Narrative Review

Dietary Modeling of Foods for Advanced CKD Based on General

Healthy Eating Guidelines: What Should Be on the Plate?
Maria Chan, MNutrDiet, GradDip, Ex&Sp, PhD, AdvAPD,1,2,3,4
John Kelly, MBBS, MD,3,4 and Linda Tapsell, PhD, FDAA, AM 2,5

Chronic kidney disease (CKD) is a major public health problem with significant clinical, societal, and psy-
chosocial burdens. Nutrition therapy has been an integral part of the medical management of patients with
CKD for more than a century, with the main goals of preserving kidney function and preventing complications.
Nutrition abnormalities may emerge well before dialysis therapy is initiated and are associated with poor
outcomes. It is therefore important to revisit nutrition management in the advanced stages of CKD to gain a
broader insight into its role and effect on patient outcomes. Traditionally, nutrition recommendations have
focused on the prescription of energy (calories) and macro- and micronutrients. Today, dietary modeling also
focuses on the evidence for food consumption on health. This review argues that advanced non2dialysis-
dependent CKD nutrition requirements to a large extent align with healthy eating guidelines for the general
population and should not be based on deprivation or be unusually restrictive. The best currently available
evidence for the CKD diet is likely to be derived from CKD nutrition prescriptions in conjunction with evidence
underpinning national dietary guidelines and evidence of healthy dietary patterns, such as Mediterranean-style
and Dietary Approaches to Stop Hypertension (DASH)-style eating. Positive messages from these dietary
patterns should improve acceptance of CKD dietary interventions among patients.
Am J Kidney Dis. -(-):---. 2016 by the National Kidney Foundation, Inc.

INDEX WORDS: Nutrition; foods; chronic kidney disease (CKD).

Maria Chan, MNutrDiet, Grad Dip, ExSpSc, PhD, AdvAPD,

was the Joel D. Kopple Award recipient at the 2015 National
Kidney Foundation Spring Clinical Meetings. This award was
established to honor an individual who has made significant
contributions to the field of renal nutrition.
N utrition is vital for optimum health because it
contributes to both survival and social needs. In
chronic kidney disease (CKD), the failing kidney loses
its principal functions of excretion and homeostatic
and hormonal regulation. Therefore, nutritional man-
agement must consider the complex interaction of
these inter-related factors affecting the patients before
dialysis therapy is needed (Table 1). Evidence-based
nutrition practice guidelines1-4 provide guiding
principles for managing these patients nutrition
requirements during the course of deteriorating kidney
function (Fig 1). The goals of dietary intervention are
to preserve kidney function with an aim toward
improving the quality and quantity of life (Box 1).
Dietary recommendations are based on prescription of
energy and nutrient levels that are derived from kidney
metabolic studies,5,6 for example, protein, sodium,
potassium, phosphorus, and uids, whereas optimal
intake of all other essential nutrients must also be
considered. These may be deduced from that of the
general population when limited data are available
(Table 2). Furthermore, dietary modications must
also consider the associated comorbid conditions, such
as cardiorenal syndrome,7,8 diabetes,9 obesity,10 and the
detrimental effects of malnutrition or protein-energy
wasting.11 In the non2dialysis-dependent CKD pop-
ulation, the prevalence of malnutrition could be as
high as 41%,12 with the carry-on effects predicting
mortality before and after dialysis therapy is
needed.13,14 Although nutrient considerations remain,
consuming adequate amounts of food remains impor-
tant. Food delivers nutrients, and food synergy is an
emerging concept that acknowledges the coordinated
effects of all biological constituents of food (including
nutrients) on health.15 Dietary modeling is an applied
mathematical system that translates the science of
energy and nutrient requirements into food-based
knowledge in developing dietary guidelines.16 The
aim is to meet the nutritional requirements of specic
target populations.
From the 1Department of Nutrition and Dietetics, The St.
George Hospital, Kogarah; 2Department of Nutrition and
Dietetics, School of Medicine, University of Wollongong,
Wollongong; 3Department of Renal Medicine, The St. George
Hospital, Kogarah; 4St. George Clinical School, School of
Medicine, The University of New South Wales; and 5Illawarra
Health and Medical Research Institute, University of Wollongong,
Wollongong, NSW, Australia.
Received March 22, 2016. Accepted in revised form September
19, 2016.
Address correspondence to Maria Chan, MNutrDiet, Grad Dip,
ExSpSc, PhD, AdvAPD, Department of Nutrition and Dietetics,
The St. George Hospital, Kogarah, New South Wales 2217,
Australia. E-mail: maria.chan@health.nsw.gov.au
 2016 by the National Kidney Foundation, Inc.
0272-6386
http://dx.doi.org/10.1053/j.ajkd.2016.09.025

Am J Kidney Dis. 2016;-(-):--- 1

 Chan, Kelly, and Tapsell

Table 1. Factors Causing Nutrition Abnormality in NonDialysis-Dependent CKD

Decreased Function
and Other Causes Factors Nutritional Abnormality

CKD related
Decreased excretion/ Uremia; buildup of fluid, electrolytes, metabolites, and
accumulation toxins; decreased urine output
Regulation/uncontrolled Acidosis; hypertension; glucose and lipid abnormalities;
homeostasis increased fibroblast growth factor 23
Hormonal imbalance Insulin resistance; increased parathyroid hormone/
osteodystrophy; decreased erythropoietin/anemia;
glucose intolerance; increased leptin
Altered bioavailability and metabolism of
nutrients; symptoms (eg, nausea, poor
appetite, gastrointestinal symptoms, taste
aversion) leading to decreased
spontaneous dietary intake, food phobia;
increased potassium, phosphorus, and
uric acid; fluid retention; augmentation of
proteinuria
Increased protein degradation and wasting,
serum lipids, and glucose
Increased protein wasting; altered vitamin
D/calcium/phosphate requirements;
increased iron, vitamin B12, and folate
requirements; increased lipids

Other related clinical Cardiorenal syndrome; intestinal barriers/altered gut
factors microbiota; comorbid conditions, eg, diabetes;
increased inflammation; increased oxidation stress;
obesity; medications; frequent hospitalization
Age and life cyclerelated Older age (.65 y); osteoporosis; sarcopenia; poor
factors dentition; increased physical inactivity; decreased
functional capacity, independence, and memory
Psychosocial factors Depression; loss of income; poor habitual eating habits;
poor nutrition knowledge, including from inappropriate
internet searching; poor food preparation skills;
perceived treatment burden
Abbreviation: CKD, chronic kidney disease.
Altered nutrient availability and metabolism,
nutrition requirements; drug-nutrient
interaction
Decreased dietary intake; altered vitamin
D/calcium/phosphate requirements;
decreased ability to obtain/prepare foods
Decreased dietary intake and/or quality;
decreased quality of life

National dietary guidelines provide guidance for
the general population on eating for better health.17,18
For example, the Australian Dietary Guidelines aim to
promote health and well-being and reduce the risk
for diet-related conditions, such as hyperlipidemia,
hypertension, obesity, and chronic diseases such as
type 2 diabetes and cardiovascular (CV) disease
(CVD) in generally well adults.17 Optimal levels of
energy and nutrients are then recommended to avoid
deciency and toxicity and minimize factors pro-
moting chronic disease.19 Foods of similar nutrient
proles are categorized into the principal core food
groups of grains, fruits and vegetables, lean meat or
meat alternatives, dairy products, and fats. These are
then modeled into dietary patterns containing foods of
sufcient quality and quantity to meet individuals
daily requirements.20 The aim of this review is to
outline the effects of foods and food components
related to the healthy eating guidelines with reference
to the development of diet plans for the CKD popu-
lation (Table 3).
GRAIN FOODS
Cereals, bread, rice, and pasta provide the body
with energy from carbohydrates, which inuence
blood glucose levels, and B vitamins, which are
important metabolic promoters. Whole grain foods
are known to reduce blood cholesterol levels,21
modulate blood glucose levels,22,23 and add meta-
bolically inert insoluble ber to the diet. Bran, for
example, regulates gut function and defecation.
Fermentable bers, such as resistant starches, resist
digestion in the small intestine and instead produce
metabolites in the colon, such as short chain fatty
acids, yielding potential effects on colon cancer and
metabolic disease prevention. The latter include
obesity and diabetes, with low glycemic index prop-
erties supporting lower postprandial glucose levels
and the corresponding insulin response.24,25 Raw oats
and barley are good sources of resistant starches.
Resistant starches also act as a synbiotica
combination of prebiotics and probiotics26,27
suggesting an important role in reducing gut dysbiotic
microbiota and hence uremic toxin production.28,29
Probiotics in supplement forms have been shown to
benet kidney health by various mechanisms,
including serum uremic toxin level reduction through
competitive colonization30 and a reduction in serum
homocysteine and triglyceride levels through
increased bacterial production of B vitamins,
including folate.31 A short-term synbiotic supplement
use in a randomized controlled trial (RCT) in patients
with CKD demonstrated a small but signicant

