Management of nutrition in patients with renal failure is challenging as malnutrition occurs in up to 40% of such patients and is associated with increased morbidity and mortality. Malnutrition has multiple contributing factors, including decreased food intake due to gastrointestinal symptoms. Providing appropriate calorie and protein intake tailored to the patient's stage of kidney disease is important to permit adequate nutrition without unnecessary restrictions. Nutritional assessment, monitoring guidelines for calories, proteins and minerals, and specialized nutrition support are crucial for managing the nutrition of renal failure patients.

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Nutrition implications in renal disease

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EDITORIAL
Management of nutrition in renal failure patients is a real challenge since
malnutrition occurs in up to 40% of patients with renal failure, and is
associated with increased morbidity and mortality in this population.
Malnutrition in renal failure is multifactorial, but gastrointestinal symptoms
frequently contribute to decreased food intake.
How will a patient manage with the actual eating? How can an innocent and
illiterate care giver balance the nutrient composition of the patient's diet?
Will the husband and wife land up in a fight over such tasteless food being
prepared and served? Will the food be eaten completely to the prescribed
quantity? One close look at such and more problems will make any clinician
realize the difficulty and pitfalls of prescribing so many do's and don't's in the
dietary management of such patients.
Amongst all this, the inevitable looser is the patient. Since there is no other
option left for them, other than a compromised diet. The resulting outcome -
Protein content may go way below the recommendations,
Potassium and sodium levels may go haywire,
Imbalance in fluid intake and phosphorous may lead to bone
demineralization
This, it would appear rational to provide calories and protein that are
appropriate for a patient’s stage of kidney disease. Only such a planning
would permit adequate nutrition without unnecessary diet restrictions.
This review provides suggestions for diet, supplements, and specialized
nutrition support in such patients. Nutrition assessment, monitoring, and
guidelines for impacting calories, proteins and minerals are also discussed.
Truly yours,
Dr. B. K. Iyer
Consulting clinical co-ordinator
BIOCORP
Mrs. Anjali (Kapse) Oberoi
Consulting clinical Nutritionist
BIOCORP

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Inside.....
Introduction 5
Nutritional assessment in kidney disease 5
Clinical assessment 5
SGA for ESRD 6
MNT interventions in renal failure 6
MNT in acute renal failure 6
MNT for chronic renal failure 7
Causes of malnutrition 8
Decreased nutrient intake 8
Increased nutrient losses 9
Increased catabolism 9
Calculating calorie needs 10
Protein 10
Sodium 11
Potassium 11
Phosphate 11
MNT support 12
Pathophysiology in ESRD 12
Specifications of albumin preparations 12
Albumen-RRT 13
Indications for albumin administration 13
Rationale for albumin in RRT patients 14
Study on oral protein supplementation 14
Egg protein and its role 17
Fast facts on Albumen-RRT 18
References 19
Notes 20-22

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Introduction
One of the first signs of
declining kidney function can
be a poor appetite, which
places nutrition services at the
forefront of early detection and
intervention. By understanding
normal kidney function and
abnormal kidney function,
appropriate nutrition
intervention can be done.
Although the traditional
surrogate markers of
malnutrition, such as
decreased muscle mass or
serum proteins have been
associated with increased
mortality, research has proven
that improving nutritional
status will alter patient
outcomes.
Nutritional Assessment in
Kidney Disease
Patient’s diet history gives a
perspective about their past
and present nutritional status,
changes that have occurred,
and areas to be addressed in
a plan of care. This involves
an evaluation of:
1. Anthropometrics,
2. Clinical assessment,
and
3. Dietary assessment.
Biochemical parameters like
serum albumin, transferrin and
pre-albumin levels are
extensively used to assess the
nutritional status. They do not
necessarily correlate with
changes in other nutritional
parameters, and can be
influenced by non-nutritional
factors like infection,
inflammation, hydration status,
peritoneal or urinary albumin
losses and acidemia.
The drop in serum albumin,
which is the most widely used
parameter of assessing
nutritional status, is not only
less specific but also lags
behind the onset of
malnutrition.Alow albumin is
seen only when PEM
manifests overtly.
Anthropometry provides a
semiquantitative estimate of
the components of body
mass, particularly the bone,
muscle and fat compartments,
and thus gives us information
concerning nutritional status.
However it requires precise
techniques of measurement
and the use of proper
equipment to give accurate
and reproducible data.
Anthropometrics
Frequently, patients with
chronic kidney disease
(CKD) may not be aware of
how sick they have been and
weight loss could be gradual.
Therefore a history including
their usual body weight over
the previous 3 months to 1
year will help determine how
poorly nourished they have
been.
For the dialysis patient, weight
may vary due to the fact that
they are urinating very little or
not at all.As a result, they may
gain fluid weight between
treatments. Weekly weighing
taken after dialysis will help
determine trends over time.
The gain for most dialysis
patients is 3-5 % of their “dry
weight,” which is the weight
achieved by the end of the
dialysis treatment, eg.:
If a patient weighs 100 kg post
dialysis, a good fluid gain in
between the dialysis would be
between 3-5 kg (100 x .03 or
100 x .05).
When the weight exceeds this
range, the patient will require
more careful monitoring and
assessment for fluid
restriction and fluid control
adherence.
Clinical Assessment
Key aspects of the clinical
assessment of the patient with
kidney disease are:
· Poor taste acuity,
· Poor wound healing,
· Bedsores, or
· Other gastrointestinal
complaints.
Poor taste acuity is often a
problem due to the waste
products or urea in the blood
leaving a metallic taste in the
mouth. Other patients may
develop an aversion to meat
products as the kidney
function declines. Animal
products are high in the
mineral zinc. If a patient is
deficient in zinc, this may
contribute to poor taste acuity.
If a patient is experiencing
poor taste, a zinc evaluation
may be needed. Alternatives
to meat may need to be
explored, including mixed
dishes, casseroles, fish,
eggs, tofu or poultry, which are
often better tolerated. Patients
with CKD are thought to have
a more compromised immune
system. As a result, wound
healing may be poor. Staying
aware of bedsores with
prompt nutritional support will

