Transcript Medical Nutrition Therapy for Renal Disorder

Medical Nutrition Therapy for Renal Disorder
And Enteral Nutrition
A. Afaghi, MPH, PhD
Qazvin University of Medical Science,
School of Medicine
Function Of The Kidney
• The main function of kidney is to maintain
homeostatic balance with respect to fluids,
electrolytes and organic solutes by continues
filtration.
• The normal kidney has the ability to perform this
function over a wide range of dietary fluctuations
in sodium, water and various solutes.
• Kidney receives 20% of cardiac output, which
filtrates 1600 L/day of blood
Function Of The Kidney
• 180 L of fluid is produced in filtering this blood
and through active reabsorbing certain
compounds, the composition of this fluid
changed to 1.5 L urine in an average day
• If the waste products are not eliminated
appropriately, the condition will be Azotomia
• Renal failure is the consequence of inability to
excretion of daily load of these waste.
azotemia
• Urea predominates in amount, depending
on the protein content of the diet. Uric
acid, creatinine (Cr), and ammonia are
present in small amounts. If normal waste
products are not eliminated appropriately,
they collect in abnormal quantities in the
blood, known as azotemia.
oliguria
• The minimum urinary volume capable of
eliminating a relatively fixed 600 mOsm of
solute is 500 mL, assuming that the kidney
is capable of maximum concentration.
• Urinary volume of less than 500 mLi day is
called oliguria;
• it is impossible for such a small urine
volume to eliminate all of the daily waste.
RENAL DISEASES
• The manifestations of renal disease are
significant. They can be ordered by degree
of severity: (1) kidney stones, (2) acute
kidney injury (AKI), (3) chronic kidney
disease (CKD), and (4) end-stage renal
disease (ESRD).
Kidney Stones (Nephrolithiasis)
• frequent occurrences between the ages of 30
and 50, predominance in males, and a high
recurrence rate. The risk doubles in those with a
family history of kidney stones
• Increased frequency of obesity, diabetes, and
metabolic syndrome have resulted in increasing
rates of nephrolithiasis among women,
decreasing the male/female ratio from 1.7: 1 to
1.3: 1
Calcium stones
• Calcium stones are the most common:
60% of stones are calcium oxalate, 10%
calcium oxalate and calcium phosphate,
and 10% calcium phosphate. Other stones
are 5% to 10% uric acid, 5% to 10%
struvite, and 1% cystine.
Type 2 diabetes and kidney stones
• Uric acid stones are common in the
presence of type 2 diabetes.
Hyperinsulinemia may also contribute to
the development of calcium stones by
increasing urinary calcium excretion
Obesity and kidney stones
• Obese stone formers excrete increased amount of
sodium, calcium, uric acid, and citrate, and have lower
urine pH.
• Obesity is the strongest predictor of stone recurrence in
• first-time stone formers.
• As body weight increases, the excretion of calcium,
oxalate, and uric acid also increases.
• Patients with higher body mass index (BMI) have a
decrease in ammonia excretion and impaired hydrogen
ion buffering
• With increasing BMI, uric acid stones become more
dominant than calcium oxalate stones, especially in men.
Weight control in stone former
• Weight control may be considered one of
the preventive modalities and in stone
formers, a BMI of 18 to 25 kg/m2 is
recommended.
Hypercalciuria
• Calcium Stones. One third to one half of patients with
calcium stones are hypercalciuric.
• Hypercalciuria describes a value of calcium in excess
of 300 mg (7.5 mmol) per day in men, 250 mg (6.25
mmol) per day in women, or 4 mg (0.1 mmol)/kg/day for
either in random urine collections of outpatients on
unrestricted diets. Causes of hypercalciuria may include:
• primary hyperparathyroidism, sarcoidosis,
• excess vitamin D intake, hyperthyroidism, glucocorticoid
• use, or renal tubular acidosis (RT A)
• A trial of combined calcium vitamin D supplementation to
prevent bone loss and fractures led to higher rates of
stone formation in women
urinary calcium and urinary oxalate
• The risk in both men and women rises with
increasing urine calcium and oxalate and
decreases with increasing citrate and urine
volume.