2 Am J Kidney Dis. 2016;-(-):---

Nutrition for Advanced CKD
Figure 1. Nutrition and lifestyle
interventions in the trajectory of
nondialysis-dependent chronic
kidney disease (CKD). Abbrevia-
tions: BP, blood pressure; CV,
cardiovascular; GFR, glomerular
filtration rate; PEW, protein-energy
wasting.
reduction in p-cresyl sulfate, a nephrovascular
toxin.32 The effect of synbiotics from whole foods on
uremic toxin metabolism has not been explored.
In the non-CKD population, strong inverse corre-
lations between whole grain consumption and
inammation, CV markers, risk for myocardial
infarction, and mortality have been observed.33-36
However, such ndings were inconsistent in other
observational37 and interventional38,39 studies,
probably due to heterogeneity in study duration,
types of whole grain ingested, and other lifestyle
factors. In a CKD cohort, high dietary ber intake
was inversely associated with inammation markers
and all-cause mortality, with a dose-response benet.
For each 10-g/d increase in total ber intake, the
odds of elevated serum C-reactive protein (CRP)
levels decreased by 38%.40 Stratied analysis
showed that total, soluble, and insoluble ber were
all associated with reduced inammation. These
protective effects are thought to be related to its
antioxidant anti-inammatory properties and altered
colonic bacterial metabolism.41 Whole grain con-
sumption has been associated with improvement in
body weight and/or body composition in the non-
CKD population.30,42 Although obesity is a risk
factor for CKD progression,43,44 the role of dietary
ber in managing overweight patients with CKD is
limited.
Despite the potential benets, 80.4% of patients
with CKD do not consume sufcient dietary ber
from grains and plant foods.12 Whole grain products
Am J Kidney Dis. 2016;-(-):---
form an important part of both the Mediterranean45
and the Dietary Approaches to Stop Hypertension
(DASH) dietary patterns.46 Traditionally, patients
with dietary potassium and phosphate restrictions are
advised to consume rened grain products instead.
Phosphorus in plants is mostly in the form of phytate,
and absorption in the gut is low (approximately 20%-
40%) compared with animal (40%-60%) or food ad-
ditive (w90%) sources.47,48 Therefore, it is feasible to
include whole grain in the diet of patients with CKD.
The general recommended minimal intake of grain
foods is 6 servings per day for a healthy 70-kg man.20
However, one must be careful with baked products
made with self-rising our and baking powder, which
Box 1. Goals of Nutritional Management in NonDialysis-
Dependent CKD Stages 3b to 5
General goal for all nondialysis-dependent CKD
 To preserve kidney function
 To maintain optimal nutritional status
 To delay onset of and alleviate uremic symptoms
 To correct electrolyte, metabolic, and fluid imbalances
 To prevent complications
 To reduce cardiovascular risk
 To improve quality of life and patient-centered outcomes
Additional goals for predialysis care
 To postpone need for dialysis
 To aim for a healthy initiation of dialysis
Additional goals for conservative management
 To improve quantity of life
Abbreviation: CKD, chronic kidney disease.
3
 Chan, Kelly, and Tapsell

Table 2. Nutrition Requirements for General Population and People With NonDialysis-Dependent CKD Stages 3b to 5

Recommendation

Energy and Nutrients General Population NDD-CKD

Energy, kcal/kg IBW/da 30-35b w30 for .60 yc,d; w35 for ,60 yc,d; and no less than 25e
Protein, g/kg IBW/d 0.84 for maleb; 0.75 for femaleb; w0.8 (range, 0.75c-1.00)d; 0.6 if severe
w1.0 for elderlyb symptomsc
Protein, % energy w15-20b 10-20d
Fat, % energy w30b w30d
Carbohydrate, % energy w50b w50d
Alcohol, % energy
Monounsaturated fat, % total fat w45b w45d
Polyunsaturated fat, % total fatf w45b; (including omega-3: w45d (RDI)g
160/610 mg for male,
90/430 mg for female)
Saturated fat, % total fat 8-10b ,7d
Vitamin B1, thiamine, mg/d 1.1-1.2b RDIg
Vitamin B2, riboflavin, mg/d 0.9-1.6b RDIg
Vitamin B6, pyridoxine, mg/d 1.3-1.7b RDIg
Vitamin B12, cyanocobalamin, mg/d 2.4b RDIg (may require supplementation)
Niacin, mg/d 14-16b RDIg
Folate, mg/d 400b RDIg (may require supplementation)
Vitamin A, retinol, mg/d 700-900b RDIg
Vitamin C, ascorbic acid, mg/d 45b RDIg
Vitamin D, ergocalciferol, mg/d 5.0 (19-50 y)b RDIg (may require supplementation)
10-15 (.50 y)b
Vitamin E, tocopherol, mg/d 7-10b RDIg
Sodium, mmol/d 20-40 adequate intakeb; 100, ,100d
tolerable upper levelb
Potassium, mmol/d 70-100 adequate intakeb 40-70 or w1 mmol/kg/dd if required
Calcium, mg/d 1,000-1,300b RDIg (may require supplementation)
Phosphorus, mg/d 1,000b 800-1,000d (if required, adjusted for
protein and PO4 binders)
Iodine, mg/d 150b RDIg
Iron, mg 8b (18 for female [19-50 y])b RDIg (may require supplementation)
Magnesium, mg/d 310-400b RDIg
Zinc, mg/d 8-14b RDIg
Dietary fiber, g/d 25-30b RDIg
Water, L/d 2.6 for maleb; 2.2 for femaleb Depending on balance
Abbreviations: CKD, chronic kidney disease; IBW, ideal body weight; NDD, nondialysis-dependent; RDI, recommended daily
intake.
a
Adjusted for age, sex, and activity level to maintain or attain IBW.
b
RDI, or other recommendations from National Health and Medical Research Council nutrient reference values for the general
Australian population.19
c
NKF-KDOQI (National Kidney Foundation2Kidney Disease Outcomes Quality Initiative) guidelines.1
d
Evidence-based practice guidelines for the nutritional management of chronic kidney disease, Australia.2
e
Protein-energy wasting classification.
f
For risk reduction of chronic diseases.
g
Limited data in CKD, refer to RDI levels.

are high in sodium and phosphate (namely, the
aerating agent calcium phosphate); reading food
labels remains important.
FRUITS AND VEGETABLES
Fruits and vegetables are a rich source of carbo-
hydrates; vitamins A (b-carotene), C, and E; potas-
sium; magnesium; and dietary ber. Green leafy
vegetables also provide iron and folic acid, whereas
legumes and dried beans are important vegetable
proteins. Other important constituents are phyto-
chemicals such as antioxidants, isoavones, avo-
noids, and polyphenols. Strong inverse associations
between consumption of fruits and vegetables and
CV risk and mortality have been observed in the
general population.49-51 Intervention studies of spe-
cic dietary patterns that emphasize high fruit and
vegetable consumption as in the Mediterranean and
DASH diets have shown reductions in mortality risk
and blood pressure, respectively.45,46 These bene-
cial effects could be related to several mechanisms:

4 Am J Kidney Dis. 2016;-(-):---

Nutrition for Advanced CKD
B vitamins and folic acid lower homocysteine
levels52 to prevent oxidative stress and endothelium
damage53; antioxidant vitamin C, avonoids, and
carotenoids prevent the oxidation of cholesterol in
the arteries54; and potassium and magnesium have
antihypertensive effects.55 In isolated supplement form,
these substances have not shown signicant clinical
benets in either the non-CKD56,57 or CKD pop-
ulations.52,58-60 Polyphenols found in blueberries and
lingonberries counteract inammation, oxidative
stress, and dysfunctional carbohydrate metabolism
and may play a role in reducing CV risk and CKD
progression.10,61
Controlled feeding studies in hypertensive patients
with CKD have shown alkali-inducing effects com-
parable to sodium bicarbonate in decreasing levels of
markers of kidney injury and preserving kidney
function without causing hyperkalemia.62-64 In these
studies, patients were advised to consume their usual
ad libitum diets with customized amounts of alkaline-
inducing fruits and vegetables (eg, apples, potatoes,
and spinach) to lower the potential renal acid load65
by half.
Fruits and vegetables are rich in nitrate, which
produces nitric oxide (NO) to initiate and maintain
endothelial vasodilatation. Low bioavailability of NO
may increase the risk for hypertension and CVD,66
both common in NO-decient patients with
CKD with decreased kidney NO production and
activation.67
Fructose is a sugar found in fruit. However, it
should not be mistaken for the undesirable effects from
excess fructose intake in the form of high-fructose corn
syrup found in sugar-loaded processed products,
including soft drinks. High-fructose corn syrup has
been associated with obesity, metabolic syndrome,
and uric acid production in the general and CKD
populations.10,68,69 Fruits and vegetables should not be
omitted from the diet to control potassium or fructose
intake because such practice may not only lead to
nutrient deciency and low-ber2related con-
stipation, but also deny the functional benets. In
non-CKD populations, lowglycemic index fruits and
vegetables (and grain foods) appear benecial in
reducing insulin resistance,70 levels of inammatory
markers (CRP),71 and uric acid levels72 and improving
glycemic control in diabetes,73 but the benecial ef-
fects on other metabolic parameters and CV risks
remain controversial.74,75 Although the effects of a
lowglycemic index diet in CKD require further study,
most ber-rich foods have a relatively low glycemic
index that may benet patients with CKD.
A U-shaped relationship exists between serum
potassium levels and mortality.76 Therefore, careful
fruit and vegetable choices and monitoring of
potassium-affecting medications, including diuretics
Am J Kidney Dis. 2016;-(-):---
and angiotensin-converting enzyme inhibitors, are
required.
The national 2 fruits & 5 vegetables campaign77
guides Australians toward healthy fruit and vegetable
consumption, which is applicable to CKD. Despite
the known benets of fruit and vegetable consump-
tion, intakes remain poor in both the general78 and
CKD populations.12
MEAT AND MEAT ALTERNATIVES
Overview
Meat and meat alternatives are the main source of
protein in the diet. Healthy choices include lean cuts
of meat, skinless poultry, eggs, sh, seafood, and
plant-based protein foods such as legumes, dried
beans, nuts, and seeds.
Optimal Protein Intake
Patients with CKD are in the chronic state of pro-
tein intolerance or protein waste intoxication, and
limiting dietary protein intake has been a common
practice to control uremia, alleviate symptoms, and
delay CKD progression,79,80 with supportive evidence
from a meta-analysis of RCTs.81 However, the
efcacy and safety of a low-protein diet in CKD is
still debated82-84 (Table 4). To date, answers to
optimal levels and types of protein foods,
including animal versus plant-based proteins, remain
controversial.81,85-87
The estimated average requirement of protein for
healthy adults is w0.6 g/kg/d, and the recommended
daily intake (RDI) is 0.75 g/kg/d with added safety
factor.88,89 In nondialysis-dependent patients with
CKD, ingestion of w0.6 g/kg/d of protein with
w25 kcal/kg/d could achieve neutral nitrogen balance
and enable consistent positive balance with improved
body mass at 30 to 35 kcal/kg/d.90,91 The traditional
low-protein diet was then set at w0.6 g/kg of ideal
body weight (IBW)/d, or up near RDI levels of
w0.75 g/kg IBW/d if not accepted by patients.1 In
CKD, high92-94 or free protein81,95 intake is asso-
ciated with increased proteinuria and faster progres-
sion rate, therefore such practices are discouraged.
Summing up these rationales, the common kidney
guidelines recommend w0.8 (range, 0.75-1.0) g/kg
IBW/d and 30 to 35 kcal/kg IBW/d of protein and
energy, respectively1-4; they must be adjusted to attain
healthy body weight and for age because the elderly
population requires higher protein of w1.0 g/kg
IBW/d.89,96 Most importantly, protein and energy
recommendations for CKD are comparable to those
for the healthy population. However, the habitual
protein intake in Australia and other typical Western
diets is well in excess of requirements, at approxi-
mately twice the RDI level.97-99
5
 6