6. 6
be needed. Diarrhoea is a
common complaint in diabetic
dialysis patients. Constipation
may occur due to fluid
restrictions, medications
required, or restriction of
foods that help relieve
constipation, such as prune
juice. Dental health will ensure
that patients get the nutrition
they need. This is particularly
important for dialysis patients
who require more protein.
Most protein foods are of
animal nature, which may
require more dentition. If
chewing problems continue,
alternative protein foods that
are easier to chew may need
to be considered.
Subjective Global Assess-ment
of Nutritional Status
of Patients [SGA] with
Chronic Renal Insuffi-ciency
and End Stage Re-nal
Disease
Subjective Global Assess-ment
[SGA] that refers to the
overall evaluation of a patient
by an experienced clinician, is
inexpensive, can be per-formed
rapidly, requires only
brief training, gives a global
score of nutrition and is repro-ducible.
It correlates the sub-jective
and objective aspects
of medical history and physi-cal
examination and also sat-isfactorily
agrees with objec-tive
methods of assessing
malnutrition. SGA is done us-ing
the 7 variables derived
from medical history and
physical examination with
each variable then scored
from 1-7, depending on the
severity.
MNT interventions in renal
Failure
Protein requirements for
patients with renal failure are
dependent on the acute or
chronic nature of the renal
failure and the presence and
type of dialysis. The nutritional
status and adequacy of
current intake of the patient
should also be considered.
Adults with chronic renal
failure who are not receiving
dialysis can usually maintain
a neutral nitrogen balance
consuming 0.6 g of protein per
kilogram if adequate calories
are ingested and most of the
protein is of high biological
value. A reduced protein
intake may decrease uremic
symptoms and delay the need

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for dialysis in a stable patient
with chronic renal insufficiency.
However, a reduced protein
intake is not advisable in the
setting of significant
malnutrition, or inadequate
calorie intake. The frequent
occurrence of malnutrition in
patients with renal failure, and
the consistent association
between markers of
malnutrition and poor
outcome in this population
emphasize the need for
appropriate and timely
nutrition intervention.
Following physiologic and
metabolic imbalances are
commonly observed but what
is noteworthy is that all stages
of CKD benefit from diet
m o d i f i c a t i o n . N u t r i t i o n
assessment and counseling
with the patient and family is
advisable; but it is the
consistent follow-up, with
modification of the nutrition
plan as clinical status
changes, that is essential.
MNT for Acute Kidney
Injury
There is no data to suggest
that a protein restriction is of
any benefit in the setting of
acute renal failure associated
with severe illness or multi-organ
dysfunction. In patients
who are acutely ill with
increasing uremia, there is a
temptation to focus on the
protein content of nutrition
support as a major contributor
to uremia.
Acute Kidney Injury [AKI] also
known as Acute renal failure
may require some diet
modifications if the patient is
still dialyzing or while
recovering from kidney failure.
These nutritional needs must
be based on the patient’s
medical condition, degree of
malnutrition, current laboratory
data, fluid status, and type and
frequency of dialysis. As a
result, diet modifications
require continual reevaluation.
Once dialysis is no longer
needed, or kidney function
returns, many diet restrictions
required while in renal failure
may no longer be needed—
such as potassium,
phosphorus, or fluid
restriction.
MNT for Chronic Kidney
Disease
CKD pogresses through
various stages and
progression from CKD stage
I to End Stage Renal Disease
is marked by irreversible and
complete loss of kidney
functions. A better
understanding of alterations in
physiologic processes and
their impact on nutrition status
helps achieve better patient
management. Thus , with the
advent of CKD, progression to
ESRD is natural and is
associated with huge
imbalance of metabolic
processes in the body. These

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alterations in the metabolic
processes occur in a very
short span ranging from a few
months to a few years. During
theCKDstage I to V, there are
physiologic and metabolic
alterations that demand a
highly specialized MNT for
various reasons.
Causes of malnutrition
• Patients with
progressive renal failure
are at increased risk for
malnutrition.
• Alteration of protein and
amino-acid metabolism
contributes to protein
wasting. As renal
function declines, the
patient becomes unable
to excrete the waste
products of nutrition
metabolism, especially
urea.
• When urea accumulates
in the blood, patients feel
nauseated and lose their
appetite.
• They often enter a
catabolic state and start
to lose their muscles and
protein stores.
Decreased nutrient intake
There are a number of factors
that contribute to malnutrition
in patients with renal failure.
Decreased intake of protein
and calories is the most
evident factor. Studies have
demonstrated that even
patients with a mild decline in
glomerular filtration rate (GFR)
(i.e. 50 mL/minute) have a
decreased calorie and protein
intake. Studies have also
documented that dietary
protein intake progressively
declines with decreasing
GFR. Overzealous diet
restrictions can also
contribute to decreased
intake. The provision of a
“renal diet” that limits protein,
salt, potassium, phosphorus
and fluid may further limit
intake in a patient with existing
malnutrition and poor oral
intake. Dietary intervention
should ideally not be instituted
until nutritional status and
eating habits have been
investigated, and the patient
demonstrates a clear need for
dietary restriction. Patients