• Reducing dairy product intake may lead to
osteoporosis, and is not recommended
Foods to Avoid for a Low Oxalate Diet
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Rhubarb
Spinach
Strawberries
Chocolate
Wheat bran and whole-grain wheat products
Nuts (almonds, peanuts, or pecans)
Beets
Tea (green, black, iced, or instant)
High doses of turmeric
Data from Siener R et al: Oxalate content of cereals and
cereal products, J Agric Food Chem 54:3008, 2006.
Uric Acid Stones
Uric acid is an end product of purine metabolism
from food, and tissue catabolism. Approximately
half of the purine load is from endogenous
sources.
Exogenous dietary sources provide the other half,.
The solubility of uric acid depends on urine
volume, the amount excreted, and urine pH. Uric
acid stones form when urine is supersaturated
with undissociated uric acid, which occurs at
urinary pH less than 5.5.
Effect of Urine pH on Stone Formation
pH
State of Urate
Likely Stone Development
<5.5
Undissociated urate
5.5-7.5
Dissociated urate
Calcium oxalate stones
>7.5
Dissociated urate
Calcium phosphate stones
Uric acid stones
Ascorbic acid & urinary oxalate
• Ascorbic acid accounts for 35% to 55%,
and glyoxylic acid accounts for 50% to
70% of urinary oxalate. In patients with
CKD, excessive vitamin C intake may lead
to stone formation. Oxalate synthesis is
not increased with a high protein diet
(Knight et aI., 2009). Because pyridoxine
acts as a cofactor in the conversion
ofglyoxylate to glycine, its deficiency could
increase endogenous oxalate production.
Milk and oxalate absorption
• Milk appears to reduce oxalate absorption
by binding it in the gut lumen as calcium
oxalate, making it less absorbable. Herbal
teas have much lower oxalate content of
31-75 urnol/L and are an acceptable
alternative (Massey, 2007). Soft drinks
and colas that contain phosphoric acid
should be avoided because of their urine
acidifying effect
Alkaline foods and renal acid load
• The most abundant alkaline foods are
plant based foods; particularly vegetables
and fruit abundant in alkalinizing
micronutrients such magnesium, calcium,
sodium,and potas ium. A more alkaline
diet consisting of a higher fruit and
vegetable intake is associated with a low
potential renal acid load (PRAL) (Remer,
1995)
ACUTE KIDNEY INJURY (AKI)
(ACUTE RENAL FAILURE)
• is characterized by a sudden reduction in
glomerular filtration rate (GFR), the
amount of filtrate per unit in the nephrons,
and altered ability of the kidney to excrete
the daily production of metabolic waste.
AKI can occur in association with oliguria
(decreased output of urine) or normal.
urine flow, but it typically occurs in
previously healthy kidneys. Duration varies
from a few days to several weeks.
Causes of AKI
• The causes of AKI are numerous, and can
occur simultaneously. These causes are
generally classified into three categories:
(1) Inadequate renal perfusion (prerenal)
(2) diseases within the renal parenchyma
(intrinsic)
(3) urinary tract obstruction (postrenal)
Medical Nutrition Therapy in AKI
• Protein. A range of recommended levels
can be found in the literature, from 0.5-0.8
g/kg for nondialysis patients to 1-2 g/kg for
dialyzed patients. With CRRT protein
losses are high, and estimated protein
needs increase to 1.5-2.5 g/kg.
• Energy: 30 to 40 kcal/kg of dry body
weight per day.
Fluid and Sodium
• Sodium is restricted, based on decreased
urinary production. In the oliguric phase
when the sodium output is very low, intake
should be low as well, perhaps as low as
20 to 40 mg/day.