Table 3. Benefits of Food for General, CV, and Kidney Health

Nutrient Intake Could

Be in Excess
in CKD if Food
Choice Is Inappropriate Important Food Components Benefits

Food (General Advice for the Dietary Pre- and Flavonoid/

Adult Population) Main Nutrient(s) Protein Na K PO4 Fiber Probiotics Antioxidants Isoflavones CV Health Kidney Health

Core food groups

Bread, cereals, and grain products Carbohydrates, PO4, Vit U U U U U U Decreased CRP (E); Decreased CRP (E);
(wholemeal/whole grain products) B and E decreased MI risk (E); decreased
low glycemic index: mortality (E)
increased insulin
sensitivity (I), decreased
uric acid (I) and CRP (I)
Fruit & vegetables (choose a variety Vit A, C, K, and Mg, U U U U U Decreased BP (I) and CV Decreased inflammation
of colored vegetables in season; folate, iron in green and all-cause mortality and oxidative stress
see plant-based protein foods leafy vegetables (E); low glycemic index: (E), acidosis (I),
below for other vegetables, eg, increased insulin markers of kidney
legumes) sensitivity (I), decreased injury (I), and drop in
uric acid (I) and CRP (I) eGFR (I)
Meat and meat alternatives Protein, PO4, iron, zinc, U U U Plant-based Plant-based Plant-based Plant-based Fatty fish: decreased CV Controlled protein: see
(including eggs; plant-based iodine, Vit B including proteins proteins proteins proteins and all-cause mortality Table 4 for supporting
proteins, eg, dried beans, B12; omega-3 fatty U U U U (E) and risk for MI, IHD, use; plant-based
legumes, nuts, seeds; lean cuts of acids and Vit D (in oily and stroke (E); plant- protein, especially
meat, skinless poultry, fish, fish); Vit E (in nuts); n- based protein: decreased soya (E & I):
especially in omega-3 fatty acid 6 fatty acids lipids (I) decreased S
rich varieties; vegetarian proteins creatinine, S PO4,
[unsalted]); avoid processed and CRP, and proteinuria
salted food
Milk and dairy, and/or alternatives Calcium, PO4, Vit B2, A, U U U U U U Increased muscle & bone Decreased
(fat-reduced varieties if needing and D (I); decreased body fat (I) albuminuria (O)
to lose weight) and uric acid (E)
U U
Am J Kidney Dis. 2016;-(-):---

Fat (mono- or polyunsaturated fats; Fat-soluble Vit, Decreased S lipids (I), BP Limited data
limit saturated fats and trans fats) essential fatty acids (I), and oxidative stress

Chan, Kelly, and Tapsell

Other foods
Alcohol (to be limited for general Alcohol U Decreased atherogenesis Limited data
health in all populations) (E), coagulation (E),
fibrinolysis (E), and
mortality (E)
(Continued)
Nutrition for Advanced CKD

Abbreviations: BP, blood pressure; CKD, chronic kidney disease; CRP, C-reactive protein; CV, cardiovascular; E, epidemiological data; EFV, extracellular fluid volume; eGFR, estimated
(I) and inflammation (I)
As kidney function deteriorates, spontaneous food

(I); decreased S lipids

microalbuminuria (E);
increased S albumin
proteinuria (I), and
intake decreases due to food aversion, with wide

Kidney Health

glomerular filtration rate; I, intervention study; IHD, ischemic heart disease; Mg, magnesium; MI, myocardial infarction; O, observational study; PO4, phosphate; S, serum; Vit, vitamin.
Decreased BP (I),
individual variation.12,100 One study reported that
13.1% and 61.2% of patients consumed ,0.75 g/kg

Decreased
IBW/d and an excess 1.0 g/kg IBW/d of protein,

EFV (I)
respectively, whereas 87.9% did not consume
adequate energy.12 Thus, patients with CKD need

Benefits

guidance to balance the control of uremia and prevent

protein-energy wasting.
Meat and Fish
CV Health

Decreased BP (I)

Decreased BP (I)
Animal protein foods are rich sources of phos-
phorus, iron, zinc, and B vitamins such as vitamin
B12, whereas oily sh provide signicant amounts of
omega-3 fatty acids and vitamin D.

Protein-rich foods from animal sources contain

Probiotics Antioxidants Isoflavones
Flavonoid/

other components, if consumed in excess, that may

cause adverse effects. Examples include purine,
U
Table 3 (Contd). Benefits of Food for General, CV, and Kidney Health

phosphorus, potential renal acid load,101 and advanced

glycation end products (AGEs),102 which increase
Important Food Components

oxidative stress, inammation, and kidney injury.

U

Wise food choices and cooking methods, for example,

steaming instead of broiling, could reduce AGE intake
by 50% and reduces serum AGE and CRP levels in
Pre- and

CKD.103 Other adverse effects, including calcium and

U

bone disorders, gout, hyperuricosuria, kidney stones,

increased cancer, and CV risk, have been associated
with protein consumption above RDI levels in the
Dietary
Fiber

general population.104
U

Omega-3 fatty acids found in oily sh confer anti-

inammatory, antiatherosclerotic, antithrombotic, and
Choice Is Inappropriate

K PO4

U
Nutrient Intake Could

antihypertensive properties and triglyceride reduction

in CKD if Food

effect.105,106 Fish consumption in the non-CKD pop-

Be in Excess

ulation has been associated with reduced risk for

Na

stroke, cardiac events/death, and all-cause mortal-

ity.105,106 Compared with nonsh eaters, 60 g/d of
Protein

sh consumption was associated with 12% reduction

in risk for death. Healthy eating guidelines recom-
mend eating 2 to 3 servings (w100 g cooked/serving)
Main Nutrient(s)

of oily sh per week, for example, salmon and tuna.107

From all core food

One study observed insufcient sh consumption in

Carbohydrates

60.8% of patients with CKD stages 4 to 5.12

groups
Salt/sodium (limit to ,100 mmol/d) Sodium

Animal Versus Plant Protein

Animal proteins are high biological value or complete
proteins and were traditionally viewed as superior to
plant-based foods, good-quality
Sugars (optimal level for energy)

animal protein food, low sugar

Dietary patterns that emphasize

plant-based proteins, which require careful planning to

Food (General Advice for the

complete the essential amino-acid prole. Plant-based

Adult Population)

proteins provide similar health benets as grains and

Healthy dietary patterns

fruits and vegetables and additional vitamin E and

omega-6 fatty acids. Consumption of plant-based pro-
teins in CKD,86 especially soy, and/or being a vegetarian
is associated with decreased levels of serum creatinine,
phosphorus, CRP, and proteinuria.108-110 Soya is a
unique plant-based protein that is of high biological
value and is a useful substitute for animal proteins.111

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 Chan, Kelly, and Tapsell

Table 4. Summary of Arguments for and Against Prescription of a Low-Protein Diet in NonDialysis-Dependent CKD

For Against

Rationale for optimal level
of protein intake
Rationale for efficacy of
low-protein diet
Rationale for low-protein
diet slowing CKD
progression rate
Rationale for renoprotective
effects of low-protein diet
Rationale for safety and
lack of adverse effects
for low-protein diet
Evidence from meta-
analyses for low-protein
diet
Likelihood of adherence to
low-protein diet
Abbreviations: ACE, angiotensin-converting enzyme; BP, blood pressure; CKD, chronic kidney disease; RDI, recommended daily
intake.
Adequate energy should be maintained; RDI level 5 0.8 Optimal level and duration of intake have
(0.75-1.0) g/kg/d, very low-protein diet 5 0.3 g/kg/d not been well defined
combined with keto-analogue of amino acids
(physiologic requirement is approximately 0.6 g/kg/d)
Improve signs and symptoms (and reduce onset) of Benefits demonstrated in experimental
peripheral neuropathy, insulin resistance, red blood cell models but lacking in clinical evidence
lipid peroxidation, osteodystrophy, albuminuria,
proteinuria
Inconsistent findings due to short study duration, inclusion Benefits demonstrated in experimental
of early and nonprogressing CKD patients, inclusion of models but lacking in clinical evidence;
nonadherent patients, unregulated use of ACE no significant slowing of progression
inhibitors, undefined treatment targets and mechanism
(eg, BP, phosphorus), when optimal adherence is
achieved, the diet can slow progression rate
May help decrease albuminuria, proteinuria, and total No additional benefit above the renin-
sodium, uric acid, and phosphate intake angiotensin-aldosterone system
blockade, BP reduction
Supervised diet management preserves nutrition status, May induce or further exacerbate
increases albumin, maintains body weight and protein malnutrition
stores, does not jeopardize survival after initiation of
dialysis therapy, improves symptom score and quality-
of-life measures
Meta-analysis supports efficacy of a protein-restricted diet Publication bias favoring studies with
in slowing progression positive results
Good adherence noted in a number of intervention Adherence is generally poor
studies, adherence can be measured by urinary
nitrogen appearance and dietary assessment