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receiving maintenance
dialysis have increased serum
leptin and elevated serum
acute phase mediators such
as IL-6 and TNF. These
mediators would be expected
to exacerbate the anorexia
and decreased oral intake in
patients with renal failure. The
presence of uremia is a more
obvious factor that adds to the
decreased appetite and
nutrient intake.
Increased nutrient losses
Patients who receive
maintenance dialysis
experience a loss of nutrients
as a direct result of the dialysis
itself. Hemodialysis results in
a loss of 6–12 grams of amino
acids, 2–3 gms of peptides,
and negligible amounts of
protein per dialysis session.
During peritoneal dialysis,
patients lose only 2–4 grams
of amino acids, but
experience a total loss of 8–9
grams of protein per day
(including 5–6 grams of
albumin). Patients on
peritoneal dialysis can lose
over 15 grams of protein each
day during periods of
peritonitis. This increased
protein loss can continue for
days after the peritonitis is
treated. Malabsorption due to
bacterial overgrowth is
another route for nutrient loss
in some patients.
Increased catabolism
Patients with renal failure
are frequently “anabolism
challenged.” The increased
acute-phase reactants
observed with renal failure
and dialysis inhibit hepatic
production of albumin and
increase catabolism of
skeletal muscle tissue.
Acidosis is an additional
factor that precipitates
catabolism in this
population. Provision of
bicarbonate to
maintenance dialysis
patients decreases the
protein catabolic rate, and
improves nutrition status.
Medical Nutrition Therapy
(MNT)
MNT recommendations will
be based on these factors:

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· Underlying condition
and treatment plan
· Presence of other
chronic diseases
· Patient - goals for care
· Advanced directives
The diet format for predialysis,
chronic kidney disease, acute
renal failure, or dialysis
patients is based on the
popular National Renal Diet of
USA. It is based on grouping
foods of similar nutrient value.
The outlook at the dietary
management of such patients
is compounded by the fact that
majority of these patients have
very poor appetite and
metallic taste in mouth
because of inadequate
creatinine and urea clearance
rate. Besides, there are 10
key tasks to attend to:
1 Iron to increase
2 Potassium to decrease
3 Sodium to decrease
sometimes and increase
at other time
4 Vitamin C to increase
5 Protein to increase BUT
6 Not to increase the
phosphorous levels !!!!!
7 Calcium to increase
8 Vitamin D to increase
9 Balance with adequate
calories and
Carbohydrates
10 Check and provide
adequate source of
glutamine, arginine and Ù-
3 fatty acids.
Calculating calorie needs
Generally, caloric calculations
should be done with actual
edema-free body weight,
determined post-dialysis for
hemodialysis, and “post-drain”
for peritoneal dialysis.
The National Kidney
Foundation recommends that
when patients are 95% or
115% of the median
standard weight (as
determined from the
NHANES II data), that an
adjusted body weight be used.
Adjusted body weight is
calculated as follows:
Adjusted weight = ideal weight
+ [(actual edema-free weight
– ideal weight) x 0.25]
Protein
The amount of protein a patient
requires will depend upon their
stage of CKD. Dialysis also is
drain to body proteins and
daily losses can occur to an
extent of 20 to 30 g in 24 hr
continuous peritoneal dialysis
[= 1 g / hr]
Source: Krause Mahan,
2000
Protein – Pre-Dialysis
Patient
Protein restriction is a part of
the Pre-ESRD diet. Since
there is a decline in the
patient’s ability to clear the
blood from the protein
metabolites due to the loss of
kidney function, a high protein
diet causes accumulation of
metabolites in the blood.
Increased protein waste
products in the blood leads to
undesirable symptoms such
as nausea, vomiting, loss of
appetite, malnutrition and
further decline in kidney
function. The recommended
protein requirement is 0.6-0.8
grams per kilogram of ideal
body weight.
Protein – Dialysis Patient
If the disease progresses to
chronic kidney failure
(ESRD), the protein restriction
is removed and additional
protein intake is
recommended. It is
recommended that dialysis
patients increase their protein
intake to 1.2 to 1.4 grams per
kilogram of their ideal body
weight.
Whole body Amino acid
turnover kinetics:
Mass balance equation:
(Non dialyzed individuals)
Q = B+I = C+S
Where
Q=AA(leucine) flux,
B = Breakdown,

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I = Intake
C = Oxidation,
S = Synthesis
Dialyzed individuals:
Q= B+I =C+D+S
where
D = Dialysate loss
Thus Haemodialysis is not
catabolic but ANTI-ANABOLIC.
HD losses = 6 to 12 g AA /
treatment depending on high
flux dialyzers, fasting or post
prandial
CAPD losses = 3 g AA /d
Bio - Compatible membranes
reduce these losses.
Complications of hypo-proteinaemia
Mortality and morbidity in
haemodialysis patients
remain high in spite of great
improvements in technology
that one would expect to
improve patient survival.
3 main topics that can
influence patient outcome and
well-being:
o The dialysis dose,
o Nutrition,
o Biocompatibility of the
dialysis procedure.
Sodium
Dietary sodium intake is
frequently restricted to 2000 –
4000 mg per day for patients
with chronic kidney disease in
an effort to aid in the control of
hypertension, and to avoid
excessive thirst and fluid
consumption in those patients
with oliguria or anuria. Salt
substitutes frequently contain
potassium chloride, and
patients should be instructed
to avoid salt substitutes that
have not been approved or
prescribed by the attending
clinician.
Potassium
Renal compensatory
mechanisms maintain normal
serum potassium levels until
GFR drops below 15–20 mL/
minute. Dietary potassium is
generally restricted to 2000–
3000 mg/day for patients
requiring hemodialysis, and
3000–4000 mg/day for
patients requiring peritoneal
dialysis. There are a number
of non-food factors that can
cause or contribute to
hyperkalemia . Correcting
underlying factors causing
hyperkalemia, such as
inadequate glucose control
will frequently allow patients a
more liberal diet restriction
that will encourage good oral
intake.
Phosphate
Patients with chronic kidney
disease frequently experience
hyperphosphatemia when
their glomerular filtration rate
(GFR) drops to 20–30 mL/
min. A dietary phosphorus