Summary of Medical Nutrition Therapy for Acute
Kidney Injury
Nutrient
Protein
Energy
Potassium
Sodium
Fluid
Phosphorus
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Amount
0.8-1 glkg IBW increasing as GFR returns to normal; 60%
should be HBV protein
30-40 kcallkg of body weight
30-50 mEq/day in oliguric phase (depending on urinary
output, dialysis,and serum K+level); replace losses indiuretic
phase
20-40 mEq/day in oliguric phase (depending on urinary
output, edema, dialysis, and serum Na" level); replace in
diuretic phase
Replace output from the previous day (vomitus, diarrhea,
urine) plus 500 mL
Limit as necessary
GFR, Glomerular filtration rate; HBV, high biologic value; lBW, ideal body
weight; K', potassium; Na', sodium.
CHRONIC KIDNEY DISEASE (CKD)
• Once approximately one half to two thirds
of kidney function has been lost,
regardless of the underlying disease,
progressive further loss of kidney function
ensues
• Diabetes is the leading risk factor for CKD
followed by hypertension.
Medical Nutrition Therapy (CKD)
• The recommended dietary protein level for CKD patients
has changed over time. Historically, these patients
received diets high in protein (up to 1.5 g/kg/day)
• However, studies have shown that a reduction of protein
intake to as low as 0.8 g/kg/day may decrease
proteinuria without adversely affecting serum albumin.
• Dietary protein has been championed as a factor that
increases glomerular pressure and thus leads to
accelerated loss of renal function. 50% to 60% of the
protein should be from animal sources
Medical Nutrition Therapy (CKD)
• The primary objectives ofMNT are to
manage the symptoms associated with the
syndrome (edema, hypoalbuminemia, and
hyperlipidemia), decrease the risk of
progression to renal failure, and maintain
nutritional stores. Patients are primarily
treated with Statins to correct
hyperlipidemia, low-sodium diets, and
diuretics
Medical Nutrition Therapy (CKD)
• Patients with an established severe protein
deficiency who continue to lose protein may
require an extended time of carefully supervised
nutritional care. The diet should attempt to
provide sufficient protein and energy to maintain
a positive nitrogen balance and to produce an
increase in plasma albumin concentration and
disappearance of edema. In most cases,
sufficient intake from carbohydrate and fats are
needed to spare protein for anabolism.
Disease of The Kidney
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Nephrotic syndrome (protein losses)
Nephritic Syndrome (hematuri)
Acute Renal failure (ARF)
Tubular defect
Renal stones
End stage disease (ESRD)
Nephrotic syndrome
• Common manifestation is loss of
glomerular barrier to protein.
• Large protein losses in the urine lead to
hypo albuminemia which consequent
edema, hypercholesterolemia,
hypercoagulability and abnormal bone
metabolism.
Cause of Disease
• More than 90% of the cases of nephrotic
syndrome stem from 3 systemic disease:
Diabetes mellitus, systemic lupus
erythematosus and amyloidosis and four
disease primarily of the kidney (minimal
change disease)
Nutritional Care
• The primary objective is to manage the
symptoms associated with the syndrome:
Edema
hypoalbuminemia
hyperlipidemia
• Decrease the risk of progression to renal
failure, and maintain nutrition stores
End-stage renal disease (ESRD)
• Reflects the kidney's inability to excrete
waste products, maintain fluid and
electrolyte balance, and produce
hormones. As renal failure slowly
progresses, the level of circulating waste
products eventually leads to symptoms of
uremia
End-stage renal disease (Uremia)
• Uremia is a clinical syndrome of malaise,
weakness, nausea and vomiting, muscle
cramps, itching, metallic taste in the
mouth, and neurologic impairment that is
brought about by an unacceptable level of
nitrogenous wastes in the body.
Medical Treatment (ESRD)
• dialysis,
• transplantation,
• or medical management progressing to
death
Medical Nutrition Therapy (ESRD, Dialysis)
• Protein: Dialysis is a drain on body protein, so
protein intake must be increased accordingly.