Nuts are an excellent source of protein, as well as
vitamin E and phytochemicals that have anti-
inammatory, antioxidant, and antiatherogenic
effects in general112 and for diabetic populations.113
One serving of nuts (w30 g) per week and per day
was associated with 4% and 27% reduction in all-
cause mortality and 7% and 31% reduction for CV
mortality, respectively.114 Understanding the reno-
protective benet of nuts alone in CKD is limited, but
considering the small quantity needed for benet, nuts
should be included in the CKD diet.
Although plant-based proteins appear to be supe-
rior to animal proteins due to the alkaline-inducing
properties or lower potential renal acid load,65
lower AGE levels,102 lower saturated fat content,
and lower absorption of phosphorus.47,48 Excess
intake of either protein foods has been associated
with detrimental effects on CKD progression.115
Therefore, plant-based protein should substitute or
partly substitute animal protein within the total
protein allowance rather than be an add-on. This is in
keeping with the dietary advice given in healthy
eating guidelines.17,20
The typical daily amount of protein food that a
healthy 70-kg man needs is equivalent to 1 medium
serving of cooked lean meat (w65 g) plus 30 g of
unsalted nuts, plus 1 medium egg or 0.5 cup/70 g
of cooked legumes/beans/lentils20 and is comparable
to that recommended in CKD.
Very Low-Protein Diet
In advanced CKD, use of a very low-protein diet116
of 0.3 g/kg IBW/d plus keto-analogue of amino acid
supplements is a known effective treatment87,117 that
recycles nitrogen and provides essential amino
acids with lesser nitrogenous waste. The types of
protein or protein-containing foods used are exible
depending on patients preferences and tolerance.
DAIRY FOODS
Milk, yogurt, cheese, and/or alternatives provide
signicant high biological value protein, calcium,
magnesium, phosphorus, and vitamins B2, B12, A,
and D for maintaining skeletal bone health,118
reducing serum uric acid levels,119 and modulating
body composition by reducing fat mass and
increasing lean body mass.120 Dairy foods also have
antimicrobial and antioxidant properties,121 and
cultured dairy products also contain probiotics that are

8 Am J Kidney Dis. 2016;-(-):---

Nutrition for Advanced CKD
important in regulating gut microbiota. Low-fat dairy
products are an essential part of the DASH diet and
carry the antihypertensive properties of vitamin D,
bioactive dairy peptides, and minerals such as cal-
cium, magnesium, and potassium,55 supported by the
stratied effects of dairy alone.122 To date, knowledge
about the effect of dairy alone in kidney health is
limited, but one observational study found an inverse
relationship between yogurt consumption and albu-
minuria in a cohort of patients with estimated
glomerular ltration rates (eGFRs) , 60 mL/min.123
General guidelines recommend 3 servings per day,
which provides w700 mg of phosphorus, close to the
daily limit of 800 to 1,000 mg for patients with CKD
with elevated parathyroid hormone and serum phos-
phate levels.124 Therefore, patients with advanced
CKD are advised to limit dairy foods to 1 serving per
day (eg, 300 mL of milk or equivalent), depending on
other intake of protein foods. To optimize health,
patients with CKD are encouraged to exercise and get
sunlight exposure for at least 1 to 2 hours per week;
supplementation of vitamin D125 and calcium may
also be required.
FATS AND OILS
Fats, oil, and margarine, of animal or plant origin,
provide the body with energy, essential fatty acids,
and fat-soluble vitamins. Dietary fats are broadly
divided into saturated and unsaturated fats, including
mono- and polyunsaturated fats. Saturated fats from
both animal (eg, lard, dripping, and poultry fats) and
plant (palm oil and cooking margarine) sources
increase serum cholesterol levels and are athero-
genic.126 These fats should be substituted by mono-
unsaturated (eg, olive or avocado oil) and
polyunsaturated (eg, omega-3 oils from walnuts and
omega-6 oils from Brazil nuts) fats for their CV
protective effects from vitamin E, an antioxidant, and
polyphenols, etc.126-128 Evidence on the effects of
dietary fat in the CKD population is limited. In the
general population, approximately 1 tablespoon
(w20 g/d) of unsaturated fats can be included daily.20
This is especially important for nondialysis-depen-
dent patients with CKD stages 4 to 5 who require
adequate nonprotein calories to maintain nitrogen
balance with added CV protection. When modeling
the diet for a 70-kg man, 3 to 4 tablespoons per day of
unsaturated fats should be included.
OTHER FOODS AND FOOD COMPONENTS
Alcohol
Alcohol (ethanol), such as spirits, wine, and beer,
provides calories with few other nutrients. In general,
excess alcohol consumption is associated with chronic
Am J Kidney Dis. 2016;-(-):---
diseases such as alcoholic liver disease, certain can-
cers, and hypertension.129 Interestingly, epidemiologic
studies have shown that moderate alcohol consump-
tion, particularly red wine, has a negative association
with atherogenesis, coagulation, and brinolysis, a
phenomenon known as the French paradox,130 and a
J-shaped relationship with mortality.131 The car-
dioprotective effect is thought to be a result of
resveratrol and other polyphenolic compounds, com-
bined with the effect of ethanol. Excess alcohol
consumption is known to have adverse effects on
kidney disease. However, observational studies show
that moderate alcohol consumption (,30 g/d for
men; ,20 g/d for women) is not a risk factor for
kidney function decline, but is not renoprotective
either.132 The general recommendation for healthy
adults is no more than 2 standard drinks (20 g of
alcohol) on any day.133 In practice, patients with
CKD are advised to limit their alcohol intake to no
more than 1 standard drink per day for optimal blood
pressure control and to avoid additional potassium
and phosphorus load.
Salt or Sodium
Sodium in the form of sodium chloride (salt) is
found naturally in food and is often used in large
quantities to preserve and process food. Other com-
mon sources of sodium in the diet are monosodium
glutamate (MSG; a avor enhancer), sodium bicar-
bonate (baking powder), and disodium phosphate
(emulsier). Sodium plays a vital role in regulating
blood pressure and blood volume through the
renin-angiotensin-aldosterone system,134 which is
impaired in patients with CKD who are also salt
sensitive135 and may lead to hypertension. High
sodium intake also increases proteinuria, attenuates
the antihypertensive effects of most antihypertensive
medications, and is associated with progression of
CKD and CVD.136,137 In the non-CKD population, a
meta-analysis of RCTs revealed that dietary sodium
restriction lowers blood pressure.138 In a CKD cohort,
a short-term RCT of sodium restriction to 60 to
80 mmol/d enhanced renin-angiotensin-aldosterone
system renin-angiotensin-aldosterone system block-
ade and reduced blood pressure, proteinuria, and
extracellular uid volume.139 In a 6-month RCT, a
customized dietary counseling and behavioral modi-
cation that aimed for a 50% reduction in sodium
intake demonstrated a signicant reduction in urinary
sodium (from 260 to 103 mmol/d) and a decrease of
systolic/diastolic blood pressure (8/2 mm Hg) from
the baseline of 149615.2 mm Hg/8566.3 mm Hg
compared to the control group, which received a
standard diet sheet only.140
A no-added-salt diet, targeting sodium , 100 mmol/d
(,2,300 mg/d), in conjunction with antihypertensive
9
 Chan, Kelly, and Tapsell

Food Energy
Essential nutrients:
Core Foods:
Macro- protein, fat, carbohydrates-fiber
Grains Micro- vitamins, minerals and trace
Fruit and vegetables elements
Meat, poultry, Other important food components:
seafood and plant- Phytochemicals, antioxidants,
based protein foods polyphenols, flavonoids, isoflavones,
Dairy nitrates etc.
Fats and water
Cardiovascular System
General good health,
Fruit & vegetables, fish,
meeting physiological
nuts, seeds & mono- /
and social needs
poly-unsaturated fats
blood pressure
Kidney inflammation
Protein controlled, oxidative stress
plant-based foods, Na
blood pressure
proteinuria
uremic toxin production
acid load, uric acid
rate of fall of GFR
inflammation

Muscle and bone

Optimal protein foods, dairy &
Gut energy
dietary fiber, pre- & pro-biotics physical strength
uremic toxin production Prevention of protein Figure 2. Symphony of foods in managing
Regulate protein assimilation energy wasting nondialysis chronic kidney disease. Abbrevia-
Improve GI microbiota sarcopenia tions: GFR, glomerular filtration rate; GI,
gastrointestinal.