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restriction of 800–1000 mg
per day should be
implemented when serum
phosphorus rises 4.6 mg/dL
(19). There is recent evidence
that phosphorus excretion is
affected when GFR drops
below 60 mL/min, contributing
to secondary hyper-parathyroidism.
The
increased serum parathyroid
hormone normalizes serum
phosphorus level until GFR
drops below 20–30.Adietary
phosphorus restriction of
800–1000 mg/day decreases
PTH levels and may reduce
bone resorption in those
patients with elevated PTH.
Patients with hyper-phosphatemia
frequently
receive calcium-containing
phosphate binders, which can
contribute to hypercalcemia or
elevation of the serum
calcium-phosphorus product.
The National Kidney
Foundation recommends that
serum calcium phosphorus
product be maintained at 55
mg/dL to prevent soft tissue
calcification. Calcium from
phosphorus binders should be
maintained below 1500 mg/
day, and total calcium intake
(supplements and diet) should
not exceed 2000 mg/day.
MNT support
Nutrition support in patients
who are unable to meet their
nutrition needs must be
supplemented with
appropriate counseling
and sound clinical advice.
Patients will benefit from
the calorie-dense, specially
formulated renal focussed
products with reduced
amounts of potassium and
phosphorus but there is no
data to suggest an
outcome advantage of
enteral feeding formula with
essential amino acids.
Reduced serum albumin is
associated with increased
morbidity and mortality in
renal failure, but this
association reflects the
presence of comorbid
conditions. Albumin
synthesis is reduced or
inhibited in humans by
acidemia and Prealbumin
levels are elevated in renal
failure, but may be
decreased immediately
after hemodialysis.
Prealbumin levels have a
strong, inverse association
with C-reactive protein and
other acute phase
reactants.
Frequently, the most
valuable nutrition
assessment must rely on an
evaluation of intake,
compared to an estimation
of the patient’s energy and
protein needs. Monitoring
oedema-free body weight
over time, in the outpatient
setting is a practical, albeit
insensitive, monitoring tool.
Interacting with a patient,
their family and caregivers,
and a review of intake will
frequently identify the
patient with nutrition
compromise.
Pathophysiology in
critically ill ESRD patients
Most critically ill patients
have a common
p a t h o p h y s i o l o g i c a l
process. Infection initiates
an inflammatory cascade
leading to the release of
various inflammatory
mediators (e.g. cytokines)
and activation of
leukocytes, resulting in
damaged endothelial
integrity, increasing
microvascular permeability
extravasation of fluids
(including albumin) into the
tissue. Such mediators
may also reprioritize
hepatic protein synthesis in
favor of acute phase
reactants at the expense of
albumin production,
leading to
hypoalbuminaemia and
poor outcome26.
Specifications of albumin
preparations
Albumin is generally
considered safe for use and
the molecular weight of
albumin is approximately
69,000 Daltons.
Commercially available
human albumin solutions for
IV use contain
approximately 96%
albumin, the remainder
being globulins. And,
although albumin is derived
from pooled human
plasma, there is no risk of
disease transmission
because it is heated and
sterilized by ultrafiltration.
100 ml of 2% albumin
increases intravascular
volume to a total of
approximately 450 ml.

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However, the volume effect
of albumin is not
predictable and depends
on blood volume, protein
levels, and capillary
permeability. Albumin is a
naturally occurring plasma
protein and has long been
considered the “gold-standard”,
the kind of
solution by which ESRD
patients would most profit.
Current research and trials
focus on the ultra high pure
recombinant human
albumin (Recombumin
20%) developed by
biotechnology that will be
available for clinical use
shortly, but definitely not
economically.
Albumen -RRT
Albumen RRT is a
specialised product from
BIOCORP consisting
principally of purified egg
elbumin for ESRD patients.
This enables easy oral
MNT intervention in such
patients. The subject of the
use of albumin as a protein
source, in clinical practice
has become more vital now
as the pathophysiology of
ESRD is now better
understood. Albumin has
several physiological
functions, and the value of
albumin administration is
increasing beyond doubt.
Clinical studies readily
demonstrate the benefits of
albumin replacement.
Indications for albumin
administration
The many indications for
albumin administration
quoted in literature are as
follows:
1. Volume replacement
therapy - Should
albumin be given for
intravascular volume
replacement in the
critically ill patient?
Hypovolemia is a
consequence of a
variety of
p a t h o p h y s i o l o g i c a l
processes, and it is
common in intensive
care patients.
Intravascular fluid
deficits occur even in
the absence of obvious
fluid loss, most likely
secondary to
g e n e r a l i z e d
modification of
endothelial barriers
resulting in capillary
leaks. Hypovolemia is a
potential killer in any
disease process and
intravenous fluids are
required to adequately
increase the circulating
blood volume. The
restoration of flow is
essential to avoid tissue
ischemia and
subsequent multiple
organ failure.
Hypovolemia is thus an
important reason to
administer albumin and
is thus largely given to
treat acute
hypovolemia, (e.g.
surgical blood loss,
trauma, haemorrhage)
and for other reasons
(e.g. infection). The
effects of albumin
depend on its movement
between the
intravascular and
e x t r a v a s c u l a r
compartments and
albumin may be without
benefit as a plasma
substitute in patients
showing capillary
leakage..
2. Support of colloid
oncotic pressure -
Maintenance of colloid
oncotic pressure is of
essence during
intravascular volume
replacement in the
critically ill patient. It is
believed that the
oncotic force of
concentrated human
albumin may help
reduce tissue oedema.
Albumin i s , thus,
considered necessary
to increase colloid
oncotic pressure to
prevent extravasation
of fluid from the
intravascular space. It
may, however,
aggravate interstitial
edema because it is not
confined to the vascular
space. Thus, the
retention of infused
albumin in the
i n t r a v a s c u l a r
compartment, and
therefore its
h a e m o d y n a m i c
efficacy, greatly varies
with regard to the
patient’s disease.
3. Maintenance of serum
albumin levels -