Protein losses of 20 to 30 g can occur during a
24-hour Peritoneal dialysis (PD), with an
average of 1 g/hour.
• Those receiving PD need 1.2 to 1.5 g/kg of body
weight. At least 50% should be HBV protein.
• Patients who receive HD three times per week
require a daily protein intake of 1.2 g/kg of body
weight
Energy, Fluid and Sodium Balance
• Depending on the patient's nutrition status
and degree of stress, between 25 and 40
kcal/kg of body weight should be provided,
with the lower amount for transplantation
and Peritoneal dialysis (PD) patients and
the higher level for the nutritionally
depleted patient
Fluid and Sodium Balance
• The vast majority of dialysis patients need
to restrict sodium and fluid intakes.
Excessive sodium intake is responsible for
increased thirst, increased fluid gain, and
resultant hypertension. Even those
patients who do not experience these
symptoms but produce minimal amounts
of urine will benefit from a reduced sodium
intake to limit their thirst and prevent large
intradialytic fluid gains.
Fluid and Sodium Balance
• In the patient who is maintained on HD,
sodium and fluid intake are regulated to
allow for a weight gain of 4 to5 lb (2 to 3
kg) from increased fluid in the vasculature
between dialyses. The goal is a fluid gain
of less than 4% of body weight. A sodium
intake of 87 to 130 mEq (2 to 3 g) daily
and a limit on fluid intake (usually about
750 mLiday
Fluid and Sodium Balance
• The fluid contained in solid foods is not
included in the 750 mL limit. Solid foods in
the average diet contribute approximately
500 to 800 mLiday of fluid. This fluid in
solid food is calculated to approximately
replace the 500 mL/day net insensible
water loss.
Lipid
• Atherosclerotic cardiovascular disease is
the most common cause of death among
patients maintained on long-term Dialysis
• Treatment of hyperlipidemia with diet or
pharmacologic agents remains
controversial.
Lipid
• Epidemiologic evidence demonstrating
increased incidence of atherosclerotic coronary
disease is balanced by studies that demonstrate
that patients with clearly defined clinical
evidence of atherosclerosis at the initiation of
dialysis are at no increased risk for a
cardiovascular event. Although routine treatment
appears unwarranted, a good case can be made
for dietary and pharmacologic treatment of
patients with ESRD with underlying lipid
disorders and evidence of atherosclerosis
Iron and Erythropoietin
• The anemia of chronic renal disease is caused
by an inability of the kidney to produce EPO, the
hormone that stimulates the bone marrow to
produce red blood cells, an increased
destruction of red blood cells secondary to
circulating uremic waste products; and blood
loss with dialysis or blood sampling. A synthetic
form of EPO, recombinant human EPO
(rHuEPO), is used to treat this form of anemia
Vitamins
• Water-soluble vitamins are rapidly lost during dialysis. In
general, ascorbic acid and most B vitamins are lost
through dialysate at approximately the same rate they
would have been lost in the urine (depending on the type
and duration of treatment), with the exception of folate,
which is highly dialyzable. Patients who still produce
urine may be at increased risk of loss of water-soluble
vitamins. Folate is recommended to be supplemented at
1 rug/day based on extra losses. Because vitamin B12is
protein-bound, losses of this B12 vitamin during dialysis
are minimal
Dialysis patient’s guide to blood values
Blood
Test
normal
value mg/dl
dialysis
value mg/dl
function
diet
BUN
4-22
<100
protein
waste
Uric acid
40-85
same
purine waste no change
Creatinine
0.7-1.5
10-15
waste
no change
of muscle
dialysis
breakdown controls
meat 3ser/d
Nutrition support
• Nutrition support is the delivery of formulated
enteral or parenteral nutrients for the purpose of
maintaining or restoring nutritional status.
Enteral nutrition (EN) refers to the provision of
nutrients into the gastrointestinal tract (GIT)
through a tube or catheter. In certain instances
EN may include the use of formulas as oral
supplements or meal replacements. Parenteral
nutrition (PN) is the provision of nutrients
intravenously.
