Coconut Water: An Unexpected Source of Urinary Citrate
Roshan M. Patel ,1Pengbo Jiang,1John Asplin,2Ignacio Granja,2Taylor Capretz,1
Kathryn Osann,3Zhamshid Okhunov,1Jaime Landman,1and Ralph V. Clayman1
1Department of Urology, University of California, Irvine, USA
2Litholink Corporation, Laboratory Corporation of AmericaHoldings, USA
3Department of Medicine University of California, Irvine, USA
Correspondence should be addressed to Roshan M. Patel; firstname.lastname@example.org
Received 3 May 2018; Revised 18 September 2018; Accepted 26 September 2018; Published 1 November 2018
Guest Editor: Ephrem Olweny
Copyright © Roshan M. Patel et al. is is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Purpose. Coconut water has long been touted for its medicinal qualities including natural hydration. We sought to determine
whether its consumption would induce changes to urinary lithogenic factors beyond changes in urine volume. Materials and
Methods. Aer Institutional Review Board approval, volunteers with no prior history of nephrolithiasis were recruited. Each
participant was randomized initially to either the coconut water or the water phase of the study. Participants kept meticulous
food and uid intake logs during the rst phase of the study and were asked to replicate that diet for the second phase. For each
phase the participant consumed L of either Taste of Nirvanapure coconut water or tap water daily for four days. Participants
were not restricted to consume additional uid of their choice during their assigned study phase. During days and of each
phase the participant collected a -hour urine specimen. Coconut water citrate and malate content were measured and were used
along with the beverage pH to calculate the total alkali content of the coconut water. Supersaturation levels were calculated using
Equil. Nonparametric paired analysis using the Wilcoxon test was performed for statistical analysis. Results. ere were adult
male and adult female participants. Each individual’s -hour urine collection had a creatinine excretion within % of the mean
for each subject’s four samples corroborating that all samples were collected properly. e two samples from each phase for each
individual were averaged. e coconut water itself was also analyzed and it was calculated to have a total alkali content of .
mEq/L. Consumption of coconut water signicantly increased urinary citrate (%, p=.), urinary potassium (%, p=.),
and urinary chloride (%, p=.), without aecting urine pH (p=.) or volume beyond that of tap water (p=.). Conclusions.
Coconut water consumption increases urinary potassium, chloride, and citrate in nonstone forming individuals.
e worldwide prevalence of kidney stones has increased
dramatically over the past few decades with calcium oxalate
nephrolithiasis continuing to be the most common type of
urolith in the United States of America. [, ] In patients with
calcium oxalate nephrolithiasis, hypocitraturia is found in up
to % of samples on quantitative -hour urine chemistry.
 e mainstay medical treatment in these patients is
potassium citrate; however, adherence to this supplement is
notoriously poor given the frequency to take the medications
(usually three times a day), the number of tablets needed,
cost, and side eects.  Alternatively, patients are also
counseled on dietary modications and they are encouraged
to increase their consumption of uids high in citrate content
(e.g., lemonade, crystal light).
(Cocos nucifera L.), which is the most naturally widespread
fruit plant on Earth.  Known to Hawaiian’s as Noelani,
meaning “dew from the heavens,” it is rich in electrolytes,
vitamins, minerals, cytokines, and proteins and has long been
touted for its medicinal qualities, including natural hydration,
high ber content, laxative and diuretic eect, antiaging
impact, antimicrobial properties, and energy enhancement.
coconut water, carbohydrate-electrolyte beverage and water.
 ey found that coconut water was well tolerated and
subjects reported having greater ease in consuming a large
BioMed Research International
Volume 2018, Article ID 3061742, 5 pages
BioMed Research International
T : Taste of Nirvana coconut water nutritional facts adjusted
to L serving size and % daily value adjusted according to FDA
Nutritional Facts % Daily Value
Serving size (L) . —
Total Fat (g)
Total Carb o hydr ate (g)
Sugar (mg) —
Protein (mg) —
Vitamin C —
amount of coconut water as opposed to an energy drink or
Gandhi et al. studied the eect of coconut water con-
sumption on ethylene glycol induced nephrocalcinosis in
male Wistar rats.  e study demonstrated that coconut
water consumption inhibited crystal deposition in renal
tissue and decreased the number of crystals in the urine.