14. 14
Hypoalbuminemia: To
treat or not to treat? The
normal serum
concentration of
albumin in healthy
adults is approximately
3.5-5.0 g/100 mL.
Because of i t s
importance as an
outcome predictor,
serum albumin level has
been added as one of
the component
parameters in the
APACHE I I I score.
However, it is to be
remembered that
changes in its values
are the result of
pathological events, and
not the cause of them.
Hypoalbuminaemia is
common in seriously ill
patients and albumin
appears to be a
nonspecific marker of
the seriousness of an
illness. Several studies
have demonstrated that
low serum albumin is
associated with poor
outcome in acutely ill
patients. The results of
a meta-analysis by
Vincent et al
incorporating 90 cohort
studies with a total of
2,91,433 patients,
show that
hypoalbuminaemia was
a potent dose
d e p e n d e n t ,
independent predictor
of poor outcome. The
decline in serum
albumin concentration
significantly raised the
odds of mortality by
137%, morbidity by
89%, prolonged the ICU
and hospital stay by
28% and 71%
respectively, and
increased resource
utilization by 66%. A
serum albumin level of
2.0 gdL-1 in critically ill
patients has been
shown to be associated
with a mortality of
nearly 100%. The
association between
hypoalbuminaemia and
poor outcomes is the
primary motivation for
clinicians in
a d m i n i s t e r i n g
exogenous albumin to
h y p o a l b u m i n a e m i c
patients27.
4. Maintenance of other
roles of serum albumin
- Albumin may also have
some additional specific
effects related to its:
· Transport function
for various drugs
and endogenous
substances;
· Assistance in the
coagulation
pathways,
· Property of free
radical scavenging
by which it modifies
m e m b r a n e
permeability,
· Management of fluid
shifts as an osmotic
agent (to pull fluid
from the interstitium)
and thereby
redistribute fluid
during dialysis and
improve oxygenation
of all tissues.
Rationale for albumin
use in patients of RRT
It is difficult to put a price
tag on the impact of protein
malnutrition on quality of
life for individuals with
ESRD. Protein malnutrition
impairs immune response,
decreases hemoglobin
levels, causes anemia, and
results in muscle wasting.
In RRT patients,
hypoalbuminaemia is a
powerful predictor of
mortality and has been
associated with as much as
a 20-fold increase in the
relative risk of death. It has
been suggested that
malnutrition, evidenced by
hypoalbuminaemia plays a
key role in mortality.
Malnutrition continues to be
a threat to hemodialysis
(HD) patients and, to a
lesser extent, patients
managed with peritoneal
dialysis (PD). Uremic
malnutrition occurs as a
result of ESRD and is
characterized by elevated
blood urea nitrogen (BUN)
and chronic inflammation
as noted by elevated
serum C-reactive protein
(CRP). Due to the chronic
nature of uremic
malnutrition, there is an
insidious loss of both
somatic and visceral
protein stores. As such,
patients present with loss of
lean body mass and
decreased serum albumin

15. 15
(hypoalbuminemia).
While malnutrition and
hypoalbuminaemia have
been used synonymously,
there is strong evidence
that inflammation also
plays a role in determining
the level of serum albumin
in such patients. Both C-reactive
protein [CRP] and
cytokine levels are
predictive of temporary
variation in albumin level as
well as survival. This is
surprising but true
considering the fact that
CRP levels are raised in
dialysis patients for only a
fraction of the time.
The evidence for protein
catabolism during and after
each haemodialysis
treatment has been
recently reviewed as it
impacts other proposed
adverse effects of HD,
including cytokine
activation, clotting, and
inflammatory responses to
pyrogens that have been
implicated as a cause of
patient morbidity and
mortality. Animal studies
suggest that decreased
protein synthesis is likely
mediated by the significant
decrease in plasma amino
acid concentrations which
occurs during dialysis
treatment. Consequently,
protein needs are higher in
CHD patients than healthy
adults, but nutrient intake is
frequently much lower. With
malnutrition likely, the
patient’s amino acid pool is
already lacking, further
compromising protein
synthesis. Hence, the
relationship between
dialysis dose and
nutritional intake and the
potential nutritional
benefits of albumin on
more frequent dialysis as
well as survival rates
clearly demonstrate that
albumin supplementation to
such patients cannot be
overlooked. In summary,
CKD and HD / CAPD
comes with a huge burden
of problems. Protein is the
major issue as it is directly
related to the mortality and
morbidity ratio in ESRD
patients. There are number
of protein sources available
in nature. However the
protein that satisfies
following criteria saves and
extends life and this is
where albumin f i t s in
perfectly.
A recent study by
Veeneman et al.
consistently revealed that
the -ve protein balance of
HD can be easily reversed
by feeding protein. The
investigators in this study
agreed that proteolysis is
not increased by dialysis
and that the catabolic
effect of dialysis is caused
by 2 factors:
· Reduced synthesis
of protein, and
· I n c r e a s e d
proteolysis and loss
of amino acids in the
dialysate.
The increased breakdown
of muscle protein during
dialysis is apparently
compensated for by liver
uptake and synthesis,
resulting in no net
proteolysis, provided the
reduction in amino acid
concentration caused by
losses in the dialysate is
compensated by feeding
the patient. In this way, in
stable hemodialyzed
patients there can be little
evidence for a major
catabolic effect of the
dialysis itself. All ESRD
patients continue to
manifest signs of
malnutrition precipitated by
dialysis but responding well
to dietary supplements.
Patients who are
“overnourished” with high
BMI values have a better
prognosis as discussed
above.
Study on oral protein
supplementation in CAPD
patients
However, dietary
supplements especially
those with high protein
value have been the subject
of criticism because of their
cost, and the theoretical
argument that they cause
a proportional reduction in
the patient’s normal dietary
intake, resulting in a net
zero benefit. This question
was addressed by a study
where the aim was was to
evaluate the effect of oral
administration of an egg
albumin-based protein
supplement on the

