c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5

Available online at www.sciencedirect.com

journal homepage: www.elsevier.com/locate/cqn

Review article

Nutritional problems in adult patients with chronic kidney

disease

Anita Saxena*
Associate Professor, Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences,
Raebarely Road, Lucknow 260014, India

article info abstract

Article history: Chronic renal failure (CRF) impairs not only appetite but also impairs immune function,
Received 28 June 2012 resulting in increased susceptibility to infections and poor wound healing and may
Accepted 8 July 2012 predispose to inflammatory diseases. Every strategy should be used to avoid complications
Available online 6 August 2012 of chronic kidney disease (CKD) manifested in uremic state including anorexia, nausea,
vomiting leading to malnutrition, fluid and electrolyte imbalance leading to volume
Keywords: overload, hyperkalemia, metabolic acidosis, and hyperphosphatemia, as well as abnor-
Chronic kidney disease malities related to hormonal or systemic dysfunction such as hypertension, anemia,
Nutrition hyperlipidemia, bone disease, pericarditis, peripheral neuropathy, and central nervous
Hyperphosphatemia system abnormalities. With decline in GFR, nutrient requirements change. Nutritional
Hyperkalemia status should be assessed periodically. Low protein diets are beneficial for CKD stages 1e5,
Fluid balance but nutritional management should be such that the nutritional status is not compro-
mised. In order to maintain proper nutritional status patients on maintenance dialysis
require high protein diet. Timely diagnosis of protein-energy-wasting (PEW) is important
for early initiation of nutritional intervention and treatment. Management of hypertension,
bone mineral disease, fluid overload and gastroparesis should be given prime importance.
Copyright ª 2012, Reed Elsevier India Pvt. Ltd. All rights reserved.

The term “protein-energy-wasting” (PEW) has been proposed 2. Diagnosis of PEW

to describe conditions such as protein-energy malnutrition,
malnutrition-inflammation complex syndrome, malnutri-
tion-inflammation atherosclerosis syndrome, kidney wasting
disease and uremic cachexia which are associated with
inadequate nutrient intake, decreased body protein and/or
reduced energy reserves.1,2 PEW defines loss of somatic and
circulating body protein mass and energy reserves2 (Table 1).
1. Causes of malnutrition
Malnutrition and inflammation are two major causes of PEW.
Table 2 summarizes nutritional and non nutritional causes
which lead to PEW in CKD population.
Timely diagnosis of PEW is important for early initiation of
intervention and treatment.1 Criteria for diagnosing PEW2 are
given in Table 3.
3. Nutritional implications and
complications of renal dysfunction
Chronic renal failure (CRF) impairs appetite.3 Several studies
have reported a statistically significant association between
poor appetite and decreased survival.4,5 PEW by virtue of its
malnutrition component may lead to impaired immune

* Tel.: þ91 9453019812 (mobile).

E-mail addresses: anitimmy@sgpgi.ac.in, anitimmy@yahoo.com.
2211-9477/$ e see front matter Copyright ª 2012, Reed Elsevier India Pvt. Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.cqn.2012.06.007
 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5 223

Table 1 e Types of malnutrition in kidney disease.2,91

Factors Type 1 Type 2

Associated with uremic syndrome Associated with MIA syndrome

Serum albumin Normal/low Low

Comorbidity Uncommon Common
Presence of inflammation No Yes
Food intake Decreased Low/Normal
Resting energy expenditure Normal Elevated
Oxidative stress Increased Markedly Increased
Protein catabolism Decreased Increased
Reversed by dialysis and nutritional support Yes No

function and host resistance, resulting in increased suscepti-
bility to infections and poor wound healing. Low protein diets
prescribed to CKD patient are also atherogenic because
patients may tend to consume high amounts of atherogenic
fat in order to maintain adequate energy. Patients may also
have low dietary mineral and vitamin intake.6 They are
susceptible to zinc, vitamin B6, vitamin C and folic acid defi-
ciencies most of which can induce alterations in host defense,
such as diminished antibody response, lymphocytic
dysfunction and impaired wound healing.7e9 Vitamin D defi-
ciency, refractory anemia and iron depletion is also a conse-
quence of PEW which may lead to increased platelet count
and/or activation and increased mycloperoxidase activity.10
Impaired host resistance, aggravated by PEW may predis-
pose to inflammatory diseases such as hepatitis C infections,
which is associated with increased death in CKD.11
In CKD population, inflammation (increased serum CRP
levels and IL6 concentrations) has been shown to be associ-
ated with increased risk of cardiovascular death.12 Inflam-
mation induces endothelial cell damage and endothelial
dysfunction, predisposing to atherosclerosis plaque
formation. Inflammation may both be a cause and a conse-
quence of PEW. Furthermore, derangements of gastrointes-
tinal tract are characteristic of malnutrition, with atrophy of
the gut lining, decreased intestinal secretion, and altered gut
flora leading to further reduction in gut function and ability to
absorb nutrients.13 Sarcopenia (muscle wasting) may lead to
reduced skeletal, respiratory and cardiac muscle function,
compromising the vital functions of these organ systems. It
may also restrict muscle based oxidative metabolism and thus
lead to a decreased antioxidant defense.14 Tissue damage can
affect protective actions of certain molecules such as gelsolin
(vitamin D binding protein) and is consumed by circulating
actin.15,16
Gradual loss of body fat content during the progression of
CKD may result in decreased sequestration of uremic toxins
and lower production of certain anti-inflammatory cytokines
and adiponectine. The endotoxinelipoprotein hypothesis17
explains the link between low levels of serum cholesterol and
increased cardiovascular disease and death in both CKD and
chronic heart failure patients; hence, higher concentrations of
unbound endotoxins occurring in the setting of low serum

Table 2 e Causes of protein-energy-wasting92 (PEW).