However, the possible antilithogenic eects of coconut water
have never been studied in humans. An anecdotal patient
encounter piqued our interest in the potential of coconut
water as an antilithogenic natural substance. In the resulting
study, our primary goal was to determine the impact of
drinking coconut water on known urinary lithogenic factors.
2. Materials and Methods
Aer Institutional Review Board approval, adult volunteers
with no prior history of nephrolithiasis were recruited. Each
participant was randomized initially to either a coconut water
or a water phase. Participants kept meticulous food and
uid intake logs during the rst phase of the study and
were asked to replicate that diet for the second phase. For
each phase, the participant consumed .L of either Taste
of Nirvanapure coconut water or tap water daily for four
percent daily value are shown in Table . Participants were
not restricted with regard to the consumption of additional
uid of their choice during the study. On days and of each
phase the participant collected a -hour urine specimen. A
washout phase of a minimum of weeks and a maximum of
weeks between phases was implemented in this study.
Citrate and malate concentrations of the coconut water
were measured using ion chromatography (Dionex, Sun-
nyvale CA). Electrolytes were measured with ion specic
electrodes and pH was measured using a pH electrode. Total
alkali of the coconut water was calculated from the citrate and
malate concentrations, the beverage pH and the pKs of the
anions. e pK of tricarboxylic acid citrate used to calculate
T : Coconut water analysi s. Each can contains .L of c oconut
Taste of NirvanaPure Coconut Water
Citrate mM/L .
Malate mM/L .
To ta l A l k a l i m E q/ L .
Na mM/L .
Cl mM/L .
anion content was ., ., and . and for dicarboxylic malate
pK was . and ., respectively. e total alkali is expressed
in milliequivalents per liter (mEq/L). Supersaturation levels
were calculated using Equil.
Nonparametric paired analysis using the Wilcoxon test
was performed for statistical analysis. Analysis was con-
A total of subjects were recruited into this study: adult
males and adult females. e average age of the male
participants was . years (- years) and for female
participants years (-). Each individual’s -hour urine
collection had a creatinine excretion within % of the
mean for each subject’s four samples corroborating that all
samples were collected properly. e two samples from each
phase for each individual were averaged. e coconut water
alkali content was .mEq/L. Each can of Taste of Nirvana
contained .L of coconut water.
e average total urine volume for the participants was
.L during both the coconut water and water phase of
the studies. Consumption of coconut water signicantly
increased urinary citrate as compared to tap water by %
(p=.). In addition, consumption of coconut water as
compared to tap water increased urinary potassium by
%(p=.) and urinary chloride by % (p=.) (Table ).
Increases in urinary citrate, potassium, and chloride with
consumption of coconut water were similar for males and
females and for younger (<=) and older subjects (>).
Numbers in these subgroups were too small to obtain statis-
tical signicance in stratied analyses.
ere was no signicant alteration in urine volume,
urine pH, supersaturation of calcium oxalate and calcium
phosphate, urine calcium, and urine sodium.
Hypocitraturia, dened as urinary citrate excretion less than
mg per day for adults, is an important metabolic abnor-
mality in stone formers with an incidence as high as %
[, ]. Citrate is a well-known inhibitor of calcium stone for-
mation through multiple mechanisms, including complexing
with calcium, preventing nucleation of both calcium oxalate
and calcium phosphate, and blocking crystal agglomeration
BioMed Research International
T : Mean values from -hour urine.
Wat e r S D ∗Coconut Water SD∗p-value
Volume (L/d) . . . . .
SSCaOx . . . . .
Ca (mEq/d) .
Oxalate (mEq/d) . . . .
Citrate (mEq/d) .
SSCaP . . . . .
pH . . . . .
SSUA . . . . .
Uric Acid (g/d) . . . . .
Na (mEq/d) . . .
K (mEq/d) . . .
Mg (mEq/d) . .
P(g/d) . . . . .
NH4 (mEq/d) . . . . .
Cl (mEq/d) . . .
Sulfate (mEq/d) . . . . .
Urea N (g/d) . . . . .
Creatinine (mEq/d) .
∗SD: standard deviation.