16. 16
nutritional status of CAPD
patients. METHODS: In
this randomized, open
label, controlled clinical
trial, 28 CAPD patients
were allocated to a study
(n = 13) or a control (n =
15) group. Both groups
received conventional
nutritional counseling; the
study group received,
additionally, an oral egg
a l b u m i n - b a s e d
supplement. During a 6-
month follow-up, a l l
patients had monthly
clinical and biochemical
evaluations and quarterly
assessments of adequacy
of dialysis and nutrition.
RESULTS: Serum albumin
Levels were not different
between groups; however,
a significant increase
(baseline vs final) was
observed in the study
group (2.64+/-0.35 vs
3.05+/-0.72 g/dL) but not
in the control group (2.66+/
-0.56 vs 2.80+/-0.54 mg/
dL). Calorie and protein
intake increased more in
the study group (calories
1331+/-432 vs 1872+/-698
kcal; proteins 1.0+/-0.3 vs
1.7+/-0.7 g/kg) than in the
control group (calories
1423+/-410 vs 1567+/-381
kcal; proteins 1.0+/-0.4 vs
1.0+/-0.3 g/kg). Similarly,
non-protein nitrogen
appearance rate (nPNA)
increased significantly
more in the study (1.00+/-
0.23 vs 1.18+/-0.35 g/kg/
day) than in the control
group (0.91+/-0.11 vs
0.97+/-0.14 g/kg/ day).
Triceps skinfold thickness
(TSF) and midarm muscle
area (MAMA) displayed a
nonsignificant trend to a
greater increase in the
study group (TSF 16.7+/-
8.7 vs 18.3+/-10.7 mm;
MAMA 23.8+/-6.2 vs
25.8+/-5.9 cm2) than in
controls (TSF 16.4+/-5.7
vs 16.9+/-7.0 mm; MAMA
28.7+/-7.8 vs 30.0+/-7.9
cm2). At the end of follow-up,
the frequency of
patients with moderate or
severe malnutrition
decreased 6% in the control
group and decreased 28%
in the study group. At the
final evaluation, the most
important predictors of
serum albumin were the
oral egg albumin-based
supplement administration
and protein intake (p
0.05); secondary
predictors (p = 0.06) were
peritoneal transport rate
and MAMA.
CONCLUSIONS: In the
study group, oral
administration of the egg
albumin-based supplement
significantly improved
serum albumin, calorie and
protein intake, and nPNA,
and, compared to controls,
this maneuver was
associated with a trend to
increased anthropometric
parameters and improved
Subjective Global
Assessment evaluation.
Oral administration of the
albumin supplement and
protein intake were the
most significant predictors
of serum albumin at the end
of follow-up. This oral
supplement may be a safe,
effective, and cheap
method to improve
nutritional status in
peritoneal dialysis
patients28.
Unfortunately, the Renal
Diet is not only
unpalatable, but it also
restricts usual dietary
choices of protein rich
foods such as beef, pork,
shellfish, dairy, beans,
nuts, and more. In a review
article by Ikizler, as
suggested, i t seems a
reasonable assumption,
that “Provision of nutrients,
either in the form of
intradialytic parenteral
nutrition or oral feeding
during hemodialysis, can
adequately compensate for
the catabolic effects of the
hemodialysis procedure.”
Oral nutritional
supplements are more
feasible to use as
compared to intradialytic
parenteral nutrition in terms
of costs and infection risks.
The issue remains however
in how to provide additional
dietary protein that:
· Contains a l l the
essential and non-essential
amino acids to
bolster the amino acid
pool,
· Can be readily
absorbed to decrease
the burden of digestion
in malnourished CHD
patients,
· Is accepted and well
tolerated by CHD

