Blood Purif 2013;36:41-46

DOI: 10.1159/000350585

Published online: May 25, 2013

Low-Protein Diet or Nutritional

Therapy
in Chronic Kidney Disease?
Vincenzo Bellizzi
Division of Nephrology, Dialysis and Renal Transplantation, San Giovanni di Dio e Ruggi
dAragona University Hospital, Salerno, Italy

initial stage, was burdened by serious

complications
and
was accessible to a very low number of patients. In
such
2013 S. Karger AG, Basel
0253-5068/13/03610041$38.00/0
E-Mail karger@karger.com

www.karger.com/bpu

Key Words
Chronic kidney disease Low-protein diet Nutrition
Salt Phosphorous Cardiovascular risk Renal death

Abstract
The use of a low-protein diet in treating chronic
kidney
disease dates back many decades. Initially, the low
intake of proteins was used to reduce uremic
symptoms. Thereafter, the hope of significantly
slowing
and
even
halting
the
progression of renal failure toward dialysis grew
among
nephrologists. This proved not to be effective and the
low-protein diet was largely abandoned. This review focuses
on the reasons why a low-protein diet, and mainly
comprehensive nutritional therapy, should still be
considered a cornerstone in the treatment of chronic
renal failure.
Copyright 2013 S. Karger AG,
Basel

Origin of Dietetic Therapy in the

Treatment of Chronic Kidney Disease

at

In the early 1960s renal replacement therapy was

an

circumstances, advanced uremic syndrome represented

a
dramatic condition with a poor outcome. Under
these
circumstances nutritional treatment of uremia
developed; it resulted in a diet comprising low amounts of
protein of high biological value and high amounts of
energy,
which was proposed for the symptomatic
treatment
of
uremia with the aim of controlling metabolic
derangements and, consequently, postponing the need for
dialysis or avoiding patient death [1]. Later,
experimental
studies hypothesized that high protein load could
cause
glomerular hyperfiltration and, as a result, the
worsening
of renal function [2]. Therefore, in the 1980s a lowprotein diet became widely used in the belief that it
could
slow down the negative progression of chronic renal
failure, thus avoiding dialysis. Many clinical studies,
however, produced controversial results and even the
largest
trial on this matter, the Modification of Diet in Renal
Disease (MDRD) study, provided negative results
regarding
a significant effect of low-protein diets on decline in
the
glomerular filtration rate (GFR) [3]. Consequently,
the
interest in the use of the low-protein diet in clinical
practice markedly reduced, and the historical aims for a use
of
dietetic therapy in chronic kidney disease (CKD), that
is
handling
of
uremic
symptoms
through
accumulation
of
protein catabolism waste products and delaying the
need

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Dr. Vincenzo Bellizzi, MD, PhD

Division of Nephrology, Dialysis and Renal Transplantation
University Hospital San Giovanni di Dio e Ruggi dAragona, Via San
Leonardo IT-84100 Salerno (Italy)
E-Mail vincenzo.bellizzi @ tin.it

for dialysis treatment, were neglected, leaving

dietetic therapy only a marginal clinical role in
the treatment of CKD [1].
Low-Protein Diet and Progression of CKD

It has been demonstrated that a low-protein diet

does
not significantly slow the worsening of CKD
measured
by the mean of GFR decline. Reduction in GFR,
however,
is not a unique or the best measure of CKD
progression.
In clinical practice renal replacement therapy
begins
with different GFR levels because of the impact of
uremic
symptoms
and
complications
of
CKD
(metabolic
derangements, hypertension, extracellular volume
expansion, hyperkalemia, etc.), independently on GFR
values.
Indeed, it is mainly the presence of clinical
complications
at the start of renal replacement treatment that
impacts
on survival in dialysis, rather than the early or late
dialysis start [4]. Thus, a treatment for nondialysis
CKD
patients which is able to reduce uremic
complications
regardless of the effect on GFR decline would
delay
the
start of dialysis and likely improve patient
outcome.
As
a matter of fact, both patient and clinician consider
renal
death, rather than GFR decline, the most
important
objective. Based on this criterion, Walser and Hill
[5]
suggested a benefit of dietetic therapy in
compliant
CKD
patients treated with a very low-protein diet,
which
delayed the start of dialysis by a median time of 1 year
without occurrence of malnutrition and with
reduced
incidence of hospitalization and death. This preliminary
evidence was confirmed by the secondary analyses of
the

