arachidonic
fats and calcium, showed the level of urinary calcium to in- acid in plasma and tissue and this is accompanied by a de-
crease in proportion to the amount of carbohydrate intake (46). crease in the excretion of calcium and oxalate, both in humans
Moreover, optimal metabolic control in diabetic patients (60) and in laboratory animals (61).
through insulin therapy leads to a considerable decrease in cal- However, a recent observational study did not confirm the exis-
cium excretion (47). tence of an association between fatty acid intake and the de-
Surprisingly, after these early reports there have been no fur- velopment of kidney stones (62). Clinical trials testing the effi-
ther studies published on the relationship between carbohy- cacy on stone prevention of high doses of ω-3 polyunsaturated
drates and calcium stone disease. Rather, interest has shifted fatty acids in the form of fish oil supplements have never been
to the relationship between metabolic syndrome, type 2 dia- performed.
betes, insulin resistance and uric acid stone disease. The as-
sociation between body size and risk of kidney stones was not-
ed for the first time in 1998, and has recently been confirmed in The role of sodium chloride
both males and females (48). It is believed that insulin resis-
tance, frequently associated with excess body weight, can alter An association between salt consumption and calcium stone
the urine acidification mechanism. It has been established for formation was first reported in a large cohort study (6), but
some time now that gouty patients and uric acid stone formers some subsequent studies failed to confirm this finding (7, 9). It
in general stand out from the rest of the normal population and should, however, be recognized that it is very difficult to make
from calcium oxalate stone formers because they have a par- reliable estimates of dietary salt intake based on food question-
ticularly acid urine pH, lower than 5.5, which leads to a marked naires, as attempted in those studies.
increase in the undissociated form of uric acid which precipi- A number of interventional studies published since 1959, re-
tates in urine (49). viewed in 1995 (63), support the notion that salt consumption
The relation between glucose intolerance and uric acid stones invariably increases calcium excretion and, conversely, salt in-
have been thoroughly investigated. Some authors found that take reduction induces a decrease in calciuria. From these
uric acid stone formers have a high incidence of type 2 dia- studies it can be estimated that an average increase of 100
betes or glucose intolerance (50-52). These patients often mmol of salt (approx. 6 g of sodium chloride) generates an av-
show an increased urinary acidity due to a reduced capacity to erage increase in calciuria equivalent to 1 mmol of calcium (40
eliminate the acid load in the form of ammonium (50). The final mg) in normal adults and 2 mmol (80 mg) in hypercalciuric
result is a higher concentration of free H+ ions (low pH), higher stone formers. These findings have important practical implica-
titrable acidity and often a decrease in citraturia. Interestingly, tions if we consider that in some countries the average con-
stone formers with type 2 diabetes prevalently form uric acid sumption of salt is at least 10-12 g/day.
stones and show a urinary risk profile very similar to that of Another relevant observation is that the calciuric effect of sodi-
gouty patients (51). The authors hypothesized that insulin re- um chloride is additive to that of the proteins as shown by an
sistance in type 2 diabetes might impair renal ammoniogenesis experiment performed in normal subjects who increased their
resulting in a low urine pH. In a subsequent study, they further salt intake from 8 g to 12 g and their protein intake from 1 to 2
supported this hypothesis by showing that patients with recur- g/kg (64): calciuria increased by about 50 mg (1.25 mmol) with
ring uric acid stone disease have severe insulin resistance each modification and by 100 mg (2.5 mmol) with both modifi-
(52). A further study showed, in a large population of stone for- cations.
mers, that urine pH is strongly inversely associated with body It is important to point out that in literature the term “sodium” is
weight (53). very often employed as synonymous of salt. This is, however,
Therefore, considering the close relationship between carbohy- misleading because when other types of sodium salts, such as

Clinical Cases in Mineral and Bone Metabolism 2008; 5(2): 135-141 137
A. Nouvenne et al.