Inflammation
1. Associated with infected vascular access sites, systemic infectious illness including tuberculosis, diabetes mellitus, myocardial infarction,
stroke, peripheral vascular ischemia, vasculitis.
2. Unassociated with clinically apparent disease such as, inflammatory reaction to vascular access catheters, grafts, peritoneal dialysis
catheters, dialysis tubing, impure dialysate, old nonfunctioning transplant kidney, kidney failure per se
Decreased food intake
1. Anorexia caused by uremic toxicity, medication, inflammatory disorders
2. Loss of taste, unpalatable prescribed diets
3. Nonanorexic causes (financial constraints), medical or surgical illness, particularly of gastrointestinal tract, impaired cognitive function,
other mental disability, physical disability, loss of dentures
Dialysate nutrient losses
1. Losses of amino acids, peptides and protein into dialysate
2. Losses of water soluble vitamins and minerals during dialysis
Metabolic acidemia
Anemia and loss of blood due to
1. Gastrointestinal bleed
2. Frequent blood sampling
Hormonal disorders
1. Resistance to anabolic hormones such as insulin, growth hormone, insulin-like growth factor-1
2. Increased levels of counter regulatory hormones such as glucagon, parathyroid hormone
Increased fecal excretion of nitrogen
Decreased level of antioxidants such as vitamin E, C, selenium, reduced glutathione (GSH)
Physical conditioning
224 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5
Table 3 e Criteria for diagnosing protein-energy-wasting (PEW).
Serum chemistry
1. Serum albumin level <3.8 g/dL
2. Serum pre-albumin level <30 mg/dL
3. Serum cholesterol level < 100 mg/dL
Body mass
1. BMI<22 kg m2 (for age >65 years), <23 kg m2(for age >65 years)
2. Unintentional weight loss over time 5% in three months; or 10% in 6 months;
Total body fat percent< 10%
Muscle mass
1. Muscle wasting, reduced muscle mass 5% in three months; or 10% in 6 months;
2. Reduced midarm muscle circumference area >10 reduction in relation to 50th percentile of reference population
3. Creatinine appearance
Dietary intake
1. Unintentional low dietary protein intake <0.8 g/kg/d for at least 2 months for maintenance dialysis patients or <0.60 g/kg/d for patients
with CKD stage 2e5 with 5 g/d of urinary protein loss.
2. Unintentional low dietary energy intake <25 kcal/kg/d for least 2 months
cholesterol may activate the proinflammtory cytokine cascade
leading to endothelial dysfunction and atherosclerosis.18
Every strategy should be used to avoid complications of
CKD manifested in uremic state including anorexia, nausea,
vomiting leading to malnutrition, fluid and electrolyte
imbalance leading to volume overload, hyperkalemia, meta-
bolic acidosis, and hyperphosphatemia, as well as abnormal-
ities related to hormonal or systemic dysfunction such as
hypertension, anemia, hyperlipidemia, bone disease, peri-
carditis, peripheral neuropathy, and central nervous system
abnormalities (ranging from loss of concentration and leth-
argy to seizures, coma, and death).
Restriction of dietary protein intake has been a relevant
part of the management of CKD for more than 100 years, but
even today, the principal goal of protein-restricted regimens is
to decrease the accumulation of nitrogen waste products,
hydrogen ions, phosphates, and inorganic ions while main-
taining an adequate nutritional status to avoid deterioration
of renal function.19,20 Every gram of nitrogen absorbed by the
body is eliminated into urine after metabolic processing.
Since, proteinuria is an important independent risk factor for
progression of CKD, nutritional intervention is directed
toward not only lowering proteinuria to a minimal level but
also to replenish losses of the same.21
3.1. Goals of nutritional therapy
Adequate nutritional support can maintain protein stores and
correct pre-existing or disease-related deficits in lean body
mass. Overnutrition, on the other hand, is associated with
altered renal hemodynamics, particularly if the excess
consists of high protein intake, high aminoacid intake, or
both. Glomerular protein trafficking induces hypermetabo-
lism and oxidative stress, and a low protein diet (LPT), is
associated with reduced oxygen consumption and mono-
aldehyde production.2,22 Nutritional intervention is directed
toward overall patient outcome and comorbid conditions such
as anemia, bone disease, and cardiovascular disease (CVD). As
glomerular filtration rate (GFR) declines, the stages of kidney
disease23 change, and the nutritional requirements also
change (Table 4). Therefore, the primary objective of nutri-
tional intervention for patients with renal disease is to
 Control progression of disease and to maintain adequate
nutritional status
 Prevent appearance of uremic symptoms
 Delay renal replacement initiation
 Improve outcomes in CKD patients
 Improve nutrition
 Build up body stores for good transplant outcome (if
planned)
 Improve quality of life
3.1.1. Energy
Increasing or decreasing energy requirement is not necessary
for patients with CKD before ESRD develops. For individuals
with CRF (GFR <25 mL/min) who are not undergoing mainte-
nance dialysis the energy intake should be 35 kcal/kg/day
provided they are below 60 years of age and 30 kcal/kg/day
those who are more than 60 years of age. Research data show
that basal rate metabolism and energy requirements in these
patients do not differ from those in healthy adults. Metabolic
balance studies of such individuals indicate that a diet
providing about 35 kcal/kg/d engenders neutral nitrogen
balance and maintains serum albumin and anthropometric
indices.24 Energy requirements are given in Table 4. Sponta-
neous reduction in energy and protein intake have been re-
ported when renal function is impaired and intake as low as
21 kcal/kg/d and 0.85 g protein/kg/d have been observed in
patients with CKD stage 3 i.e., GFR <30 mL/min. With
restricted protein intake risk for intake of hypocaloric diet
increases when GFR declines below 50 mL/min. Careful eval-
uation of protein energy intake is necessary to prevent setting
in of PEW.
3.1.2. Protein restriction
Multiple well-designed randomized controlled human trials
have evaluated both the efficacy and safety of protein
restriction in patients with progressive CKD.25e29 Moderate
protein restriction (0.6e0.8 g/kg per day) is associated with
a modest but not significant benefit of protein restriction on
progression of renal disease. It is generally well tolerated and
does not lead to malnutrition in patients with CKD providing
caloric goals are met, dietary protein is of high biologic value,
 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5 225

Table 4 e Stages of chronic kidney disease23 and changes in nutrient requirement.

Stage Description GFR mL/min/1.73 m2 Nutrient requirement

1 Kidney damage (presence of protein >90 Recommended dietary allowances

in urine) with normal GFR Energy 30e35 kcal/kg/d
(35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d)
Water soluble Vitamins and minerals as per RDA
2 Kidney damage with mild 60e<89 Low protein 0.6e0. 75 g/kg/d
decrease in GFR Energy 30e35 kcal/kg/d
(35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d)
Phosphorus 800e1000 mg
Non-calcium based phosphate binder with meals
Calcium 1000e1500 mg/d
Sodium <2.4 g/d
Potassium 1 mEq/kg
Cholesterol <200 mg/d
Water soluble Vitamins and minerals as per RDA
3 Moderate decrease in GFR 30e59 Low protein 0.6e0.75 g/,
Energy 30e35 kcal/kg/d
(35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d)
Phosphorus 800e1000 mg
Non-calcium based phosphate binder with meals
Calcium 1000e1500 mg/d
Sodium <2.4 g/d
Potassium 1 mEq/kg
Cholesterol <200 mg/d
Water soluble Vitamins and minerals as per RDA
4 Severe reduction in GFR 15e<30 Low protein 0.6 g-75/kg/d,
Energy 30e35 kcal/kg/d
(35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d)
Phosphorus 800e1000 mg
Non-calcium based phosphate binder with meals
Calcium 1000e1500 mg/d
Sodium <2.4 g/d
Potassium 1 mEq/kg
Cholesterol <200 mg/d
Water soluble vitamins and minerals as per RDA
5 Kidney failure <15 Low protein 0.6 g/kg/d,
(End-stage renal disease) if on conservative management,
1.2e1.3 g/kg/d if on
maintenance dialysis phosphorus 800e1000 mg
Energy 30e35 kcal/kg/d
(35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d)
Non-calcium based phosphate binder with meals
Calcium 1000e1500 mg/d
Sodium <2.4 g/d
Potassium 1 mEq/kg
Cholesterol <200 mg/d
Water soluble Vitamins and minerals as per RDA6
Treat anemia with folic acid, B12,
iron supplements (check iron profile)
and erythropoietin stimulating agents
as per requirements of the patients.