MDRD study [6, 7]. Furthermore, a recent

Cochrane
review in nondiabetic patients showed that a lowprotein
diet prolongs renal survival [8]. Similarly, in
patients
with type I diabetes a reduced intake of
proteins
in
the
long term, even not influencing the decline in GFR,
leads
to a reduction of relative risk of renal death by
77%
[9].
Therefore, low-protein diets may significantly
modify
the clinical course of CKD, delaying dialysis
start
by
about 1 year in either nondiabetic or diabetic
patients.
Clinical Effects of a Low-Protein Diet

Because of the major scientific interest in the

progression of CKD and the negative results of the MDRD
study,
the metabolic effects of a low-protein diet in
CKD
have
been basically neglected. However, it has been
evidenced
that even a slight actual reduction of protein
intake of
42

Blood Purif 2013;36:41-46

DOI: 10.1159/000350585

Bellizzi

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0.2 gram per kilogram body weight per day is sufficient

to
achieve significant metabolic improvements in
uremic
state, metabolic acidosis and hyperphosphatemia
[10].
A
recent randomized controlled trial, comparing the
metabolic effects of two different low-protein diets
(mild
or
moderately
low-protein),
evidenced
that
prescription
of
a 0.6-g/kg/day diet compared with a 0.8-gram
diet
allowed a better control of both metabolic acidosis and
hyperparathyroidism in the entire study population,
which
also included noncompliant patients; that study
demonstrated that metabolic advantages of low-protein diets
in
CKD occur even if adherence to diet prescription is
incomplete [11]. In addition, a very low-protein
diet
is
much more efficacious on calcium-phosphorus
metabolism, further reducing the levels of both phosphorus
and
parathyroid hormone [12]. It has been demonstrated
that
the greater reduction of protein intake in CKD
improves
the lipid profile by reducing the levels of
cholesterol,
triglycerides and also lowering lipoprotein AI and the
ApoAI:Apo-B ratio [13, 14]. Interestingly, the very lowprotein diet improves several major modifiable
cardiovascular risk factors associated with the uremic state.
Indeed,
randomized studies have shown that low-protein
diets
reduce proteinuria [15, 16], improve anemia [17] and
improve hypertension [13]. In addition, an interaction
between nutrition, either salt intake or serum
phosphate
levels, and cardiorenal protection has recently been
suggested. A randomized trial compared the shortterm
effects of dietary salt restriction added to angiotensincon-

verting enzyme inhibitors (ACEi) and dual

angiotensin
blockade, or their combination, on proteinuria and
blood
pressure in nondiabetic CKD stage 1-2 patients
already
on ACEi; reduction of salt intake to the amount
recommended by guidelines (6 g per day) enhances the
urinary
protein lowering effect of either ACEi alone or dual
angiotensin blockade, and low salt plus ACEi alone
is,
by
itself, even more efficacious than dual angiotensin
blockade without low salt on both proteinuria and
hypertension [18]. A secondary analysis of a combination
of
the
RENAAL and IDNT studies evaluated the same
interaction in the long term, showing that in patients on
angiotensin receptor blockers (ARBs) the lower salt
intake
is
associated with reduced renal and cardiovascular
risk;
hence, dietary salt restriction potentiates renal
and
cardiac protective effect of ARBs even in the long term
[19].
The relationship between serum phosphorus, CKD
progression and efficacy of ACEi has also been evaluated
in
patients from the REIN study; the highest serum
phosphorus is associated with increased renal death and
the
urinary protein-lowering effect of ACEi declines as
serum

phosphorus increases, suggesting that phosphorus

is
an
independent predictor of CKD progression and may
impact on the renoprotective effect of ACEi [20].
Similarly,
the interaction between serum phosphorus and the
antiproteinuric effect of a very low-protein diet has
been
explored; in this setting either the higher serum
phosphorus
or the greater phosphate intake were associated with
lower urinary protein reduction due to a low-protein
diet;
in
contrast, the major reduction of proteinuria was
obtained
with lower intakes of phosphorus and lower serum
phosphorus levels, suggesting that phosphorus
impacts
on
proteinuria [21]. Thus, reduced phosphorus intake
and
serum phosphorus levels can also enhance the effects of
a
low-protein diet on proteinuria and, likely, CKD
progression to renal death. In summary, in CKD the whole
nutritional treatment reduces uremic signs and symptoms
and
delays the start of dialysis, allowing the patient to
commence dialysis with lower cardiovascular risk (table 1).
Adherence to a Low-Protein Diet

