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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
4 
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
5 
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 
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
7 
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
8 
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
9 
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:
10 
· 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,
11 
 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
12 
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.
13 
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 
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 
(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 
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 
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 
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 
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 
Notes
21 
Notes
22 
Notes
23 
Inside of back page for pack shot 
of Albumen -RRT
24 
Produced and presented as a service to the medical profession by Biocorp, Pune, India and edited on their behalf by Dr. B. K. Iyer, 
consulting clinical co-ordinator 
Back page for ad and pack shot of 
our entire product range

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Rrt

  • 1. 1 Nutrition implications in renal disease
  • 2. 2 Inner page for photo of our entire range of products
  • 3. 3 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
  • 4. 4 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
  • 5. 5 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
  • 7. 7 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
  • 8. 8 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
  • 9. 9 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:
  • 10. 10 · 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,
  • 11. 11 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
  • 12. 12 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.
  • 13. 13 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
  • 23. 23 Inside of back page for pack shot of Albumen -RRT
  • 24. 24 Produced and presented as a service to the medical profession by Biocorp, Pune, India and edited on their behalf by Dr. B. K. Iyer, consulting clinical co-ordinator Back page for ad and pack shot of our entire product range