and metabolic acidosis is avoided. Low protein diet (0.6e0.8 g/
kg per day) should be used in select predialysis patients who
are highly motivated to follow such a diet. According to KDOQI
guideline 24,30 individuals with CRF (GFR <25 mL/min) who
are not undergoing maintenance dialysis institution of
a planned low-protein diet providing 0.60 g/kg/d should be
considered. For individuals who will not accept such a diet or
who are not able to maintain adequate daily energy intake
with such a diet, an intake of up to 0.75 g protein/kg/d may be
prescribed.30 Target dietary protein intake for people with
diabetes and CKD stages 1e4 should be the RDA of 0.8 g/kg
body weight per day.31
3.1.2.1. Efficacy of low protein diet. Relatively small studies
have suggested that a low protein diet may protect against
progression of CKD in at least some diseases, such as diabetic
nephropathy and chronic glomerular diseases.32e35 It has
been shown that in diabetic nephropathy, the rate of decline
in GFR slowed by 75 percent with dietary protein restriction.36
Even patients with an initial GFR as low as 15 mL/min
226 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5
appeared to benefit.34 In contrast to these positive results,
a much larger controlled trial (Northern Italian Cooperative
Study Group) involving patients with a variety of renal
diseases found that a low protein diet produced only a small,
not statistically significant trend toward benefit at two years.36
There were, however, two potential problems with this study:
the GFR was measured indirectly by the often inaccurate
creatinine clearance and, more importantly, noncompliance
with protein restriction minimized the difference in dietary
intake between control and treated groups. Protein intake
(as estimated from the formula derived below) has been close
to 1 g/kg per day in the control group in most studies. Whereas
protein intake was reduced by 29e43 percent in the treated
group in the smaller successful trials.32e34
It was reduced by only 16 percent in the Italian trial.36
Difficulty with compliance occurred despite the availability
of much greater dietary counseling and monitoring than is
available to the typical practitioner.
Modification of Diet in Renal Disease (MDRD) study
analyzed patients with nondiabetic CKD and a mean GFR of
39 mL/min per 1.73 m2 (all patients with GFR less than 55 mL/
min per 1.73 m2).37 Protein intake was 1.3 or 0.58 g/kg per day
with or without aggressive blood pressure control and followed
for a mean of 2.2 years. The achieved protein intake in the low
protein group was between 0.6 and 0.8 g/kg per day. Despite
good compliance, there appeared to be little overall benefit
with the low protein diet. A similar lack of substantial benefit
was noted in a second part of this study involving patients with
more advanced disease (mean GFR 19 mL/min per 1.73 m2) who
were randomized to a low protein diet or a very low protein diet
(0.3 g/kg per day) with a ketoacid-amino acid supplement. A
long-term follow-up analysis of the MDRD study38,39 reflected
on outcomes during the first six years after the trial ended, the
next six year period, and the total 12-year period. Analysis of
outcomes after the first six years revealed a small but signifi-
cant benefit of low-protein intake on renal failure and all-cause
mortality (hazard ratios of 0.68, CI 0.51e0.93 and 0.66, CI
0.50e0.87, respectively). However, there was no benefit of
protein restriction when outcomes between 6 and 12 years
were analyzed. Another trial also provided evidence of modest
benefit from dietary protein restriction (control group mean
protein intake 1.06 g/kg per day) versus protein intake 0.8 g/kg
per day, higher than the desired level of 0.6 g/kg per day in
treatment group) in nondiabetic CKD.40
Reviews published in 2006 and 2008 evaluated eight
randomized controlled trials that compared low protein diets
(0.3e0.6 g/kg per day) with standard protein intake (>0.8 g/kg
per day) in nondiabetic.41,42 Low protein diet was associated
with a decreased risk of need for dialysis, kidney trans-
plantation, or death during follow-up (RR 0.69, 95% CI
0.56e0.86). These studies provide some evidence that a low
protein diet may benefit some patients with CKD. Some
studies have evaluated the effects of a very low protein diet in
patients with significant proteinuria or reduced GFR. Study on
nephrotic syndrome patients evaluated the effects of a very
low protein diet (0.3 g/kg per day supplemented with 10e20 g/
day of essential amino acids), which was administered for an
average of ten months in 16 patients.43,44
Eleven of the 16 patients with clearances below 30 mL/min
upon entrance into the study exhibited modest improvement
with treatment, but all eventually required dialysis. Among
the remaining five patients with clearances greater than
30 mL/min, however, dietary treatment for 3e14 months
resulted in several beneficial effects such as decreased
proteinuria (9.3 versus 1.9 g/day), increased serum albumin
concentration (2.5 versus 3.8 g/dL), increased GFR (52 versus
70 mL/min) and upon resumption of a relatively normal diet,
four of the five patients continued to remain in clinical
remission (or near-remission) at a follow-up of 6e24 months.
Some44 studies suggest that a very low protein diet may
help delay the requirement for renal replacement therapy
among patients with near-end-stage renal failure (GFR of less
than 6e10 mL/min). Nutritional studies in patients with CKD
suggest that protein intake can be safely lowered to 0.6 g/kg
per day.28 However, a very low protein diet has been associ-
ated with increased mortality over the long term.
Lower levels of protein ingestion are associated with
diminished energy intake and significant, but small, absolute
declines in serum transferrin, body weight, percent body fat,
and arm muscle area at a mean follow-up of 2.2 years (http://
www.uptodate.com/contents/protein-restriction-and-progre
ssion-of-chronic-kidney-disease/abstract/16) and increased
risk of death among patients who received the very low
protein diet compared to patients who received the low
protein diet (hazard ratio 1.92, 95% CI 1.15e32).39 However,
these observations suggest that there are important long-term
safety risks associated with the very low protein diet among
patients with advanced CKD. Modest protein restriction to
0.6e0.8 g/kg per day appears to be safe. We observed moderate
to severe malnutrition with high CRP levels, low albumin
levels, protein intake of 0.8 g/kg/d and energy intake of
25e28 kcal/kg/d in our patients (SGPGI, Lucknow) on mainte-
nance hemodialysis (Unpublished data).
To prevent malnutrition:
 Patients should maintain adequate caloric intake.
 At least 60 percent of the ingested protein must be of high
biologic value or contain a high percentage of essential
amino acids.25
 Metabolic acidosis should be treated to prevent skeletal
muscle stimulation and protein breakdown and to limit net
nitrogen loss.
 Properly supervised resistance training may help maintain
muscle mass.45
3.1.2.2. Hyperkalemia. Hyperkalemia is a common clinical
problem that is most often a result of impaired urinary potassium
excretion due to acute or chronic kidney disease and/or disorders
or drugs that inhibit the renineangiotensinealdosterone axis.
Therapy for hyperkalemia due to potassium retention is
ultimately aimed at inducing potassium loss.46e48 In some cases,
the primary problem is movement of potassium out of the cells,
even though the total body potassium may be reduced. Redis-
tributive hyperkalemia most commonly occurs in uncontrolled
hyperglycemia (e.g., diabetic ketoacidosis or hyperosmolar
hyperglycemic state). In these disorders, hyperosmolality and
insulin deficiency are primarily responsible for the transcellular
shift of potassium from the cells into the extracellular fluid,
which can be reversed by the administration of fluids and insulin.
 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5 227