sodium bicarbonate and sodium citrate, were compared with 60 mg/day in the normocalciuric stone former, and as much as
sodium chloride on an equimolar basis, they did not increase 160 mg/day in the hypercalciuric stone former with a specific
urinary calcium (65, 66), leading to the conclusion that the cal- hypersensitivity to calcium intake. However, viewed in terms of
ciuria-producing effect of kitchen salt is due to its chloride con- urine supersaturation, the implication of the changes in oxalate
tent (67). excretion are anything but trivial: changing from the low calci-
There is substantial agreement that the salt increases calciuria um diet to a normal calcium diet does not increase calcium ox-
through its inhibiting effect on the tubular reabsorption of calci- alate supersaturation, but actually reduces it by approx. 10%.
um (68). Thirdly, when we recommend the dietary limitation of milk and
Additionally, it should also be pointed out that the increase in dairy products, patients are likely to increase their animal pro-
sodium chloride in the diet is also accompanied by a significant tein intake in the form of meat, fish and poultry, leading to all
decrease in urinary citrate (69), which on its own increases the the potential unfavorable consequences mentioned earlier.
lithogenic risk. The mechanism by which salt reduces urinary The pathophysiological considerations reported so far agree
citrate is uncertain. According to a widely-shared view, it is re- with the results achieved in large follow-up studies (6-9). Ac-
lated to the bicarbonaturic effect of the salt intake elicited by cording to these studies, the risk of becoming a stone former,
extracellular volume expansion causing a decrease in the ex- for men and women alike, is much lower in those who habitual-
tracellular pH. ly consume relatively high quantities of calcium (> 1000
Although there are no randomized studies testing the capacity mg/day) than in those who consume lower quantities (< 600
of a low salt diet to reduce kidney stone formation on its own, mg/day). Finally, a 5-year randomized study conducted on
there is evidence suggesting that a low salt intake may improve male hypercalciuric calcium stone formers showed that a low
the beneficial effects of a low animal protein intake (42). calcium diet, achieved through the elimination of milk and dairy
A balanced diet for the prevention of renal stones should con- products, is less efficacious in the prevention of stone recur-
tain no more than 6 g/day of sodium chloride, an amount also rences than a normal-calcium, low-animal protein, low-salt diet
fulfilling the recommendations provided in the updated report of (42).
the Joint National Committee on Prevention, Detection, Evalua- In conclusion, in the light of current knowledge, idiopathic stone
tion and Treatment of High Blood Pressure (70). To this end, it formers should not be deprived of normal quantities of milk and
is important to inform the patient about the “hidden sources” of dairy products.
salt.

The role of fruit and vegetables

The role of milk and dairy products
Doctors are hesitant in advising stone formers to eat fruit and
The recommended daily intake of calcium can be satisfied by vegetables, because these foods are the most important di-
foods such as milk (approx. 120 mg per 100 ml), yogurt (ap- etary source of oxalate, part of which is undoubtedly absorbed
prox. 120 mg per 100 g) and cheese (on average approx. 700 to be excreted with the urine. However, their higher urinary ox-
mg per 100 g). Abstaining from such foods leads to a very low- alate notwithstanding (77), vegetarians show a prevalence of
calcium intake (approx. 400 mg/day). stone disease about half that of omnivores (32).
Calcium intake affects calciuria: in normal subjects an increase How can we explain this apparent paradox?
in calcium intake brings about an increase in calciuria equiva- First of all, we must point out that only a few vegetables have
lent to 8% of the increased amount, rising to 20% in hypercalci- demonstrated to significantly increase oxaluria: spinach,
uric stone formers due to their peculiar ability to hyperabsorb rhubarb, beets, nuts, chocolate, tea, wheat bran and strawber-
intestinal calcium (71). This means, for example, that changing ries (78).
from a diet containing 400 mg of calcium to one containing Although a sizable proportion of urinary oxalate may derive
1200 mg, can increase calcium excretion in a normal subject from diet, up to 50% (79), there is great variability from person
from 120 mg/day to 180 mg/day, and in a hypercalciuric sub- to person in intestinal absorption rate. Since about 8-10% of id-
ject from 240 mg/day to 400 mg/day. This is the reason why, iopathic stone formers show hyperoxaluria (80) and 20-30% of
for many years now, physicians have been advising patients these show intestinal oxalate hyperabsorption (81), we can
with calcium stone disease to reduce or eliminate their intake reasonably assume that the problem of oxalate hyperabsorp-
of milk and dairy products. In the light of current knowledge, tion should affect no more than 2-3% of idiopathic stone form-
this indication does not appear to be sound for three important ers.
reasons. In the great majority of cases oxalate absorption rate is rather
Firstly, the low calcium diet may not succeed in reducing calci- low, about 6% with the usual dietary intake (79, 81), a propor-
uria in a large percentage of subjects (72), while it can cause a tion rising very little with the higher intakes due to the flattening
negative calcium balance (72) which, over prolonged periods, of the absorption process (79, 82). Hence, important variations
can lead to the onset of osteopenia/osteoporosis (73). in intake, namely from 50 mg/day to 250 mg/day, as it may oc-
Secondly, reducing calcium intake increases intestinal absorp- cur with a free diet, causes the oxaluria to usually increase 4-5
tion of oxalate (74,75). Oxalate is prevalently absorbed in the mg/day only (79). Perhaps this is due to the saturation of the
small intestine and colon, where, in the presence of high calci- transporters or to the supersaturation of calcium oxalate rising
um concentration, it can form non absorbable calcium oxalate to such a level in the intestinal lumen as to cause the crystal-
salt; conversely, if calcium level in this site is low, the oxalate lization of this salt hindering its absorption.
will be more easily absorbed in the form of sodium or potassi- Finally, as already mentioned previously, the absorption of di-
um oxalate. It has been estimated that oxalate excretion de- etary oxalate is strongly affected by the simultaneous dietary
creases by an average of 1.9 mg (0.02 mmol) for each 100 mg intake of calcium (74, 76). Some Authors have shown that
increase of calcium intake per day (76). For instance, a change even hyperoxaluria brought about by a high consumption of ox-
in daily calcium intake from 400 mg to 1200 mg brings about a alate-rich foods can be reduced by the simultaneous consump-
decrease in oxalate excretion from 40 mg/day to 24 mg/day. tion of milk and dairy products (83, 84).
The oxalate decrease of 16 mg/day might appear trivial when On the other hand, fruit and vegetables display an antilithogen-
compared with the concurrent increase in calciuria, which ac- ic effect.
cording to the example previously reported, should amount to In general, fruit and vegetables have a low content in protein