It has been shown that it is possible to reach high

adherence to a low-protein diet if you obtain the
understanding and satisfaction of the patient [22].
Psychosocial
factors (knowledge, achieving the objective,
satisfaction,
attitude, support) are the most important
determinants
of adherence to treatment and, in contrast,
inadequate
communication between physician and patient
represents a major cause of reduced adherence. Indeed, if
the
physician who prescribes the low-protein diet is not
fully

convinced of the effectiveness of the treatment,

results
are
poor; conversely, a convinced doctor obtains the
best
patient compliance. On the other hand, in clinical
practice
even a slight reduction of protein intake is associated
with
significant metabolic improvement, despite
compliance
to prescription being incomplete. Indeed, the
actual
reduction of only 0.2 g/kg/day of protein intake,
regardless
of both the amount of prescribed protein and the
degree
of adherence to diet prescription, induces
significant
improvement in serum urea, metabolic acidosis and
phosphate levels [10]. As a result, very low-protein
diets,
regardless of reduced adherence, achieves better
metabolic
effects. A recent study compared two lowprotein
diets
with 0.60 and 0.35 g/kg/day of protein; the
study
group
on the 0.35-gram diet reached a major
improvement
in
lipid profile, proteinuria, calcium-phosphate
balance
and
hypertension, despite a lower number of
patients
being
adherent to prescription; this effect was
related
to
the
lower protein intake actually achieved [17].
The same
Low-Protein Diet or Nutritional
Therapy in CKD?

Table 1. Effects of protein intake restriction in CKD

CKD
Renal death is more reliable than reduction in GFR
progression to assess the progression of CKD to end-stage
renal disease.
Renal death is delayed by almost 1 year by the
low-protein diet.
Clinical
benefits

One additional year without dialysis is a very good

result for CKD patients and physicians too.
Low-protein diet significantly affects the
major
modifiable
cardiorenal
risk
factors
(proteinuria,
hypertension, anemia, hyperphosphatemia,
etc.).

discovery
of
nutritional abnormalities due to the close
monitoring
of
the nutritional status, thereby reducing the risk of
malnutrition. Indeed, in all studies on low-protein diets,
malnutrition is extremely rare, even with very low-protein
diets
[26, 27]. In a recent randomized trial, in which more
than
400 stage 3-5 CKD patients were followed for 30
months,
Blood Purif 2013;36:41-46
DOI: 10.1159/000350585

43

Additional Low-protein diet enhances the cardiorenal

advantages protective effect (BP lowering, antiproteinuric) of
ARBs.
Low-protein diet represents the only treatment
for
proteinuric nephropathy when ARBs cannot be
used.

held true for higher amounts of dietary protein

prescription; indeed, in a further study comparing daily
protein prescriptions of 0.80 and 0.55 g/kg, in the
lower protein group the adherence was lower (27 vs.
53%), but also the actual protein intake was lower and,
consequently, both metabolic acidosis and calciumphosphate
balance
improved [11]. Hence, compliance to a low-protein
diet is certainly low, but convinced doctors can
increase the compliance and even a minimal
reduction of 0.2 g/day of protein intake, regardless of
the degree of compliance, has to be considered of
clinical relevance.

In CKD the amount of dietary protein needed to

maintain a neutral nitrogen balance is about 0.55
g/kg/day,
provided adequate energy intake [23]. In the majority
of
patients who have been prescribed a low-protein diet,
the
amount of protein intake is much higher and it
rarely
drops below the safe threshold; however, it is quite
common for energy intake to reduce and this may cause
malnutrition [24, 25]. Prescription of a nutritional
treatment,
that is a low-protein diet, allows the early

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Safety of a Low-Protein Diet

Table 2. Possible limitation of protein intake restriction in

CKD

Compliance
similar
including

Adherence to low-protein diet is low,

to
the adherence to all chronic therapies,
ACEi.
Low-protein diet has beneficial, metabolic
and
clinical effects also in cases of reduced
compliance.

Malnutrition The risk of malnutrition increases when

energy
intake is reduced, but that associated with
the
prescription of low-protein intakes is
negligible. Low-protein diets do not
increase the risk of
malnutrition either during or after the
long-term treatment.