medication appears to be safe, feasible, and cost-
effective for reducing CV risk, CKD progression, and
dosage of antihypertensive medication.141
Added Sugars
Sugars occur naturally in foods, but added sugars in
processed food have become a public health concern.
In the general population, short-term controlled
studies142 have shown that added sugar increases
blood pressure and serum lipid levels independent of
body weight and is associated with CV mortality.143
However, these ndings were not replicated in
another large study of 353,751 people,144 but positive
associations between high-fructose corn syrup on
all-cause and CVD mortality were observed. No
association between sugar intake and risk for devel-
oping kidney and/or cardiorenal disease has been
established.145,146 Sensible use of sugars provides
nonprotein calories to spare protein and prevent
catabolism. In one RCT, supplementation with
maltodextrin, a glucose polymer, improved dietary
adherence to a protein-restricted diet (0.6-0.8 g/kg/d)
and resulted in a signicant reduction in proteinuria.147
General dietary recommendations are that 5% to 15%
of energy from added sugars is acceptable.18,148,149
Foods Common to Healthy Dietary Patterns
Dietary patterns synergize the additive effects of
foods and food constituents on health, and a sys-
tematic review and meta-analysis of RCTs revealed
that healthy eating patterns are effective in reducing
blood pressure and CV risk in the non-CKD popula-
tion.150 Diets included in the analysis were the highly
studied DASH diet and regional specialty diets such
as the Mediterranean and Nordic diets. Regional diets
adopt the local culture and include fresh produce that
is rich in sh, dairy, and plant-based foods (eg, whole
grains, legumes, nuts, and seeds) and low in meat,
sweets, and alcohol. It is not known whether these
healthy eating patterns can be extrapolated to effec-
tive CKD management because data are limited and
inconsistent. Epidemiologic studies151,152 revealed
that Western diets high in saturated fat and processed
and fried foods are associated with albuminuria and
rapid eGFR decline in the CKD population. No sig-
nicant associations between the prudent diet pattern
and albuminuria or GFR decline were observed. On
average, DASH-style eating was associated with a
decreased risk for eGFR decline and albuminuria.
However, the stratied data indicated an association
between DASH diet adherence scores in the top

10 Am J Kidney Dis. 2016;-(-):---

Nutrition for Advanced CKD
quartile and reduced risk for rapid eGFR decline, but
not albuminuria.151 Furthermore, secondary analysis
of the DASH low-sodium trial showed improved
blood pressure but no interactions with eGFR.153
Adherence to the Mediterranean diet independently
predicted survival in CKD,154 although a 12-month
RCT of a Mediterranean-style ad libitum diet
showed signicant improvement in kidney function
(eGFR) from baseline, but no change in urinary
albumin-creatinine ratio. The overall benets were
not found to be different from a low-fat diet for
CVD management.155 A 3-month RCT156 of adding
Mediterranean diet to the standard NKF-KDOQI
(National Kidney Foundation2Kidney Disease Out-
comes Quality Initiative) diet recommendations1 re-
ported signicant improvement in serum albumin and
lipid proles, and reduced levels of markers of
inammation (CRP and brinogen) and lipid peroxi-
dation (thiobarbituric acid reactive substances). The
original DASH and Mediterranean diets emphasize
diet quality, but the total quantity of protein foods
included is high. For instance, the DASH diet is a
high-protein diet that provides w1.4 g/kg/d (w18%
protein in a 2,100-kcal/d meal plan), almost twice the
RDI levels, and is not desirable in CKD. This prob-
ably explains the discrepancy between outcomes in
these studies because dietary protein was not
controlled. No doubt the plant-based components of
these diets are CV protective,157 and potassium or
phosphorus levels can be modied to safe levels in
patients with advanced CKD if required. The safety
and efcacy of these diets in the CKD population,
either in their original formats or modied to meet the
CKD-specic nutrient prescription with moderate
levels of protein, requires further research. The best
currently available evidence for the CKD diet is likely
to be the combined CKD nutrition prescription in
conjunction with the national dietary guidelines and
Mediterranean- and DASH-style eating.
CONCLUSIONS
The goal of CKD nutrition therapy is to target
an optimal set of food choices to meet energy and
nutrient requirements, adjusted to match the disease
state (Fig 2). This review suggests that a concurrent
consideration of renal nutrition requirements and pop-
ulation health dietary guidelines will enable identi-
cation of an appropriate diet for people with CKD
stages 3b to 5 (Table 3). Patients should be made aware
that the CKD diet aligns with healthy eating guidelines
for the general population; it therefore is not based on
deprivation or excessive restriction. This positive
message may improve acceptance among patients (and
the kidney community). Dietary modeling is needed to
develop the diet plan for future intervention studies.
Am J Kidney Dis. 2016;-(-):---
These studies would need to consider changing
requirements during the course of deteriorating kidney
function, such that there will be no single diet plan
(or particular set amounts of foods) to suit the lifelong
disease trajectory of CKD. A framework for modeling,
adapting, and monitoring the diet to meet the individ-
ual needs of each patient with CKD is essential.
ACKNOWLEDGEMENTS
Support: None.
Financial Disclosure: The authors declare that they have no
relevant nancial interests.
Peer Review: Evaluated by 2 external reviewers, a Co-Editor,
Education Editor Gilbert, and Editor-in-Chief Levey.
REFERENCES
1. The National Kidney Foundation. K/DOQI clinical practice
guidelines for nutrition in chronic renal failure. 2000. http://www2.
kidney.org/professionals/KDOQI/guidelines_nutrition/doqi_nut.html.
Accessed January 1, 2016.
2. Ash S, Campbell K, MacLaughlin H, et al. Evidence based
practice guidelines for the nutritional management of chronic
kidney disease. Nutr Diet. 2006;63(suppl 2):S33-S45.
3. Cano N, Fiaccadori E, Tesinsky P, et al. ESPEN guidelines
on enteral nutrition: adult renal failure. 2006. http://espen.info/
documents/ENKidney.pdf. Accessed January 1, 2016.
4. The UK Renal Association. Nutrition in CKD, prevention of
undernutrition in CKD (guidelines 2.1-2.6); 2010. http://www.
renal.org/guidelines/modules/nutrition-in-ckd#sthash.zZMWgxMC.
dpbs. Accessed January 1, 2016.
5. Kopple JD, Massry SG, Kalantar-Zadeh K (eds). Textbook of
Nutritional Management of Renal Disease. 3rd ed. Elsevier
Publishing: Philadelphia; 2013.
6. Steiber AL, Kopple JD. Vitamin status and needs for people with
stages 3-5 chronic kidney disease. J Ren Nutr. 2011;21(5):355-368.
7. Levey AS, Beto JA, Coronado BE, et al. Controlling the
epidemic of cardiovascular disease in chronic renal disease:
What do we know? What do we need to know? Where do we go
from here? Special report from the National Kidney Foundation
Task Force on Cardiovascular Disease. Am J Kidney Dis.
1998;32(5)(suppl 3):S1-S199.
8. Bock JS, Gottlieb SS. Cardiorenal syndrome: new perspec-
tives. Circulation. 2010;121(23):2592-2600.
9. Danaei G, Lu Y, Singh GM, et al. Global Burden of
Metabolic Risk Factors for Chronic Diseases C. Cardiovascular
disease, chronic kidney disease, and diabetes mortality burden of
cardiometabolic risk factors from 1980 to 2010: a comparative
risk assessment. Lancet Diabetes Endocrinol. 2014;2(8):634-647.
10. Stenvinkel P. Obesitya disease with many aetiologies
disguised in the same oversized phenotype: has the overeating
theory failed? Nephrol Dial Transplant. 2015;30(10):
1656-1664.
11. Kovesdy CP, Kalantar-Zadeh K. Why is protein-energy
wasting associated with mortality in chronic kidney disease?
Semin Nephrol. 2009;29(1):3-14.
12. Chan M, Kelly J, Batterham M, Tapsell L. A high preva-
lence of abnormal nutrition parameters found in predialysis
end-stage kidney disease: is it a result of uremia or poor eating
habits? J Ren Nutr. 2014;24(5):292-302.
13. Lawson JA, Lazarus R, Kelly JJ. Prevalence and prognostic
signicance of malnutrition in chronic renal insufciency. J Ren
Nutr. 2001;11(1):16-22.
11