Many of these patients have a significant deficit in whole body
potassium and must be monitored carefully for the development
of hypokalemia during therapy.
Hyperkalemia generally develops in the patient who is
oliguric or who has an additional problem such as a high-
potassium diet, increased tissue breakdown, or hypo-
aldosteronism (due in some cases to the administration of an
ACE inhibitor or ARB).49 Impaired cell uptake of potassium
also may contribute to the development of hyperkalemia in
advanced chronic kidney disease. Hyperkalemia due to ACE
inhibitor or ARB therapy is most likely to occur in patients in
whom the serum potassium concentration is elevated or in
the high normal range prior to therapy. In addition to treating
hyperkalemia, there are several measures that can help
prevent hyperkalemia in patients with chronic kidney
disease. These include ingestion of a low potassium diet (e.g.,
less than 40e70 meq/day [1500e2700 mg/day] or 1 mEq/kg/d)
(Table 5) and avoiding, if possible, the use of drugs that raise
the serum potassium concentration such as non-steroidal-
anti-inflammatory drugs. Nonselective beta-blockers make
the postprandial rise in the serum potassium concentration
but do not produce persistent hyperkalemia.
3.1.3. Approach to hyperphosphatemia
Dietary manipulations should be considered as one of the
main approaches in the management program of CKD
patients and that a reasonable number of patients with
moderate or severe CKD benefit from dietary protein phos-
phorus restriction.19 To optimally manage elevated phosphate
levels in patients with CKD, it is important to first assess the
presence or absence of other mineral abnormalities, vascular
calcifications, and note the administration of concurrent
therapies. Therefore baseline phosphate, calcium, and para-
thyroid hormone (PTH) levels must be obtained and then on
an ongoing basis, particularly after changes in therapeutic
measures. Among dialysis patients, aim is to maintain serum
phosphate levels between 3.5 and 5.5 mg/dL. Initial step
should be to restrict dietary phosphate to 900 mg/day.
Among dialysis patients with elevated phosphate levels
that are refractory to maintenance dialysis therapy and diet,

Table 5 e Potassium content of common foods.a

High-potassium foods Moderate-potassium foods Lower-potassium foods

Citrus fruits Cantaloupe Apple, Apple juice, Apple sauce

Apricots Figs (2 whole) Apricot nectar
Banana (1 small) Grapefruit Blackberries
Dates (1/4 cup) Grapefruit juice Blueberries
Honeydew melon Mango nectar Cranberries and Cranberry juice
Nectarines Papaya Fruit cocktail
Orange juice Peach (fresh) Gooseberries
Prune juice Pear (fresh) Grape juice
Melons Rhubarb Grapes
Kiwi Prunes (5) Lemon or lime (1)
Tomatoes Raisins Papaya nectar
Sweet potatoes Cherries Pear (canned)
Spinach Asparagus Pear nectar
Beans (baked, kidney, lima, pinto) Broccoli Pineapple
Avocado Celery Plums
Beets Kale Raspberries
Brussels sprouts Mixed vegetables Strawberries
Chard Peas Tangerines
Greens (beet, collard, etc.) Peppers Watermelon
Kohlrabi Potato Cabbage
Parsnips Summer squash Cauliflower
Pumpkin Turnips Mustard greens
Zucchini Broccoli
Alfalfa sprouts
Bamboo shoots (canned)
Corn
Cucumber
Eggplant
Green beans
Lettuce (1 cup)
Mushrooms
Radishes
Water chestnuts
Watercress

a Source: United States Department of Agriculture (USDA) National Nutrient Database for Standard Reference, Release 17-1 (www.nal.usda.
gov/fnic/foodcomp/Data/SR17/wtrank/sr17a306.pdf (PDF, 211 KB); accessed June 3, 2005); Nutritive value of Indian Foods Gopalan G, Rama
Sastri BV and Balasubramaniam SC, National Institute of Nutrition, 1996 Indian Council of Medical Research Hyderabad.
228 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5

administration of phosphate-binding agents is a must. Table 6
shows approach to treating hyperphosphatemia based upon
the serum calcium level.
Some patients do not achieve the recommended serum
phosphate goals with the regimen given in Table due in part to
the use of various agents to help control PTH levels. Vitamin D
analogs may contribute, raising both phosphate and calcium
concentrations. A possible alternative is the use of cinacalcet,
which acts by a different mechanism and produces significant
reductions in PTH, calcium, and phosphate levels. More
frequent and more intensive dialysis can also lower phos-
phate levels.50
Extremely long and/or frequent dialysis, such as that
provided by nocturnal hemodialysis, clears a large amount of
phosphate. Among patients with refractory hyper-
phosphatemia, nocturnal hemodialysis is an option among
those who are willing to accept this form of dialysis.
Avoid aluminum hydroxide except for short-term therapy
(four weeks for one course only) of severe hyperphosphatemia.
Many such patients are candidates for parathyroidectomy.51
First step in the management of hyperphosphatemia in
patients with stage 3e5 CKD not on dialysis is to restrict die-
tary phosphate to 900 mg/day. Among patients with serum
phosphate levels greater than target levels despite dietary
phosphorus restriction after one month, administer phos-
phate binders. While restricting dietary phosphates following
points must be considered:
1. Restrict phosphate but nutritional status should not be
compromised.
2. Approximately 900 mg per day level/day is acceptable.
3. Phosphate restriction includes processed foods and colas
but high biologic value foods such as meat and eggs should
not be restricted (Table 7).
A large number of dialyzed patients having either overt or
borderline malnutrition are advised protein supplements.
Plant-derived phosphorus is less easily absorbed because it is
in the form of phytate phosphorus, and the human intestine
does not secrete phytase, the enzyme required for absorption.
The patient should be encouraged to avoid unnecessary die-
tary phosphate (as in phosphorus-containing food additives,
dairy products, certain vegetables, many processed foods, and
colas) while increasing the intake of high biologic value
sources of protein (such as meat and eggs).52,53
Table 6 shows strategies for management with and
without comorbidities. Since hypercalcemia is unusual in
CKD stage 3e5, evaluation for secondary non-PTH mediated
causes should be undertaken if PTH values are not signifi-
cantly elevated and patients are not receiving active vitamin
D therapy. Primary hyperparathyroidism can be present in
hypercalcemic patients with stage 3e4 CKD and when
serum phosphate level is low in the absence of phosphate
binders. In patients without comorbidities, but high phos-
phate levels, dose of calcium-containing phosphate binders
is generally increased until the serum phosphate falls to
normal values. The safe dose of calcium is not known in
stage 3 and 4 CKD but likely exceeds the 1500 mg/day limit
in end stage renal disease patients suggested by the K/DOQI
work group.54 The 2009 KDIGO practice guidelines provide
recommendations for the evaluation and management of
chronic kidney disease-mineral and bone disorder (CKD-
MBD).55
3.1.3.1. Calcium. Close attention to the prevention and
management of cardiovascular disease should be a priority
among patients identified with chronic renal dysfunction.
Increased intake of calcium for treating hyperphosphatemia
enhances coronary arterial calcification which may be asso-
ciated with the development of coronary atherosclerosis. The
combination of hypercalcemia (calcium >10.2 mg/dL cor-
rected for serum albumin) and persistent hyper-
phosphatemiais a limitation with calcium therapy and active
vitamin D analog administration, possibly leading to extra-
skeletal calcium phosphate deposition. Dose of calcium-based
phosphate binders should be decreased or therapy dis-
continued, and/or therapy should be switched to sevelamer to
control phosphate (Table 6).50 In addition, the dose of active
vitamin D sterols should be lowered or therapy should be
discontinued until calcium levels return to 8.4e9.5 mg/dL. In
dialysis dependent hypocalcemic patients, calcium supple-
ments should be taken in between the meals and non-calcium
based phosphate binders should be administered with meals.
Since patients on maintenance dialysis are advised to take
high protein diet, therefore in these patients dietary calcium
(especially from milk and milk products) should also be taken