BioMed Research International
and growth . Oral potassium citrate, available in various
forms, increases urinary citrate levels and urinary pH; it is the
main treatment for hypocitraturia associated nephrolithiasis
Despite its proven ecacy, compliance with potassium
term follow-up of stone formers who were treated with
potassium citrate, only % consistently took the medication
. In addition, given that potassium citrate therapy is costly,
upward o USD/month for three times daily dosing of
meq, alternative dietary therapies have been evaluated .
reported to signicantly increase urinary citrate levels .
some doubt on the eectiveness of lemonade therapy. Ko et
al. performed a crossover design trial comparing potassium
dierence in urinary citrate or urine pH in the lemonade
group, while the potassium citrate group demonstrated sig-
pH (%). Using controlled metabolic conditions, Odvina
and colleagues measured urinary stone risk factors and
demonstrated that orange juice had a greater alkalinizing and
urinary citrate per ml of orange juice was mg compared
to only mg during lemonade consumption. Similarly, uri-
nary pH was higher by . units in the orange juice group
compared with lemonade and control phases of the study.
Halebian et al. performed quantitative analysis of citrate
content amongst commercially available beverages. Grape-
tent (.mmol/L), followed by lemon juice (.mmol/L),
orange juice (.mmol/L), pineapple juice (.mmol/L),
and home-made lemonade (.mmol/L). Crystal Light had
the highest concentration of citrate (.mmol/L) among
non-juice beverages . However, because of how the body
absorbs and metabolizes citrate, only a small amount of
dietary citrate reaches the urine. Instead, urinary citrate
excretion depends closely on acid-base physiologic states. In
a state of acid loading, the proximal tubule reabsorbs citrate.
On the contrary, during alkali loading, there is decreased
renal tubule reabsorption of citrate, which thereby increases
urinary citrate excretion .
Given the importance of systemic alkalinization and its
eect on renal citrate handling, Eisner et al. analyzed lemon-
ade and diet sodas to determine citrate and malate as alkali
as alkali, far lower than several other beverages such as Diet-
Up (. mEq/L), Diet Sunkist Orange (. mEq/L), and
Sierra Mist Free (. mEq/L). e pH of lemonade is usually
less than , so most citrate in lemonade is present as citric
acid, limiting the amount of alkali delivered. e majority of
beverages tested did not have signicant measurable malate
as alkali, except for Diet Sunkist Orange, Diet Canada Dry
Ginger Ale, and Diet Orange Crush. e total alkali content
was highest in Diet Sunkist Orange (. mEq/L), Diet-Up
(. mEq/L), and Diet Canada Dry Ginger Ale (. mEq/L)
. Of note, coconut water, at . mEq/L, has far greater
In our study, despite relatively low citrate content (.
mmol/L), coconut water therapy revealed a signicant
increase in urinary citrate excretion from baseline (mean
increase of mg/d). is citraturic eect is likely due to the
very high total alkali load (. mEq/L), which is higher than
e high total alkali load is mainly a function of the high pH
of coconut water and the malate content. Of note is that this
increase in citrate occurred in nonstone forming individuals
with a normal citrate at baseline; whether there would be a
stone-formers has yet to be tested. Interestingly, we did not
record a signicant change in urinary pH. Our ndings
also revealed signicant increase in urinary potassium and
chloride, which may be explained by the high potassium
and chloride content of coconut water. e coconut water
studied contains approximately mg/L (. mEq) of
potassium, which is % of the Food and Drug administration
daily recommended value for adults . Of note, potassium
Of interest, coconut water contains a signicant amount
of chloride, which is unusual for a fruit beverage. Potassium
content of a beverage is oen used as a gauge of alkali content
on the assumption that most potassium is accompanied by
organic anions. In coconut water, this assumption is not
point highlights the need for direct measurement of organic
anions and pH to assess the alkali content of a beverage.
e ideal dietary therapy for decreasing urinary stone risk
factors should be low in calories, animal protein, sodium, and
oxalate and high in citrate and total alkali load. Compared to
commercially available grapefruit and orange juice, coconut
water has approximately % less calories and % less
sugar content.While there is less overall citrate content
compared to other citrus beverages, the very high alkali
load is associated with a signicant and substantial citraturic
eect. Indeed, coconut water may represent a more ideal
beverage for increasing urinary citrate compared to lemon
juice, lemonade, and other beverages.
To our knowledge, this is the rst analysis of coconut
water for its antilithogenic properties in humans and the
results are promising. Additionally, dierences in pH and
supersaturation of calcium oxalate between the two groups
may have reached signicance if suciently powered. We
chose initially to include only individuals with no prior
history of nephrolithiasis to determine if coconut water
consumption would change urinary stone risk factors. Future
studies with larger sample sizes are needed to evaluate if the
citraturic eect of coconut water is operational in calcium
stone forming patients with hypocitraturia.