17. 17
patients,
· Can be easily
dispensed and
consumed at the
dialysis unit or at home,
and
· Complies with the
recommended dietary
restriction for CHD
patients.
Standard oral nutritional
supplements which are
commonly used for CHD
patients are high in sugar
and electrolytes and do not
comply with recommended
renal diet restrictions. The
high sugar content can
diminish appetite for
regular meals, cause
osmotic diarrhea, and
elevate blood sugars in
diabetics. Unfortunately, up
until now, these
supplements have been the
only products available to
clinicians and patients. Not
any more!
In addition to enhanced
immunity with potentially
fewer infections, the
benefits of Albumin intake
for dialysis patients can be
illustrated withthe costs
associated with anemia
management in ESRD.
There are several
contributing factors to the
etiology of anemia in
ESRD such as insufficient
iron stores and iron
utilization, recurrent
infections and malnutrition.
Any of the commercial
forms of the replacement
drug for the hormone
erythropoietin used to treat
anemia in CHD patients,
form the single most
expensive item in ESRD
care. This is always
prescribed once the ESRD
patient’s serum hemoglobin
level has dropped below 12
gm/dL. Production of
erythropoietin and
hemoglobin are both
dependent on adequate
protein intake. Protein
malnutrition increase
resistance to the
biotechnolgically produced
external erythropoietin
supplement. Therefore,
higher doses would be
required in the presence of
malnutrition. Adequate iron
stores and iron utilization,
both of which are
influenced by body
proteins, are also required
for efficacy of the
biotechnolgically produced
external erythropoietin
supplement therapy. As
nutritional status improves
as measured by increased
albumin levels, less of the
biotechnolgically produced
external erythropoietin
supplement is needed, thus
aiding to cut down therapy
maintenance costs in
ESRD patients.
Egg whte helps lower
phosphorus
Phosphorus levels declined
in dialysis patients who ate
egg whites instead of meat
for one meal a day as per
a study done by Lynn M.
Taylor, MS, RD, and Ted
Markewich, BA, of DaVita
Carroll County Dialysis in
suburban Maryland. 6 men
and 7 women (mean age
62 years) with serum
phosphorus levels higher
than 3.9 mg/dL were
enrolled. The first 4 weeks
of the study (baseline)
consisted of data
collection. Then, for one
meal per day over the
following 6 weeks, patients
substituted 8 ounces of
pasteurized liquid egg
whites for meat. The 8
ounces of egg whites
contained 24 grams of
protein and 28 mg of
phosphorus. 12 patients
(92%) had a decrease in
phosphorus, the
researchers reported here
at the National Kidney
Foundation's 2008 Spring
Clinical Meetings. Mean
phosphorus levels declined
significantly from 5.54 mg/
dL at baseline to 4.63 mg/
dL during the study. Mean
p a t i e n t - r e p o r t e d
phosphorus intake also
declined significantly, from
692 to 572 mg/day. “Egg
whites are an effective
component of the renal diet
for lowering serum
phosphorus while
maintaining the albumin
level, the authors
concluded.31
Is egg protein all it’s
cracked up to be?
Eggs have the highest
biological value (BV) of any
food protein, which means
that the amino acids found
in eggs are converted into
body tissue more

18. 18
efficiently than any other
known dietary protein. Egg
protein possesses the
highest possible Protein
Digestibility Corrected
Amino Acid Score
(PDCAAS), the most
commonly used measure
of protein quality [not
forgetting milk and soya
protein]. Research
suggests that diets higher
in animal protein and lower
in carbohydrates can help
ESRD patients maintain
muscle mass during
dialysis, thus improving
body composition. This is
of great importance since
lean body mass is the
single most important
determinant of resting
energy expenditure.
Egg albumin: Easy and
abundantly available
aource
In one evaluation, the most
important predictors of
serum albumin were the
oral egg albumin-based
supplement administration
and protein intake (p
0.05); secondary
predictors (p = 0.06) were
peritoneal transport rate
and MAMA (Mid Arm
Muscle Area). Oral
administration of the
albumin supplement and
protein intake were the
most significant predictors
of serum albumin at the end
of follow-up. This oral
supplement may be a safe,
effective, and cheap
method to improve
nutritional status in
peritoneal dialysis
patients.30
Fast Facts: Albumen-
RRT
Albumen-RRT contains
egg albumin, which is an
excellent source of all the
essential and non-essential
amino acids. Albumen-RRT
is stable as a ready to use
powder form at room
temperature. As such, the
product can be mixed with
food as sprinkles or liquid,
or taken, as is available–
providing 7grams of
protein in only 10g. of the
powder.
Conclusions
The benefits provided by
orally administered
Albumin in ALBUMEN-RRT
are as good as expensive
parenteral albumin at a
fraction of the cost. Such a
supplementation enables
the attending clinician to
meet a l l the exacting
demands of the dietary
management of ESRD
patients. By not only
meeting the protein
demands but also the
needs for intervention into
the mineral requirements,
ALBUMEN-RRT is a unique
product that is designed
specifically for such
patients.