Table 6 e Treating hyperphosphatemia based upon the serum calcium level.

Patient’s calcium level Treatment

>9.5 mg/dL Non-calcium containing phosphate binder (Sevelamer or lanthanum) rather than calcium containing binders
Between 8.4 and 9.5 mg/dL a) Without comorbidities-

i) calcium-based phosphate binder (up to 1500 mg of elemental calcium from binders alone).
ii) Higher doses of calcium if patients are not receiving vitamin D analogs or who have hypocalcemia
while being treated with calcimimetics.
iii) If phosphate remains above 5.5 mg/dL despite this strategy, add non-calcium containing phosphate binder

b) Presence of a dynamic bone disease, low PTH levels, and/or vascular calcification:

i) Prefer non-calcium based phosphate binder

<8.4 mg/dL Calcium based phosphate binders
 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5
Table 7 e High and low phosphorus containing foods.a
High phosphorus foods
Dairy foods: milk (condensed milk, evaporated milk, dried milk.),
cheese (cheddar, Edam, Gruyere, Cheese spreads, cheese sauce),
yogurt, ice cream
Calcium enriched milk
Peanut butter
Beans (baked, kidney, lima, pinto)
Nuts and peanut butter
Processed meats (hot dogs, canned meat)
Cola Pepsi
Canned iced teas and lemonade
Bran cereals
Egg yolks
a Source: United States Department of Agriculture (USDA) National Nutrient Database for Standard Reference, www.nal.usda.gov/fnic/
foodcomp/Data/SR17/wtrank/sr17a305.pdf (PDF, 211 KB) June 3, 2005); Nutritive value of Indian Foods Gopalan G, Rama Sastri BV and Balasu-
bramaniam SC, National Institute of Nutrition, 1996 Indian Council of Medical Research Hyderabad.
into account, both while prescribing calcium supplements
and while calculating total calcium intake/day.
3.1.3.2. Sodium and its association with hypertension. Hyper-
tension is a common comorbidity associated with CKD. There
is a large body of evidence that patients with CKD have
a substantial increase in cardiovascular risk that can be in part
explained by an increase in traditional risk factors such as
hypertension, diabetes, and the metabolic syndrome. CKD
alone is also an independent risk factor for cardiovascular
disease.56 Among patients with CKD, the risk of death,
particularly due to cardiovascular disease, is much higher
than the risk of eventually requiring dialysis therefore
hypertension requires not only medical management but also
nutritional management which includes dietary salt and fat
and cholesterol restriction, changes in life style. 2011 KDIGO
clinical practice guideline for management of blood pressure
in CKD states that goal blood pressure depends upon the
degree of proteinuria:
 In patients with proteinuric CKD (500e1000 mg/day or
more), the blood pressure should be lowered to less than
130/80 mmHg.
 In patients with nonproteinuric CKD (less than
500e1000 mg/day), the blood pressure should be lowered to
less than 140/90 mmHg in all patients, and to less than
130e135 mmHg systolic if it can be achieved without
producing significant side effects.
Sodium balance remains virtually normal until very late in
the course of CKD, because the kidney can markedly increase
the amount of sodium excreted per nephron by reducing
tubular sodium reabsorption. Although sodium balance is
maintained, the kidney loses its ability to adapt to large vari-
ations in salt intake. Indeed, intake of large amounts of
229
Low phosphorus foods
Milk/Dairy Foods/Eggs
Cottage cheese, Ricotta cheese, cream cheese,
Cream, sour cream
Egg whites
Liquid non-dairy creamer
Sherbet
Pasta rice
Rice and corn cereals
Popcorn
Green beans
Lemon-lime soda
Root beer
Powdered iced tea and lemonade mixes
Biscuits and Cakes
Cream crackers, water biscuits, digestives, plain sweet biscuits,
shortbread, crumpets, cream biscuits
Sugars
All sugars, jams, honey, golden syrup,
Cordials and soft drinks, (not cola, Pepsi)
sodium can easily overwhelm the excretory capacity of the
failing kidney and result in fluid retention, edema, and
hypertension. Likewise, if diuretics are used overzealously,
the patient may become volume-depleted, with further
aggravation of the kidney failure.57 Clinically evident edema is
uncommon until the GFR falls to less than 15 mL/min/1.73 m2.
However, edema can occur at higher GFR levels in patients
with glomerular disease and significant proteinuria (i.e.,
nephrotic syndrome) and in those with heart failure. The
cornerstone of treatment of edema (and hypertension) is
restriction of dietary sodium to a level lower than that rec-
ommended for uncomplicated hypertension (<100 mEq/day;
2.3 g of sodium or 6 g of salt).58 If sodium restriction is not
effective or not achieved, diuretics should be used.59 Thiazide
diuretics are usually ineffective if the serum creatinine level is
greater than 3 mg/dL (>265 mmol/L). Thus, more potent loop
diuretics are the agents of choice in patients with CKD. The
initial aim is to determine the threshold dose that is effective.
Patients with advanced CKD may require doses of furosemide
(Lasix) as high as 400 mg per day. Lack of response to high
doses of loop diuretics often is due to noncompliance with
dietary sodium restriction. In such cases, a combination of
a thiazide diuretic or metolazone (Mykrox, Zaroxolyn) given
before the loop diuretic may induce diuresis. For maximum
efficacy, the thiazide diuretic should be given 30 min before
the loop diuretic. Potassium-sparing diuretics (e.g., spi-
ronolactone [Aldactone]) are contraindicated because of the
risk of inducing hyperkalemia.
The NKF-KDOQI Guidelines on Hypertension and Antihy-
pertensive Agents in CKD recommended a version of the
DASH diet with modifications for CKD stages 3 to 4.56,60 These
modifications decreased dietary protein from 1.4 g/kg body
weight per day to 0.6e0.8 g/kg body weight per day, as well as
restricted phosphorus (0.8e1.0 g/d) and potassium (2e4 g/d).
Based on concerns about potential detrimental effects of
230 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5
high-protein diets on the kidney and evidence for kidney and
survival benefits at approximately the RDA level in diabetes
and CKD stages 1e2, the Work Group concluded that a protein
intake that meets, but does not exceed, the RDA would be
prudent at earlier stages of CKD (Table 8). The ADA endorses
a dietary protein intake of 0.8 g/kg body weight per day for
people with DKD.61 An additional restriction to 0.6 g/kg body
weight per day is suggested should glomerular filtration rate
begin to decrease. The dietary protein recommendation
should be based on idealized body weight because obesity,
which is highly prevalent in the diabetes and CKD population,
otherwise would lead to overestimating the dietary protein
recommendation.62
Dietary sodium reduction to 2.3 g/d (100 mmol/d) is rec-
ommended based on the DASH and DASH-Sodium diets.60
Because most people with diabetes and CKD have hyperten-
sion characterized by enhanced sodium retention, this limi-