14. Chan M, Kelly J, Batterham M, Tapsell L. Malnutrition
(Subjective Global Assessment) scores and serum albumin levels,
but not body mass index values, at initiation of dialysis are in-
dependent predictors of mortality: a 10-year clinical cohort study.
J Ren Nutr. 2012;22(6):547-557.
15. Jacobs DR, Gross MD, Tapsell LC. Food synergy: an
operational concept for understanding nutrition. Am J Clin Nutr.
2009;89(suppl):1543S-1548S.
16. Tapsell L, Flood V, Probst Y, Charlton K, Williams P.
Nutrition tools: dietary assessment, food databases and dietary
modelling. In: Food, Nutrition and Health. Tapsell L (ed). South
Melbourne, Victoria, Australia: Oxford University Press; 2013;
pp 282-320.
17. National Health and Medical Research Council (NHMRC).
Australian Government Eat for Health, Australian Dietary Guide-
lines. 2013. https://www.nhmrc.gov.au/_les_nhmrc/publications/
attachments/n55_australian_dietary_guidelines_130530.pdf. Accessed
January 1, 2016.
18. Center for Nutrition Policy and Promotion, US Department
of Agriculture (USDA). 2015-2020 Dietary Guidelines for
Americans. 2015. http://www.cnpp.usda.gov/2015-2020-dietary-
guidelines-americans. Accessed January 1, 2016.
19. National Health and Medical Research Council (NHMRC),
Australian Government. Nutrient Reference Values (NRV) for
Australia and New Zealand. 2005. http://www.nrv.gov.au/.
Accessed January 1, 2016.
20. National Health and Medical Research Council (NHMRC),
Australian Government. Australian Guide to Healthy Eating,
Eat for Health, Australian Dietary Guidelines. 2013. https://www.
eatforhealth.gov.au/food-essentials/how-much-do-we-need-each-day/
recommended-number-serves-adults. Accessed January 1, 2016.
21. Kelly SA, Summerbell CD, Brynes A, Whittaker V,
Frost G. Wholegrain cereals for coronary heart disease. Cochrane
Database Syst Rev. 2007;2:CD005051.
22. Riccardi G, Rivellese AA. Effects of dietary ber and
carbohydrate on glucose and lipoprotein metabolism in diabetic
patients. Diabetes Care. 1991;14(12):1115-1125.
23. Post RE, Mainous AG 3rd, King DE, Simpson KN. Dietary
ber for the treatment of type 2 diabetes mellitus: a meta-analysis.
J Am Board Fam Med. 2012;25(1):16-23.
24. Birt DF, Boylston T, Hendrich S, et al. Resistant starch:
promise for improving human health. Adv Nutr. 2013;4(6):
587-601.
25. Hasjim J, Lee S-O, Hendrich S, et al. Characterization of a
novel resistant-starch and its effects on postprandial plasma-glucose
and insulin responses. Cereal Chem J. 2010;87(4):257-262.
26. Topping DL, Fukushima M, Bird AR. Resistant starch as a
prebiotic and synbiotic: state of the art. Proc Nutr Soc. 2003;62(1):
171-176.
27. Fuentes-Zaragoza E, Snchez-Zapata E, Sendra E, et al.
Resistant starch as prebiotic: a review. Starch. 2011;63:406-415.
28. Rossi M, Klein K, Johnson DW, Campbell KL. Pre-, pro-,
and synbiotics: do they have a role in reducing uremic toxins? A
systematic review and meta-analysis. Int J Nephrol. 2012;2012:
673631.
29. Rossi M, Johnson DW, Campbell KL. The kidney-gut axis:
implications for nutrition care. J Ren Nutr. 2015;25(5):399-403.
30. Good CK, Holschuh N, Albertson AM, Eldridge AL.
Whole grain consumption and body mass index in adult women:
an analysis of NHANES 1999-2000 and the USDA pyramid
servings database. J Am Coll Nutr. 2008;27(1):80-87.
31. Taki K, Takayama F, Niwa T. Benecial effects of Bidobac-
teria in a gastroresistant seamless capsule on hyperhomocysteinemia
in hemodialysis patients. J Ren Nutr. 2005;15(1):77-80.
12
Chan, Kelly, and Tapsell
32. Rossi M, Johnson DW, Morrison M, et al. Synbiotics
Easing Renal Failure by Improving Gut Microbiology
(SYNERGY): a randomized trial. Clin J Am Soc Nephrol.
2016;11(2):223-231.
33. Butcher JL, Beckstrand RL. Fibers impact on high-
sensitivity C-reactive protein levels in cardiovascular disease.
J Am Acad Nurse Pract. 2010;22(11):566-572.
34. Ning H, Van Horn L, Shay CM, Lloyd-Jones DM. Asso-
ciations of dietary ber intake with long-term predicted cardio-
vascular disease risk and C-reactive protein levels (from the
National Health and Nutrition Examination Survey Data
[2005-2010]). Am J Cardiol. 2014;113(2):287-291.
35. Helns A, Kyr C, Andersen I, et al. Intake of whole grains
is associated with lower risk of myocardial infarction: the
Danish Diet, Cancer and Health Cohort. Am J Clin Nutr.
2016;103(4):999-1007.
36. Wu H, Flint AJ, Qi Q, et al. Association between dietary
whole grain intake and risk of mortality: two large prospective
studies in US men and women. JAMA Intern Med. 2015;175(3):
373-384.
37. Holmberg S, Thelin A, Stiernstrom EL. Food choices and
coronary heart disease: a population based cohort study of rural
Swedish men with 12 years of follow-up. Int J Environ Res Public
Health. 2009;6(10):2626-2638.
38. Ampatzoglou A, Atwal KK, Maidens CM, et al. Increased
whole grain consumption does not affect blood biochemistry, body
composition, or gut microbiology in healthy, low-habitual whole
grain consumers. J Nutr. 2015;145(2):215-221.
39. Brownlee IA, Moore C, Chateld M, et al. Markers of
cardiovascular risk are not changed by increased whole-grain
intake: the WHOLEheart study, a randomised, controlled dietary
intervention. Br J Nutr. 2010;104(1):125-134.
40. Krishnamurthy VM, Wei G, Baird BC, et al. High dietary
ber intake is associated with decreased inammation and all-
cause mortality in patients with chronic kidney disease. Kidney
Int. 2012;81(3):300-306.
41. Evenepoel P, Meijers BK. Dietary ber and protein:
nutritional therapy in chronic kidney disease and beyond. Kidney
Int. 2012;81(3):227-229.
42. ONeil CE, Zanovec M, Cho SS, Nicklas TA. Whole grain
and ber consumption are associated with lower body weight
measures in US adults: National Health and Nutrition Examination
Survey 1999-2004. Nutr Res. 2010;30(12):815-822.
43. Kambham N, Markowitz GS, Valeri AM, Lin J,
DAgati VD. Obesity-related glomerulopathy: an emerging
epidemic. Kidney Int. 2001;59(4):1498-1509.
44. Hsu CY, Iribarren C, McCulloch CE, Darbinian J, Go AS.
Risk factors for end-stage renal disease: 25-year follow-up. Arch
Intern Med. 2009;169(4):342-350.
45. Trichopoulou A, Bamia C, Trichopoulos D. Anatomy of
health effects of Mediterranean diet: Greek EPIC prospective
cohort study. BMJ. 2009;338:b2337.
46. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the
effects of dietary patterns on blood pressure. DASH Collaborative
Research Group. N Engl J Med. 1997;336(16):1117-1124.
47. Kalantar-Zadeh K, Gutekunst L, Mehrotra R, et al. Un-
derstanding sources of dietary phosphorus in the treatment of
patients with chronic kidney disease. Clin J Am Soc Nephrol.
2010;5(3):519-530.
48. Cupisti A, Kalantar-Zadeh K. Management of natural and
added dietary phosphorus burden in kidney disease. Semin
Nephrol. 2013;33(2):180-190.
49. Wang X, Ouyang Y, Liu J, et al. Fruit and vegetable