138 Clinical Cases in Mineral and Bone Metabolism 2008; 5(2): 135-141
Dietary treatment of nephrolithiasis

and sodium chloride, a high content in potassium and magne- 2. Advise patients to drink enough water to bring the urinary
sium, and a moderate alkalinizing potential deriving from an- volume up to at least 2 liters /day. It is extremely important to
ions such as bicarbonate and citrate. This peculiar composition instruct patients to drink the water a little at a time, and to con-
may explain some favorable effects of fruit and vegetables on sume a water load of approx. 500 ml before going to bed. An-
some of the most important urinary stone risk factors. It has other essential aspect is to show patients how to measure uri-
been shown that high potassium intake, inherent in the large nary volume by themselves periodically, e.g. once a month.
consumption of fruit and vegetables, is associated with a re- Other fluids may be consumed but not in substitution of water.
duced stone risk (6-9). It has also been shown that these foods If the patient consumes regular quantities of milk and dairy
can increase citrate excretion in patients with idiopathic calci- products, the water should not contain high quantities of calci-
um stone disease, up to curing conditions of pronounced um, e.g. not more than 100 mg/L, in order to avoid excessive
hypocitraturia in some cases (24, 25, 85). Moreover, they can calcium loads, especially between meals.
increase the excretion of magnesium (85), another calcium 3. Advise patients to limit animal protein intake, by reducing
crystallization inhibitor, and they can decrease calcium excre- above all the consumption of meat and its derivatives; the total
tion (86). Finally, they can increase the urine pH (85, 87) with of proteins deriving from meat, fish, chicken, eggs, milk and
favorable effects on the solubility of uric acid. cheese should not exceed 50-60 g/day.
By converse, the elimination of fruit and vegetables from the di- 4. Advise patients to avoid excessive carbohydrates. Refined
et of normal subjects causes unfavourable changes in stone ones, in particular, should not exceed 20 g per day. It might be
risk due to the significant increase in the supersaturation for useful to replace sucrose with sweeteners such as saccharine
calcium oxalate and calcium phosphate (85). or aspartame.
Give the above considerations, we encourage physicians to 5. Advise patients to avoid excess of saturated fats, shifting the
advise their patients to consume fruit and vegetables regularly, calorie requirement to foods rich in omega-3 fatty acids, such
regardless if they are calcium or uric acid stone formers, pro- as olive oil, anchovies, sardines and mackerel.
vided that they exercise moderation in the consumption of 6. Advise patients to limit sodium chloride consumption to no
foods known to elicit a marked hyperoxaluric effect. more than 6 g/day. To this end, it is extremely important for pa-
tients to be aware of the “hidden sources” of salt and to avoid
the use of mixed prepacked foods which tend to be very salty.
The role of vitamins 7. Advise patients to consume milk, yogurt and cheese regular-
ly, but not excessively and to avoid cheeses containing large
The vitamins most implicated in stone risk are vitamin D (cal- quantities of sodium chloride.
citriol), vitamin C (ascorbic acid) and vitamin B6 (pyridoxine). 8. Advise patients to consume fruit and vegetables daily, taking
A recent follow-up study did not find any association between care to avoid foods containing very high quantities of oxalate.
vitamin D intake and stone risk (9). It has been known for many 9. Do not give patients vitamin D supplements; allow, if re-
years, however, that some idiopathic hypercalciuric subjects quested, vitamin C supplements of not more than 1500 mg/
have an excess of calcitriol in the blood or, in any case, an day; avoid vitamin B6 deficiencies.
overregulation of its receptors, leading to hyperabsorption of in- 10. Advise patients to use, as far as possible, fresh or frozen
testinal calcium (88). Except in special cases, therefore, it is products, not prepacked or precooked foods. If this is not pos-
not advisable to give vitamin D supplements to stone formers, sible advise them to purchase products bearing a label on
especially in association with pharmacological calcium supple- which the content of sodium chloride and other nutrients are
ments. listed.
Vitamin C supplementation is a widespread practice due to its
alleged preventive action against tumors and degenerative dis-
eases. Being a precursor of oxalate and potentially capable of References
increasing oxaluria, vitamin C taken in excessive amount could
be dangerous in nephrolithiasis. Truly (89-100), high intakes of 11. Yoshida O, Terai A, Ohkawa T, Okada Y. National trend of the in-
ascorbic acid causes a rise in oxaluria, but of up to 1500 cidence of urolithiasis in Japan from 1965 to 1995. Kidney Int.
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