tation should apply. Recommendations for phosphorus and
potassium are the same for CKD with and without diabetes.
Phosphorus binders may be needed in patients with advanced
CKD because of the emphasis on whole grains and dairy
products. Table 9 lists high and low sodium containing foods.
The Institute of Medicine established guidelines for intake of
omega-3 fatty acids. Adequate intake of alpha-linolenic acid
was established as 1.6 g/d for men and 1.1 g/d for women, with
substitution of up to 10% of these amounts by the more physi-
ologically potent eicosapentaenoic acid (EPA) and docosahex-
aenoic acid (DHA).63 The AHA and the KDOQI CPGs for CVD in
dialysis patients recommend including 1 serving of cold-water
fish in the diet 3 times per week.64,65 It is possible that 3 serv-
ings of cold-water fish, such as salmon, mackerel, herring, and
albacore tuna, would provide EPA and DHA in excess of the 10%
of adequate intake amounts for men and women. In the opinion
of the Work Group, these recommendations may be considered
for the diabetes and CKD population.
Table 8 e A balanced approach to nutrition in CKD with or
without diabetes: macronutrient.56
Nutrient Stage of CKD
1e2 1e4 3e4
Sodium (g/d) <2.3
Total fata (% of calories) <30
Saturated fat (% of calories) <10
Cholesterol (mg/d) <200
Carbohydrate 50e60
(% of ca calories)
Protein (g/kg/d, % of calories)
No diabetes 1.4 (w18) 0.5e0.8 (w8e13)
Diabetes 0.8 (w10) 0.5e0.8 (w8e13)
Phosphorus (g/d) 1.7 0.8e1.0
Potassium (g/d) >4 2.4
Note: Adapted from the DASH diet and NKF-KDOQITM CPGs for
hypertension and antihypertensive agents in CKD, modified for
diabetes and stages of CKD.92
a Adjust so total calories from protein, fat, and carbohydrate are
100%. Emphasize such whole-food sources as fresh vegetables,
whole grains, nuts, legumes, low-fat or nonfat dairy products,
canola oil, olive oil, cold-water fish, and poultry.
3.1.3.3. Restriction of fat. Restriction of fat 20 g/d is advisable
(Table 8). Avoid saturated fats (red meat, poultry, whole milk,
butter, lard) and hydrogenated vegetable oils. Preference
should be given to monounsaturated fats such as corn oil,
safflower oil, olive oil, peanut oil, canola oil. Foods containing
trans-fatty acids like commercially baked goods (cakes,
pastries and biscuits, French fries, doughnuts) should best be
avoided.56
3.1.3.4. Metabolic acidosis. There is an increasing tendency to
retain hydrogen ions among patients with chronic kidney
disease. This can lead to a progressive metabolic acidosis.
Bicarbonate supplementation may slow the progression of
chronic kidney disease. Bone buffering of some of the excess
hydrogen ions is associated with the release of calcium and
phosphate from bone, which can worsen the bone disease.
Uremic acidosis can increase skeletal muscle breakdown and
diminish albumin synthesis, leading to loss of lean body mass
and muscle weakness. Classical studies in humans demon-
strated the powerful effect of chronic metabolic acidosis,
induced experimentally or resulting from chronic kidney
disease, on the loss of bone mineral. Bone fractures are
a relatively common manifestation of chronic metabolic
acidosis. Chronic metabolic acidosis contributes, in part, to
the osteodystrophy in patients with chronic kidney disease.66
Acidemia engenders protein catabolism and negative protein
balance and enhances degradation of protein and amino
acids.67,68 Acidemia due to metabolic acidosis is associated
with increased oxidation of branched chain amino acids
(valine, leucine and isoleucine),69,70 increased protein degra-
dation and PNA and decreased albumin synthesis. Arterial pH
of 7.43e7.45 is associated with a more positive protein
nitrogen balance than an arterial pH of 7.36e7.38.71 The
administration of bicarbonate increases serum albumin and
the lean body mass.72 When academia occurs repetitively
Table 9 e Food sources of sodium.a
High-sodium foods Lower-sodium alternatives
Salt Salt-free herb seasonings
Chutney Frozen vegetables
Pickles Plain rice
Papdams Plain noodles
Coconut water Unsalted popcorn
Tomato sauce
Canned vegetables
Hot dogs
Packaged rice with sauce
Packaged noodles with sauce
Frozen vegetables with sauce
Canned soup
Snack foods
a United States Department of Agriculture (USDA) National
Nutrient Database for Standard Reference, Release 17-1 (www.nal.
usda.gov/fnic/foodcomp/Data/SR17/wtrank/sr17a307.pdf (PDF,
211 KB)).
Adapted from National Renal Diet (Harvey KS. A Healthy Food Guide
for People on Dialysis. Chicago, IL: American Dietetic Association
Renal Practice Group; 2002).
 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5
before hemodialysis treatments, alkali supplements can
prevent this from occurring.1 Predialysis or stabilized serum
bicarbonate levels should be maintained at or above 22 mmol/
L.67 According to K/DOKI guideline 15,66 in CKD Stages 3, 4 and
5, measurement and monitoring of the serum levels of total
CO2 is warranted or in patients on maintenance dialysis. Steps
to keep the measured serum levels of CO2 above 22 mmol/L
are warranted for improvement in bone histology, and to
ameliorate excess protein catabolism. The frequency of these
measurements should be based on the stage of CKD. If
necessary, supplemental alkali salts should be given to ach-
ieve this goal.66 The use of exogenous alkali salts containing
citrate may increase the absorption of dietary aluminum in
patients with CKD, both before dialysis and in those treated
with dialysis; therefore, citrate alkali salts should be avoided
in CKD patients exposed to aluminum salts.
3.1.3.5. Fluid balance. The kidneys are the key organs to
maintain the balance of the different electrolytes in the body
and the acidebase balance. Progressive loss of kidney function
results in a number of adaptive and compensatory renal and
extrarenal changes that allow homeostasis to be maintained
with glomerular filtration rates in the range of 10e25 mL/min.
With glomerular filtration rates below 10 mL/min, there are
almost always abnormalities in the body’s internal environ-
ment with clinical repercussions.73 Other factors that
contribute to the development of fluid volume overload are
proteinuria and increased renin. Proteinuria occurs in
response to damage of the glomeruli. High blood pressure can
cause sclerotic changes in the glomeruli with a resultant loss
of protein, especially albumin in the urine.74,75 The loss of
albumin in the urine contributes to fluid shifting from the
intravascular space to the interstitial space because of
decreased oncotic pressure. As a response to decreased GFR,
aldosterone is released from the adrenal cortex, causing the
kidneys to reabsorb sodium and water. Fluid retention in turn
results in the development of respiratory and cardiovascular
clinical manifestations.76 Sodium and intravascular volume
balance are usually maintained via homeostatic mechanisms
until the GFR falls below 10e15 mL/min. However, the patient