consumption and mortality from all causes, cardiovascular disease,
Am J Kidney Dis. 2016;-(-):---
Nutrition for Advanced CKD
and cancer: systematic review and dose-response meta-analysis of
prospective cohort studies. BMJ. 2014;349:g4490.
50. Leenders M, Boshuizen HC, Ferrari P, et al. Fruit and
vegetable intake and cause-specic mortality in the EPIC study.
Eur J Epidemiol. 2014;29(9):639-652.
51. Ivey KL, Hodgson JM, Croft KD, Lewis JR, Prince RL.
Flavonoid intake and all-cause mortality. Am J Clin Nutr.
2015;101(5):1012-1020.
52. Mann JF, Sheridan P, McQueen MJ, et al. Homocysteine
lowering with folic acid and B vitamins in people with chronic
kidney diseaseresults of the renal Hope-2 study. Nephrol Dial
Transplant. 2008;23(2):645-653.
53. Malinow MR, Bostom AG, Krauss RM. Homocyst(e)ine,
diet, and cardiovascular diseases: a statement for healthcare
professionals from the Nutrition Committee, American Heart
Association. Circulation. 1999;99(1):178-182.
54. Voutilainen S, Nurmi T, Mursu J, Rissanen TH. Caroten-
oids and cardiovascular health. Am J Clin Nutr. 2006;83(6):
1265-1271.
55. Sacks FM, Brown LE, Appel L, et al. Combinations of
potassium, calcium, and magnesium supplements in hypertension.
Hypertension. 1995;26(6):950-956.
56. Desai CK, Huang J, Lokhandwala A, et al. The role of
vitamin supplementation in the prevention of cardiovascular dis-
ease events. Clin Cardiol. 2014;37(9):576-581.
57. Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG,
Gluud C. Antioxidant supplements for prevention of mortality in
healthy participants and patients with various diseases. Cochrane
Database Syst Rev. 2012;3:CD007176.
58. Jun M, Venkataraman V, Razavian M, et al. Antioxidants
for chronic kidney disease. Cochrane Database Syst Rev. 2012;10:
CD008176.
59. Sahni N, Gupta KL. Dietary antioxidents and oxidative stress
in predialysis chronic kidney disease patients. J Nephropathol.
2012;1(3):134-142.
60. Jamison RL, Hartigan P, Kaufman JS, et al. Effect of ho-
mocysteine lowering on mortality and vascular disease in
advanced chronic kidney disease and end-stage renal disease: a
randomized controlled trial. JAMA. 2007;298(10):1163-1170.
61. Saldanha JF, Leal Vde O, Stenvinkel P, Carraro-
Eduardo JC, Mafra D. Resveratrol: why is it a promising therapy
for chronic kidney disease patients? Oxid Med Cell Longev.
2013;2013:963217.
62. Goraya N, Simoni J, Jo C, Wesson DE. Dietary acid
reduction with fruits and vegetables or bicarbonate attenuates
kidney injury in patients with a moderately reduced glomerular
ltration rate due to hypertensive nephropathy. Kidney Int.
2012;81(1):86-93.
63. Goraya N, Simoni J, Jo CH, Wesson DE. A comparison of
treating metabolic acidosis in CKD stage 4 hypertensive kidney
disease with fruits and vegetables or sodium bicarbonate. Clin J
Am Soc Nephrol. 2013;8(3):371-381.
64. Goraya N, Simoni J, Jo CH, Wesson DE. Treatment of
metabolic acidosis in patients with stage 3 chronic kidney disease
with fruits and vegetables or oral bicarbonate reduces urine
angiotensinogen and preserves glomerular ltration rate. Kidney
Int. 2014;86(5):1031-1038.
65. Remer T, Manz F. Potential renal acid load of foods and its
inuence on urine pH. J Am Diet Assoc. 1995;95(7):791-797.
66. Kobayashi J, Ohtake K, Uchida H. NO-rich diet for
lifestyle-related diseases. Nutrients. 2015;7(6):4911-4937.
67. Modlinger PS, Wilcox CS, Aslam S. Nitric oxide, oxidative
stress, and progression of chronic renal failure. Semin Nephrol.
2004;24(4):354-365.
Am J Kidney Dis. 2016;-(-):---
68. Ferder L, Ferder MD, Inserra F. The role of high-fructose
corn syrup in metabolic syndrome and hypertension. Curr
Hypertens Rep. 2010;12(2):105-112.
69. Johnson RJ, Nakagawa T, Sanchez-Lozada LG, et al.
Sugar, uric acid, and the etiology of diabetes and obesity.
Diabetes. 2013;62(10):3307-3315.
70. Juanola-Falgarona M, Salas-Salvado J, Ibarrola-Jurado N,
et al. Effect of the glycemic index of the diet on weight loss,
modulation of satiety, inammation, and other metabolic risk
factors: a randomized controlled trial. Am J Clin Nutr.
2014;100(1):27-35.
71. Schwingshackl L, Hoffmann G. Long-term effects of low
glycemic index/load vs. high glycemic index/load diets on
parameters of obesity and obesity-associated risks: a systematic
review and meta-analysis. Nutr Metab Cardiovasc Dis. 2013;23(8):
699-706.
72. Juraschek SP, McAdams-Demarco M, Gelber AC, et al.
Effects of lowering glycemic index of dietary carbohydrate on
plasma uric acid: the OmniCarb randomized clinical trial. Arthritis
Rheum. 2016;68(5):1281-1289.
73. Thomas D, Elliott EJ. Low glycaemic index, or low gly-
caemic load, diets for diabetes mellitus. Cochrane Database Syst
Rev. 2009;1:CD006296.
74. Kristo AS, Matthan NR, Lichtenstein AH. Effect of diets
differing in glycemic index and glycemic load on cardiovascular
risk factors: review of randomized controlled-feeding trials.
Nutrients. 2013;5(4):1071-1080.
75. Sacks FM, Carey VJ, Anderson CA, et al. Effects of
high vs low glycemic index of dietary carbohydrate on car-
diovascular disease risk factors and insulin sensitivity: the
OmniCarb randomized clinical trial. JAMA. 2014;312(23):
2531-2541.
76. Korgaonkar S, Tilea A, Gillespie BW, et al. Serum potas-
sium and outcomes in CKD: insights from the RRI-CKD Cohort
Study. Clin J Am Soc Nephrol. 2010;5(5):762-769.
77. Australian Government, Department of Health and Aging.
The Go for 2 Fruit & 5 Vegetables Campaign. 2008. www.
gofor2and5.com.au/. Accessed January 1, 2016.
78. Australian Bureau of Statistics. Daily intake of fruit and veg-
etables. 4364.0.55.003 - Australian Health Survey: updated results,
2011-2012. Canberra, Australia. 2013. http://www.abs.gov.au/
ausstats/abs@.nsf/Lookup/C549D4433F6B74D7CA257B820017
9569?opendocument. Accessed January 1, 2016.
79. Bergstrom J. Discovery and rediscovery of low protein diet.
Clin Nephrol. 1984;21(1):29-35.
80. Walser M, Mitch WE, Maroni BJ, Kopple JD. Should
protein intake be restricted in predialysis patients? Kidney Int.
1999;55(3):771-777.
81. Fouque D, Laville M. Low protein diets for chronic kidney
disease in non diabetic adults. Cochrane Database Syst Rev.
2009;3:CD001892.
82. Mitch WE, Remuzzi G. Diets for patients with chronic
kidney disease, still worth prescribing. J Am Soc Nephrol.
2004;15(1):234-237.
83. Johnson DW. Dietary protein restriction as a treatment for
slowing chronic kidney disease progression: the case against.
Nephrology (Carlton). 2006;11(1):58-62.
84. Thilly N. Low-protein diet in chronic kidney disease: from
questions of effectiveness to those of feasibility. Nephrol Dial
Transplant. 2013;28(9):2203-2205.
85. Levey AS, Adler S, Caggiula AW, et al. Effects of dietary
protein restriction on the progression of moderate renal disease in
the Modication of Diet in Renal Disease Study. J Am Soc
Nephrol. 1996;7(12):2616-2626.
13