Coconut water consumption increases urinary potassium,
chloride, and citrate in nonstone forming individuals without
altering the urine pH.
BioMed Research International
e datasets generated during and/or analyzed during the
current study are available from the corresponding author on
Conflicts of Interest
e authors declare that there are no conicts of interest
regarding the publication of this article.
is study was funded by the UC Irvine Department of
 C. D. Scales Jr., A. C. Smith, J. M. Hanley et al., “Prevalence of
kidney stones in the United States,” European Urology,vol.,
p. , .
ciuria and formation of calcium renal stones,” Nature Reviews
ment of stone disease,” Current Opinion in Urology,vol.,no.
, pp. –, .
long-term medical treatment of kidney stones,” e Journal of
 E.B.C.Lima,C.N.S.Sousa,L.N.Menesesetal.,“Cocos nucifera
(L.) (Arecaceae): a phytochemical and pharmacological review,”
Brazilian Journal of Medical and Biological Research,vol.,no.
, pp. –, .
position and biological properties of coconut (Cocos Nucifera
L.) water,” Molecules,vol.,no.,pp.–,.
 M. Saat, R. Singh, R. G. Sirisinghe, and M. Nawawi, “Rehy-
dration aer Exercise with Fresh Young Coconut Water,
Carbohydrate-Electrolyte Beverage and Plain Water.,” Journal of
Physiological Anthropology and Applied Human Science,vol.,
eect of coconut water (Cocos nucifera L.) on ethylene glycol
induced nephrocalcinosis in male wistar rat,” International
Brazilian Journal of Urology,vol.,no.,pp.–,.
 L. L. Hamm and K. S. Hering-Smith, “Pathophysiology of
hypocitraturic nephrolithiasis,” Endocrinology and Metabolism
Clinics of North America,vol.,no.,pp.–,.
 C. Y. C. Pak, “Medical management of urinary stone disease,”
Nephron Clinical Practice, vol. , no. , pp. c–c, .
 E. S. Hyams, R. Gupta, J. Melamed, S. S. Taneja, and O. Shah,
“Renal involvement by chronic myelomonocytic leukemia
requiring nephroureterectomy,” Reviews in Urology, vol. , no.
, pp. –, .
 D. Mattle and B. Hess, “Preventive treatment of nephrolithiasis
Britton, “Long-Term Treatment of Calcium Nephrolithiasis
with Potassium Citrate,” eJournalofUrology,vol.,no.,
pp. –, .
 C. Jendle-Bengten and H.-G. Tiselius, “Long-term follow-up
of stone formers treated with a low dose of sodium potassium
citrate,” Scandinavian Journal of Urology,vol.,no.,pp.–
 GoodRx, “Potassium Citrate,” , https://www.goodrx.com/
 M. A. Seltzer, R. K. Low, M. Mcdonald, G. S. Shami, and
M. L. Stoller, “Dietary manipulation with lemonade to treat
hypocitraturic calcium nephrolithiasis,” e Journal of Urology,
vol. , no. , pp. –, .
 S. G. Ko, E. L. Paquette, J. Cullen, K. K. Gancarczyk, P.
R. Tucciarone, and N. S. Schenkman, “Comparison Between
Lemonade and Potassium Citrate and Impact on Urine pH
and -Hour Urine Parameters in Patients with Kidney Stone
 C. V. Odvina, “Comparative value of orange juice versus
lemonade in reducing stone-forming risk.,” Clinical journal of
the American Society of Nephrology : CJASN,vol.,no.,pp.
 G. E. Haleblian, V. A. Leitao, S. A. Pierre et al., “Assessment of
citrate concentrations in citrus fruit-based juices and beverages:
Implications for management of hypocitraturic nephrolithia-
sis,” Journal of Endourology,vol.,no.,pp.–,.
 B. H. Eisner, J. R. Asplin, D. S. Goldfarb, A. Ahmad, and M. L.
Stoller, “Citrate, Malate and Alkali Content in Commonly Con-
sumed Diet Sodas: Implications for Nephrolithiasis Treatment,”
e Journal of Urology, vol. , no. , pp. –, .
 F. A. D. Administration, Ed., Labeling Daily Values,.