with mild to moderate chronic kidney disease, despite being
in relative volume balance, is less able to respond to rapid
infusions of sodium and is therefore prone to fluid overload.
Therefore, as kidney disease progresses, limiting fluid intake
is necessary in order to correct edema.
In CKD stages 1e3 urine output is generally normal. Except
in edematous states, a daily fluid intake of 1.5e2 L may be
recommended.73 Urine output drops as kidney failure prog-
resses therefore, most dialysis patients urinate very little or
not at all, and therefore fluid restriction between treatments is
very important. Daily fluid restriction should be based
according to insensible fluid losses þ urine output þ amount
to replace additional losses (e.g., vomiting, diarrhea, enteros-
tomy output)  amount to be deficited.77
Without urination, fluid builds up in the body and causes
fluid overload. In such patients, daily requirement of fluid
depends upon e i) the amount of urine output in 24 h, ii) the
amount of weight gain between the dialysis treatment,
iii) amount of fluid retention, iv) levels of dietary sodium,
v) congestive heart failure.
231
Patients with chronic kidney disease and volume overload
generally respond to the combination of dietary sodium
restriction and diuretic therapy, usually with a loop diuretic
given daily. Limiting sodium intake may also help decrease
progression of chronic kidney disease by lowering intra-
glomerular pressure (Table 4). Water overload may result in
hyponatremia and a decrease in water intake may lead to
hypernatremia. Hyponatremia does not usually occur with
glomerular filtration rates above 10 mL/min. The use of
diuretics in volume overload in CKD is useful to force natri-
uresis. Thiazides have little effect in advanced CKD. Loop
diuretics are effective and should be used in higher than
normal doses. The combination of thiazides and loop diuretics
can be useful in refractory cases.73 Weight and volume should
be monitored regularly in the hospitalized patient with CKD.
In oliguric patients, the best advise to avoid fluid overload
is to
 Avoid or minimize eating food with high content of water
(soups, fruit juices, grapes, melons, coconut water).
 Use measuring glasses for proper charting of fluid intake.
 Allow sips of water if patients feels dryness of mouth.
 Minimize sodium intake. It is best to avoid salty foods.
 If possible, freeze juices (with low potassium content) in an
ice tray and suck them to minimize thirst.
 Avoid extreme heat. Do not go out in the sun when its too
hot.
3.1.4. Nutritional status, indications for nutritional support
and monitoring nutritional adequacy in CKD
Individuals undergoing maintenance dialysis (CKD Stage 5D)
who are unable to meet their energy requirements with food
intake for an extended period of time should receive nutrition
support.78 Unfortunately, there is no single optimal laboratory
test to assess and monitor nutritional adequacy in CKD
patients. Criteria for diagnosis of PEW are given in Table 3. No
single measure provides a comprehensive indication of
nutritional status. Measures of intake, visceral and somatic
protein stores, body composition, and functional status
identify different aspects of nutrition status. Malnutrition
may be identified with greater sensitivity and specificity using
a combination of factors.
Patients with CKD who are on a protein-restricted diet
should be carefully monitored with close follow-up every
three to six months for adequate caloric intake and evidence
of protein malnutrition.79 Body weight, serum albumin, pre-
albumin, and cholesterol should be checked on every visit.
More frequent monitoring (i.e., monthly) may be necessary in
patients with advanced CKD (i.e., stages 4 and 5). Comple-
mentary measures for assessment should include medical
history, physical examination, anthropometry (height, body
weight, body mass index (BMI), skin fold thickness, mid upper
arm mid upper arm muscle mass), waist/hip ratio. Subjective
global assessment (SGA) score correlates with objective
measures (albumin/weight/intake/anthropometry). Change in
SGA rating by 1 point decreases relative risk of death by 25%. A
higher SGA score is associated with a lower relative risk of
death and fewer hospitalized days/year (CANUSA study).
Methods of body composition like bioelectrical impedance
analysis, infrared reactance and DEXA should be used to
232 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5
estimate water compartments and changes in body muscle,
fat and protein stores. This will help in attainment of dry
weight.
Assessment of dietary Intake should be done at least once
a month using, 1. Diet history questionnaires, 2. Food weigh-
ing and 3. Observation. Food weighing is a little difficult for
patients who visit dialysis units on out patient basis. Assess-
ment of food intake using diet history questionnaires is
therefore more appropriate for such patients. Egg white, fish,
chicken, milk and milk products (curd, chenna/paneer),
dehusked (without outer covering to prevent hyper-
phosphatemia) lentils kidney beans, soy protein (milk and
cheese marketed as Tofu) are good sources of protein with
HBV for patients on maintenance dialysis.
3.1.4.1. Predialysis serum creatinine. This is a direct indicator
of protein intake and muscle mass. It is directly proportional
to skeletal muscle mass & dietary muscle intake According to
NKF/KDOQI guideline 5 predialysis Serum Creatinine
of<10 mg/dL is considered as high risk for PEW which
warrants thorough evaluation of PEW. Mortality risk increases
with creatinine below 9e11 mg/dL in patients on MHD or PD.
But these data are based on Western population with signifi-
cantly different body frame and size. A predialysis serum
creatinine of higher than 10 mg/dL is not tolerated by Indian
patients and they become highly uremic (anorexia, vomiting,
loss of taste). Therefore, the threshold levels of predialysis
serum creatinine for Indian are much lower than those rec-
ommended by NKF/KDOKi guidelines. A low predialysis or
stabilized serum creatinine level in MD patients suggests
decreased skeletal muscle mass and or low dietary protein
intake. Therefore in Indian patients, low stabilized predialysis
creatinine of between 2 and 4.5 mg/dL with negligible residual
renal function should be investigated for low dietary protein
intake and skeletal muscle wasting and risk for high mortality.
3.1.4.2. Anorexia. Chronic renal failure impairs appetite.3
Major proportion of patients treated with HD consume less
protein and energy than is recommended. Factors that
contribute to anorexia like underdialysis (to overcome this
factor switch over to thrice weekly dialysis in place of twice
weekly dialysis therapy), comorbidity, medication (in such
circumstances discontinuing phosphate binders and iron and
vitamin supplements for a short period of time helps improve
appetite) psychosocial factors should be immediately