86. Chauveau P, Combe C, Fouque D, Aparicio M. Vegetari-
anism: advantages and drawbacks in patients with chronic kidney
diseases. J Ren Nutr. 2013;23(6):399-405.
87. Piccoli GB, Vigotti FN, Leone F, et al. Low-protein diets in
CKD: how can we achieve them? A narrative, pragmatic review.
Clin Kidney J. 2015;8(1):61-70.
88. Atinmo T, Beaton GH, Calloway D, et al. Energy and protein
requirements. In: Technical Report Series 724, 1st ed. Geneva,
Switzerland: World Health Organization; 1985. http://www.fao.org/
docrep/003/aa040e/aa040e00.HTM. Accessed January 1, 2016.
89. Australian Government, National Health and Medical
Research Council (NHMRC). Dietary protein. Nutrient Reference
Values (NRV) for Australia and New Zealand. 2006. [updated
September 9, 2015]. http://www.nrv.gov.au/nutrients/protein.htm.
Accessed January 1, 2016.
90. Kopple JD, Shinaberger JH, Coburn JW, Rubini ME.
Protein nutrition in uremia: a review. Am J Clin Nutr. 1968;21(5):
508-515.
91. Kopple JD, Monteon FJ, Shaib JK. Effect of energy intake
on nitrogen metabolism in nondialyzed patients with chronic renal
failure. Kidney Int. 1986;29(3):734-742.
92. Friedman AN. High-protein diets: potential effects on the
kidney in renal health and disease. Am J Kidney Dis. 2004;44(6):
950-962.
93. Knight EL, Stampfer MJ, Hankinson SE, Spiegelman D,
Curhan GC. The impact of protein intake on renal function decline
in women with normal renal function or mild renal insufciency.
Ann Intern Med. 2003;138(6):460-467.
94. Huang MC, Chen ME, Hung HC, et al. Inadequate energy
and excess protein intakes may be associated with worsening renal
function in chronic kidney disease. J Ren Nutr. 2008;18(2):
187-194.
95. Meloni C, Tatangelo P, Cipriani S, et al. Adequate protein
dietary restriction in diabetic and nondiabetic patients with chronic
renal failure. J Ren Nutr. 2004;14(4):208-213.
96. Kurpad AV, Vaz M. Protein and amino acid requirements
in the elderly. Eur J Clin Nutr. 2000;54(suppl 3):S131-S142.
97. Australian Bureau of Statistics. Australian Health Survey:
Nutrition First Results - Foods and Nutrients, 2011-12. 2014.
http://www.abs.gov.au/ausstats/abs@.nsf/detailspage/4364.0.55.
0072011-12. Accessed January 1, 2016.
98. Halkjar J, Olsen A, Bjerregaard LJ, et al. Intake of total,
animal and plant proteins, and their food sources in 10 countries in
the European Prospective Investigation into Cancer and Nutrition.
Eur J Clin Nutr. 2009;63(suppl 4):S16-S36.
99. Fulgoni VL. Current protein intake in America: analysis of
the National Health and Nutrition Examination Survey, 2003
2004. Am J Clin Nutr. 2008;87(suppl):1554S-1557S.
100. Ikizler TA, Greene JH, Wingard RL, Parker RA,
Hakim RM. Spontaneous dietary protein intake during progression
of chronic renal failure. J Am Soc Nephrol. 1995;6(5):1386-1391.
101. Remer T. Inuence of diet on acid-base balance. Semin
Dial. 2000;13(4):221-226.
102. Uribarri J, He JC. The low AGE diet: a neglected aspect of
clinical nephrology practice? Nephron. 2015;130(1):48-53.
103. Uribarri J, Peppa M, Cai W, et al. Restriction of dietary
glycotoxins reduces excessive advanced glycation end products
in renal failure patients. J Am Soc Nephrol. 2003;14(3):
728-731.
104. Delimaris I. Adverse effects associated with protein intake
above the recommended dietary allowance for adults. ISRN Nutr.
2013:http://dx.doi.org/10.5402/2013/126929.
105. Nestel P, Clifton P, Colquhoun D, et al. Indications for
omega-3 long chain polyunsaturated fatty acid in the prevention
14
Chan, Kelly, and Tapsell
and treatment of cardiovascular disease. Heart Lung Circ.
2015;24(8):769-779.
106. Zhao LG, Sun JW, Yang Y, et al. Fish consumption and
all-cause mortality: a meta-analysis of cohort studies. Eur J Clin
Nutr. 2016;70(2):155-161.
107. Heart Foundation, Australia. Position statement, sh and
seafood. 2015. http://heartfoundation.org.au/images/uploads/main/
Programs/PRO-169_Fish_and_seafood_position_statement.pdf.
Accessed January 1, 2016.
108. Anderson JW. Benecial effects of soy protein con-
sumption for renal function. Asia Pac J Clin Nutr. 2008;17(suppl
1):324-328.
109. Jing Z, Wei-Jie Y. Effects of soy protein containing iso-
avones in patients with chronic kidney disease: a systematic
review and meta-analysis. Clin Nutr. 2016;35(1):117-124.
110. Zhang J, Liu J, Su J, Tian F. The effects of soy protein on
chronic kidney disease: a meta-analysis of randomized controlled
trials. Eur J Clin Nutr. 2014;68(9):987-993.
111. Young VR. Soy protein in relation to human protein and
amino acid nutrition. J Am Diet Assoc. 1991;91(7):828-835.
112. Bolling BW, Chen CY, McKay DL, Blumberg JB. Tree
nut phytochemicals: composition, antioxidant capacity, bioac-
tivity, impact factors. A systematic review of almonds, Brazils,
cashews, hazelnuts, macadamias, pecans, pine nuts, pistachios and
walnuts. Nutr Res Rev. 2011;24(2):244-275.
113. Tapsell LC, Batterham MJ, Teuss G, et al. Long-term
effects of increased dietary polyunsaturated fat from walnuts on
metabolic parameters in type II diabetes. Eur J Clin Nutr.
2009;63(8):1008-1015.
114. Grosso G, Yang J, Marventano S, et al. Nut consumption
on all-cause, cardiovascular, and cancer mortality risk: a system-
atic review and meta-analysis of epidemiologic studies. Am J Clin
Nutr. 2015;101(4):783-793.
115. Bernstein AM, Treyzon L, Li Z. Are high-protein,
vegetable-based diets safe for kidney function? A review of the
literature. J Am Diet Assoc. 2007;107(4):644-650.
116. Aparicio M, Bellizzi V, Chauveau P, et al. Protein-
restricted diets plus keto/amino acids - a valid therapeutic
approach for chronic kidney disease patients. J Ren Nutr.
2012;22(2)(suppl):S22-S24.
117. Brunori G, Viola BF, Parrinello G, et al. Efcacy and
safety of a very-low-protein diet when postponing dialysis in the
elderly: a prospective randomized multicenter controlled study.
Am J Kidney Dis. 2007;49(5):569-580.
118. Rizzoli R. Dairy products, yogurts, and bone health. Am J
Clin Nutr. 2014;99(suppl):1256s-1262s.
119. Choi HK, Liu S, Curhan G. Intake of purine-rich foods,
protein, and dairy products and relationship to serum levels of uric
acid: the Third National Health and Nutrition Examination Survey.
Arthritis Rheum. 2005;52(1):283-289.
120. Abargouei AS, Janghorbani M, Salehi-Marzijarani M,
Esmaillzadeh A. Effect of dairy consumption on weight and body
composition in adults: a systematic review and meta-analysis of
randomized controlled clinical trials. Int J Obes (Lond).
2012;36(12):1485-1493.
121. Nongonierma AB, FitzGerald RJ. Bioactive properties of
milk proteins in humans: a review. Peptides. 2015;73:20-34.
122. McGrane MM, Essery E, Obbagy J, et al. Dairy con-
sumption, blood pressure, and risk of hypertension: an evidence-
based review of recent literature. Curr Cardiovasc Risk Rep.
2011;5(4):287-298.
123. Yacoub R, Kaji D, Patel SN, et al. Association between
probiotic and yogurt consumption and kidney disease: insights
from NHANES. Nutr J. 2016;15(1):10.
Am J Kidney Dis. 2016;-(-):---
Nutrition for Advanced CKD
124. Lorenzo Sellares V, Torregrosa V. [Changes in mineral
metabolism in stage 3, 4, and 5 chronic kidney disease (not on
dialysis)]. Nefrologia. 2008;28(suppl 3):67-78.
125. Chan M, Johnson D. Vitamin D therapy (supplementa-
tion) in early chronic kidney disease, KHA-CARI Guidelines
(Kidney Health Australia-Caring for Australasians with Renal
Impairment). 2012. http://www.cari.org.au/CKD/CKD%20early/
Vitamin_D_Therapy_ECKD.pdf. Accessed January 1, 2016.
126. Hooper L, Martin N, Abdelhamid A, Davey Smith G.
Reduction in saturated fat intake for cardiovascular disease.
Cochrane Database Syst Rev. 2015;6:CD011737.
127. Hohmann CD, Cramer H, Michalsen A, et al. Effects of
high phenolic olive oil on cardiovascular risk factors: a systematic
review and meta-analysis. Phytomedicine. 2015;22(6):631-640.
128. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and
lifestyle recommendations revision 2006: a scientic statement
from the American Heart Association Nutrition Committee.
Circulation. 2006;114(1):82-96.
129. Shield KD, Parry C, Rehm J. Chronic diseases and
conditions related to alcohol use. Alcohol Res. 2013;35(2):
155-173.
130. Lippi G, Franchini M, Favaloro EJ, Targher G. Moderate
red wine consumption and cardiovascular disease risk: beyond
the French paradox. Semin Thromb Hemost. 2010;36(1):59-70.
131. Plunk AD, Syed-Mohammed H, Cavazos-Rehg P,
Bierut LJ, Grucza RA. Alcohol consumption, heavy drinking, and
mortality: rethinking the J-shaped curve. Alcohol Clin Exp Res.
2014;38(2):471-478.
132. Buja A, Vinelli A, Lion C, Scafato E, Baldo V. Is mod-
erate alcohol consumption a risk factor for kidney function
decline? A systematic review of observational studies. J Ren Nutr.
2014;24(4):224-235.
133. Department of Health, Australian Government. Reduce
your risk: new national guidelines for alcohol consumption. 2006.
[updated November 2013]. http://www.alcohol.gov.au/internet/
alcohol/publishing.nsf/Content/guide-adult. Accessed January 1,
2016.
134. Kobori H, Nangaku M, Navar LG, Nishiyama A. The
intrarenal renin-angiotensin system: from physiology to the
pathobiology of hypertension and kidney disease. Pharmacol Rev.
2007;59(3):251-287.
135. Boero R, Pignataro A, Quarello F. Salt intake and kidney
disease. J Nephrol. 2002;15(3):225-229.
136. Weir MR, Fink JC. Salt intake and progression of chronic
kidney disease: an overlooked modiable exposure? A commen-
tary. Am J Kidney Dis. 2005;45(1):176-188.
137. Humalda JK, Navis G. Dietary sodium restriction: a
neglected therapeutic opportunity in chronic kidney disease. Curr
Opin Nephrol Hypertens. 2014;23(6):533-540.
138. He FJ, Li J, Macgregor GA. Effect of longer term modest
salt reduction on blood pressure: Cochrane systematic review and
meta-analysis of randomised trials. BMJ. 2013;346:f1325.
139. McMahon EJ, Bauer JD, Hawley CM, et al. A randomized
trial of dietary sodium restriction in CKD. J Am Soc Nephrol.
2013;24(12):2096-2103.
140. de Brito-Ashurst I, Perry L, Sanders TA, et al. The role of
salt intake and salt sensitivity in the management of hypertension
in South Asian people with chronic kidney disease: a randomised
controlled trial. Heart. 2013;99(17):1256-1260.
Am J Kidney Dis. 2016;-(-):---
141. McMahon E, Campbell KL. Altered dietary salt for people
with CKD. Nephrology. 2015;20(10):758-759.
142. Te Morenga LA, Howatson AJ, Jones RM, Mann J.
Dietary sugars and cardiometabolic risk: systematic review and
meta-analyses of randomized controlled trials of the effects on
blood pressure and lipids. Am J Clin Nutr. 2014;100(1):65-79.
143. Yang Q, Zhang Z, Gregg EW, et al. Added sugar intake
and cardiovascular diseases mortality among US adults. JAMA
Intern Med. 2014;174(4):516-524.
144. Tasevska N, Park Y, Jiao L, et al. Sugars and risk of
mortality in the NIH-AARP Diet and Health Study. Am J Clin
Nutr. 2014;99(5):1077-1088.
145. Karalius VP, Shoham DA. Dietary sugar and articial
sweetener intake and chronic kidney disease: a review. Adv
Chronic Kidney Dis. 2013;20(2):157-164.
146. Johnson RJ, Segal MS, Sautin Y, et al. Potential role of
sugar (fructose) in the epidemic of hypertension, obesity and the
metabolic syndrome, diabetes, kidney disease, and cardiovascular
disease. Am J Clin Nutr. 2007;86(4):899-906.
147. Wu HL, Sung JM, Kao MD, et al. Nonprotein calorie
supplement improves adherence to low-protein diet and exerts
benecial responses on renal function in chronic kidney disease.
J Ren Nutr. 2013;23(4):271-276.
148. National Health and Medical Research Council (NHMRC),
Australian Government. Macronutrient balance, nutrient reference
values (NRV) for Australia and New Zealand. 2005 [updated
20-4-2014]. https://www.nrv.gov.au/chronic-disease/macronutrient-
balance. Accessed January 1, 2016.
149. Johnson RK, Appel LJ, Brands M, et al. Dietary sugars intake
and cardiovascular health: a scientic statement from the American
Heart Association. Circulation. 2009;120(11):1011-1020.
150. Ndanuko RN, Tapsell LC, Charlton KE. Dietary patterns
and blood pressure in adults: a systematic review and meta-
analysis of randomized controlled trials. Adv Nutr. 2016;7(1):
76-89.
151. Lin J, Fung TT, Hu FB, Curhan GC. Association of
dietary patterns with albuminuria and kidney function decline in
older white women: a subgroup analysis from the Nurses Health
Study. Am J Kidney Dis. 2011;57(2):245-254.
152. Gutierrez OM, Muntner P, Rizk DV, et al. Dietary
patterns and risk of death and progression to ESRD in individuals
with CKD: a cohort study. Am J Kidney Dis. 2014;64(2):
204-213.
153. Tyson CC, Kuchibhatla M, Patel UD, et al. Impact of
kidney function on effects of the Dietary Approaches to Stop
Hypertension (Dash) Diet. J Hypertens (Los Angel). 2014. http://
dx.doi.org/10.4172/2167-1095.1000168.
154. Huang X, Jimenez-Moleon JJ, Lindholm B, et al. Medi-
terranean diet, kidney function, and mortality in men with CKD.
Clin J Am Soc Nephrol. 2013;8(9):1548-1555.
155. Diaz-Lopez A, Bullo M, Martinez-Gonzalez MA, et al.
Effects of Mediterranean diets on kidney function: a report from
the PREDIMED trial. Am J Kidney Dis. 2012;60(3):380-389.
156. Mekki K, Bouzidi-bekada N, Kaddous A, Bouchenak M.
Mediterranean diet improves dyslipidemia and biomarkers in
chronic renal failure patients. Food Funct. 2010;1(1):110-115.
157. Buil-Cosiale P, Zazpe I, Toledo E, et al. Fiber intake and
all-cause mortality in the Prevencion con Dieta Mediterranea
(PREDIMED) study. Am J Clin Nutr. 2014;100(6):1498-1507.
15