Table 3. Schedule for nutritional treatment in CKD

CKD GFR
Protein intake
stage ml/min g/kg/day
1
2
3a
3b
4

Note

90
89 - 60
59 - 45
44 - 30

normal: 1.2 - 1.0

salt, fat, energy, fiber
normal: 1.2 - 1.0
salt, fat, energy, fiber
lower-normal: 0.8 salt, fat, energy, fiber
low protein: 0.7 - 0.6 salt, fat, energy, fiber,
attention to
phosphate
29 - 15 low protein: 0.7 - 0.6 salt, fat, energy, fiber,
attention
to
phosphate
<0.6
ketoanalogs
<15
low protein: max. 0.6 salt, fat, energy, fiber,
attention to
phosphate
0.3 - 0.4 ketoanalogs

Table 4. Summary of nutritional treatment in CKD

- The best time to start the nutritional treatment in

CKD
is
unknown.
- The best nutritional treatment in CKD is unknown.
- From early stages of CKD several metabolic
derangements
and cardiovascular risk factors appear associated with
uremia, which are corrected by the nutritional
treatment.
- Nutritional treatment in CKD represents a major part
of the
conservative treatment.
- Since the first visit, CKD patients have to be educated
about
a

healthy diet (low salt, low saturated fats, high fibers,

low
energy).
- Protein restriction has to be progressively
increased
according to CKD stages.
- Physical activity should complement the
nutritional
treatment.

44

Blood Purif 2013;36:41-46

DOI: 10.1159/000350585

only 3 subjects developed malnutrition (i.e. less than

1%)
[28]; in contrast, 40-50% of patients on a free diet
spontaneously reduce both protein and energy intake,
developing overt malnutrition at the start of dialysis and
thus
demonstrating that a free diet, in contrast to a lowprotein one, may cause malnutrition. Recently, Dukkipati
et
al. [29] stated that a low-protein diet provides
adequate
amounts of protein for all CKD patients and does not
adversely affect their body composition. Overall, the
side
effects of nutritional treatment in CKD are scant and
can
be easily prevented with careful clinical monitoring
(table2).

[30].
This approach educates the patient in proper
nutrition
from the early stages of the disease and avoids
abrupt
changes in eating habits, allowing better adaptation and,
hence, adherence to dietary treatment (table 3).

Low-Protein Diet or Nutritional Therapy?

Low-protein intake alone, although relevant, represents

only a part of the nutritional treatment in CKD. It is essential since it affects uremic symptoms, phosphate and acidoBellizzi

Which Diet and When to Start It in CKD?

highly prevalent from the initial stages of the disease and

they are also the cause of faster CKD progression. Accordingly, in CKD the first aim of nutritional treatment is
the
early and strict restriction of energy, salt and saturated fat
intake. Regarding protein intake, a threshold of GFR for
starting a low-protein diet has not yet been defined;
the
common opinion among nephrologists is to start a
lowprotein diet when GFR falls below 60 ml/min/1.73
m2
(CKD 3). Such reduction should be obtained progressively, based on both the CKD stage and current protein
intake. Recently, an international expert consensus defined
this strategy: in CKD stages 1 and 2, when the usual protein intake is greater than 1.5 g/kg/day, patients should be
instructed to reduce the usual protein intake to 1.2-1.0 g/
kg/day, which is the intake indicated for the general population; in CKD stage 3, when uremic and
cardiovascular
complications develop, a reduction to 0.8 g/kg/day of protein is recommended, which represents the lower level of
the recommended intake for the general population; when
the GFR falls below 30 ml/min (CKD 4), which represents
a minor portion of the entire CKD population, it is
time
to introduce the low-protein diet (0.6 g/kg/day)

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In CKD, overweight, obesity and hypertension are

sis. Nevertheless, the entire nutritional treatment also

concerns a number of cardiovascular and renal risk factors.
On
the whole, as is the case with many chronic diseases
which
have a strong relationship with food where the
use
of
healthy diets (low energy, low salt, low saturated fats,
low
sugar, etc.) is recommended to improve both
cardiovascular risk and survival, also in CKD a healthy CKD diet, reduced in energy, saturated fats, eventually sugars, but
also
reduced in proteins and several micronutrients
(phosphorus, acids, salt, potassium), has to be recommended in
order to control metabolic derangements, renal outcome
and
cardiovascular risk.

Conclusions

In CKD, a low-protein diet has a minimal effect on

the
decline in GFR, but it is capable of delaying renal
death
(i.e. the start of renal replacement therapy) by
almost
1
year. Nonetheless, the main pathophysiological
rationale
for nutritional treatment in CKD is to prevent the
onset
and reduce the worsening of either metabolic
derangements or cardiorenal risk factors associated with
CKD.
Although high-degree scientific evidence is lacking,
commencing a nutritional treatment is recommended
from
the early stages of CKD, along with the progressive
implementation of a low-protein diet according to
disease
stage (table 4).

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