addressed. Dialysis regimen should be regularly monitored
and modified to treat intensification of the patient’s uremic
state that is caused by superimposed illness. Maintain KT/V of
1.2 in HD patients.
Because of the number of factors affecting the nutritional
and metabolic status in patients with advanced chronic
kidney disease or who are on maintenance dialysis, the
prevention and treatment of PEW of chronic kidney disease
should involve a comprehensive combination of maneuvers
to diminish protein and energy depletion, in addition to
therapies that will avoid further losses. The available evidence
suggests that nutritional supplementation, administered
orally or parenterally, is effective in the treatment of main-
tenance dialysis patients with PEW in whom oral dietary
intake from regular meals cannot maintain adequate
nutritional status. Increased oral nutrient intake during dial-
ysis and at home is the ideal choice for this intervention.79 In
clinical practice, the advantages of intradialytic oral nutri-
tional supplements include proven efficacy and compliance.
Therefore, at a minimum, oral nutritional supplementation
given intradialytically should be attempted in maintenance
dialysis patients with PEW, accompanied by individualized
dietary advice for appropriate intake at home. In ones who
cannot tolerate oral feeding, intradialytic parenteral nutri-
tional is a good alternative.80
Approximately one-third of maintenance dialysis patients
have mild to moderate protein-energy malnutrition, and about
6e8 percent of these individuals have severe malnutrition.81
These statistics are of major concern because markers of
protein-energy malnutrition are strong predictors of morbidity
and mortality. The causes of protein-energy malnutrition in
patients with chronic renal failure are given in Table 2. There is
some evidence that the nutritional status of the hemodialysis
patient can be influenced by the biocompatibility of the mem-
brane.82e84 In particular, the elaboration of cytokines from cells
activated after contact with BICM may be responsible for
increased protein catabolism. One report demonstrated net
protein catabolism when normal subjects were exposed to (not
dialyzed by) cellulosic membranes but not when exposed
biocompatible polysulfone or PAN membranes.85 It was esti-
mated that a 150 min exposure to the cuprophane membrane
resulted in the net degradation of approximately 15e20 g of
muscle protein (measured by the release of amino acids). Of
interest, the net release of amino acids occurred 3 h after the
end of dialysis, not during dialysis, and continued for as long as
six and one-half hours after dialysis. This time course is similar
to that of monocyte activation, the release of cytokines, and
their subsequent action on muscle cells.82
Two other observations are compatible with a beneficial
effect of biocompatible membranes (BCM) on nutritional
status. In one study, for a given dose of dialysis, protein intake
(reflected by the protein catabolic rate) increased to a greater
extent in patients dialyzed with PAN membranes compared to
those treated with cuprophane membranes.83 In a multi-
centeric trial, patients treated with BCMs had higher plasma
levels of albumin and insulin-like growth factor-1 and
a greater degree of body-mass weight gain during the 18
months of the study.84
3.1.4.3. Gastroparesis. Gastroparesis can be a contributing
factor to decreased food intake by delaying gastric emptying,
thereby increasing the feeling of fullness. This complication is
most common in diabetics (possibly affecting as many as 20 to
30 percent of diabetics with end-stage renal disease), but can
also occur in nondiabetics.86,87 If gastroparesis is suspected
from the history, the rate of gastric emptying can be accu-
rately assessed by various methods, such as ingestion of
a radiolabeled test meal with simultaneous gastric scanning.
Patients with severe gastroparesis may be unable to tolerate
any form of oral supplementation. Intravenous infusion and
intradialytic parenteral nutrition (IDPN) or total parenteral
nutrition (TPN) depending upon urine output in case of dial-
ysis dependent patients may be beneficial. TPN is required in
patients with severe malabsorption. Although generally well
tolerated, TPN solutions typically contain added potassium,
 c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5
phosphorus, and magnesium. Thus, patients with end-stage
renal disease receiving TPN are at risk for the development
of hyperkalemia, hyperphosphatemia, and hyper-
magnesemia. Elimination of the added electrolytes can
prevent these problems but carries the reverse risk of elec-
trolyte deficiencies with prolonged therapy.
3.1.4.4. Obesity. Weight excess is associated with increased
renal risk. Data in overt obesity suggest a role for altered renal
hemodynamics. Study on the relation between BMI and renal
hemodynamics in 102 healthy, non-obese (BMI <30 kg/m2)
subjects suggests that the impact of BMI on renal function is
not limited to overt obesity as in subjects with BMI <30 kg/m2,
a higher BMI is associated with higher FF, that is, a higher GFR
relative to effective renal plasma flow. This suggests an
altered afferent/efferent balance and higher glomerular
pressure (i.e., a potentially unfavorable renal hemodynamic
profile) that may confer enhanced renal susceptibility when
other factors, such as hypertension or diabetes are super-
imposed.88 Elevated BMI is not a biologically significant
predictor of diminished GFR and therefore may be an insuf-
ficiently accurate measure of risk for the metabolic syndrome
and CKD.89 Hypertension is a common obesity-related health
problem and visceral obesity seems to be the major culprit.
Obesity-related HTN pandemic and its CVD and CKD conse-
quences call for prevention and treatment of obesity and to
treat HTN to goal.90 It is recommended that obese patients be
motivated to lose body weight by encouraging physical
activity without compromising their nutritional status.
4. Summary
Chronic renal failure (CRF) impairs not only appetite but also
impairs immune function and host resistance, resulting in
increased susceptibility to infections and poor wound healing
and may predispose to inflammatory diseases. Every strategy
should be used to avoid complications of chronic kidney
disease (CKD) manifested in uremic state including anorexia,
nausea, vomiting leading to malnutrition, fluid and electrolyte
imbalance leading to volume overload, hyperkalemia, meta-
bolic acidosis, and hyperphosphatemia. With decline in GFR,
nutrient requirements change. Nutritional status should be
assessed. Timely diagnosis of PEW is important for early
initiation of nutritional intervention and treatment. Manage-
ment of hypertension, bone mineral disease, fluid overload
and gastroparesis should be given prime importance.
Conflicts of interest
The author has none to declare.
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