19. 19
References
1. MehrotraR,KoppleJD.Nutritional
managementof maintenance di-alysis
patients:whyaren’twedo-ingbetter?
AnnRevNutr,2001;21:
343-379.
2. Kopple JD. Pathophysiology of
protein-energy wasting in chronic
renal failure. J Nutr, 1999;129(1S
Suppl):247S-251S.
3. Strid H, Simren M, Stotzer P, et
al. Patients with chronic renal
failure have abnormal small
intestinal motility and a high
prevalence of small intestinal
bacterial overgrowth. Digestion,
2003;67(3):129-137.
4. VanVlemB, Schoonjans R,Van-holder
R, et al. Delayed gastric
emptying in dyspeptic chronic
hemodialysis patients. Am J
KidneyDis,2000;36(5):962-968.
5. CapelliJP,KushnerH,Camiscioli
TC, Chen SM, Torres MA. Effect
of intradialytic parenteral nutrition
on mortality rates in endstage
renal disease care.AmJ Kidney
Dis, 1994; 23(6): 808- 816.
6. Mitch WE, Price SR. Mecha-nisms
activating proteolysis to
causemuscleatrophyincatabolic
conditions. J Ren Nutr, 2003;
13(2):149-152.
7. Natl.KidneyFound.IInit.K-DOQ.
Clinical practice guidelines for nu-trition
in chronic renal failure.Am
J Kidney Dis, 2000; 35:S1-S140.
8. Bergstrom J, Furst P, Alvestrand
A, et al. Protein and energy in-take,
nitrogen balance, and
nitrogenlossesinpatientstreated
with continuous ambulatory
peritoneal dialysis. Kidney Int,
1993; 44: 1048- 1057.
9. Walser M, MitchWE,Maroni BJ,
Kopple JD. Should protein intake
be restricted in predialysis pa-tients?
Kidney Int, 1999; 55( 3):
771-777.
10. Ikizler TA, Pupim LB, Brouillette
JR,etal.Hemodialysisstimulates
muscle and whole body protein
lossandalterssubstrateoxidation.
Am J Physiol Endocrinol Metab,
2002;282:E107-E116.
11. ScheinkestelCD,KarL, Marshall
K, Bailey M, Davies A, Nyulasi I,
Tuxen DV. Prospective
randomized trial to assess caloric
and protein needs of critically ill,
anuric,ventilatedpatientsrequiring
continuous renal replacement
therapy.Nutrition,2003;19(11-12):
909-16.
12. Bellomo,etal.AprospectiveCom-parativeStudyofModerateVshigh
protein Intake for Critically Ill Pa-tients
with Acute Renal Failure.
RenalFailure,1997; 19:111-120.
13. Macias WL, Alaka KJ, Murphy
MH,etal.Impactofnutritionalregi-menonprotein
catabolismandni-trogen
balance in patients with
acute renal failure. JPEN, 1996;
20: 56- 62.
14. Allon M: Hyperkalemia in End-
Stage Renal Disease: Mecha-nisms
and Management. J Am
SocNephrol,1995;6:1134-1142.
15. National Kidney Foundation. K/
DOQIClinical Practice Guidelines
forManagingBoneMetabolismin
ChronicKidneyDisease.AmJKid-neyDisease,
2003;42(suppl1):S1-
S92.
16. FiaccadoriE,MaggioreU,Giacosa
R,etal.Enteralnutritioninpatients
with acute renal failure.KidneyInt,
2004;65(3):999-1008.
17. HolleyJL,KirkJ.Enteraltubefeed-ing
in a cohort of chronic
hemodialysispatients. JRenNutr,
2002; 12( 3): 177- 182.
18. KaysenGA,DubinJA, MullerHG,
et al. Inflammation and reduced
albuminsynthesisassociatedwith
stable decline inserumalbumin in
hemodialysis patients.Kidney Int,
2004;65(4):1408-1415.
19. KaysenGA,DubinJA, MullerHG,
et al. Relationships among
inflammation nutrition and
physiologic mechanisms
establishing albumin levels in
hemodialysis patients.Kidney Int,
2002;61(6):2240-2249.
20. Moshage H. Cytokines and the
hepatic acute phase response. J
Pathol, 1997;191:257-266.
21. Moshage HJ, Janssen JAM,
FranssenJH,HafkenscheidJCM,
Yap SH. Study of the molecular
mechanisms of decreased liver
synthesis of albumin in
inflammation. J Clin Invest, 1987;
79: 1635- 1641.
22. BellizziV, Di IorioBR,Terracciano
V, et al. Daily nutrient intake
represents a modifiable
determinant of nutritional status in
chronic haemodialysis patients.
Nephrol Dial Transplant, 2003;
18(9):1874-1881.
23. KloppenburgWD,StegemanCA,
de Jong PE, Relating protein in-taketonutritionalstatusinhaemo-dialysis
patients: how to normal-ize
the protein equivalent of total
nitrogen appearance (PNA)?
NephrolDialTransplant, 1999;14(
9):2165-2172.
24. RaoM,SharmaM,Juneja R, et al
Calculated nitrogen balance in
hemodialysispatients:influenceof
protein intake. Kidney Int, 2000;
58(1):336-345.
25. Kalantar-Zadeh K, Kopple JD.
Trace elements and vitamins in
maintenancedialysispatients.Adv
Ren Replace Ther, 2003; 10(3):
170-182.
26. YeunJY, LevineRA,MantadilokV
etal.C-reactiveproteinpredictsall
- cause and cardiovascular mor-talityinhaemodialysispatients.
Am
J Kidney Dis 2001; 35: 469-76.
27. Vincent JL, Dubois MJ, Navickis
RJ,WilkesMM.Hypoalbuminemia
in acute illness: Is there a ration-aleforintervention.
AnnSurg2003;
237:319-34.
28. LGonzalez-Espinoza,JGutierrez-
Chavez, FM del Campo, HR
Martinez-Ramirez, L Cortes-
Sanabria, E Rojas-Campos, AM
Cueto-Manzano, Randomized,
open label, controlled clinical trial
of oral administration of an egg
albumin-basedproteinsupplement
to patientsoncontinuousambula-tory
peritoneal dialysis, Perit. Dial.
Int. 2005 25: 173-180.
29. Blood Purification 1999;17:159-
165.
30. Perit Dial Int 25(2): 173-180 2005
31. Blood Purification 1999;17:159-
165.
30. Perit Dial Int 25(2): 173-180 2005

20. 20
Notes

21. 21
Notes

22. 22
Notes

23. 23
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24. 24
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