Enteral and parenteral nutrients
• PN should be used in patients who are or
will become malnourished and who do not
have sufficient gastrointestinal function
• EN decreases the incidence of
hyperglycemia when compared with PN.
ENTERAL NUTRITION
• By definition, enteral implies using the
GIT, primarily via "tube feeding." When a
patient has been determined to be a
candidate for EN, the location of nutrient
administration and type of enteral access
device is selected.
ENTERAL NUTRITION
Nasoenteric Routes and tube placement
• Nasogastric (Cervical pharyngostomy or
esophagostomy, Gastrostomy)
• Nasoduodenal (Gastrostomy)
• Nasojejunal (Jejunostomy)
(duodenum, jejunum, ileum are 3 sections of
small intestine)
Nasogastric tubes (NGTs)
• are the most common way to access the GIT.
They are generally appropriate only for those
requiring short-term EN, which is defined as 3 or
4 weeks. Typically, the tube is inserted at the
bedside by a nurse or dietitian. The tube is
passed through the nose into the stomach.
• Patients with normal gastrointestinal function
tolerate this method, which takes advantage of
normal digestive, hormonal, and bactericidal
processes in the stomach. Rarely, complications
can occur
Factors to Consider When
Choosing an Enteral Formula
• Ability of the formula to meet the patient's nutritional
requirements
• Caloric and protein density of the formula (i.e., kcal/mL,
g protein/mL, kcal :nitrogen ratio)
• Gastrointestinal function of the patient
• Presence of lactose, which may not be tolerated
• Sodium, potassium, magnesium, and phosphorus
content of the formula, especially in cardiopulmonary,
renal, or
• hepatic failure
• Type of protein, fat, carbohydrate, and fiber in the
formula tolerable for the patient's digestive and
absorptive capacity
• Viscosity of the formula related to tube size and method
of feeding
Monitoring the Patient Receiving
Enteral Nutrition
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Abdominal distention and discomfort
Fluid intake and output (dail )
Gastric residuals (every 4 hr) if appropriate
Signs and symptoms of edema or dehydration (daily)
Stool output and consistency (daily)
Weight (at least 3 times/wk)
Nutritional intake adequacy (at least 2 times/wk)
Serum electrolytes, blood urea nitrogen, creatinine, (2-3
times/wk)
• Serum glucose, calcium, magnesium,
phosphorus,(weeklyor as ordered)
Macronutrients, vitamins, minerals, fluids
• 30% to 85% of Energy as CHO
• 15% and 30% of the total kilocalories of
standard formulas are provided by lipids
• 15% Energy as protein
MCT (Medium chain triglyceride)
• MCTs can be added to enteral formulas
because they do not require bile salts or
pancreatic lipase for digestion and are absorbed
directly into the portal circulation. Most formulas
provide 0% to 85% of fat as MCTs.
• MCTs do not provide the essential linoleic or
linolenic acids; they must therefore be provided
in combination with long-chain triglycerides.
• MCT is available naturally in milk and coconut oil
Omega-3
• Formulas contain a combination of
(omega-3 fatty acids and (omega-6 fatty
acids. The (omega-3 fatty acids include
eicosapentaenoic acid and
docosahexanoic acid. These are
considered advantageous compared with
(omega-6 fatty acids because of their anti
inflammatory effect
Vitamins, Minerals, and Electrolytes
• Most, but not all available formulas are
designed to meet the dietary reference
intakes (DRls) for vitamins and minerals if
a sufficient volume is taken.
Fluid
• Fluid needs for adults can be estimated at 1 mL of water
per kilocalorie consumed, or 30 to 35 mL/kg of usual
body weight Without an additional source of fluid, tubefed patients may not get enough free water to meet their
needs, particularly when concentrated formulas are
used.
• Standard (1 kcallmL) formulas contain approximately
85% water by volume, but concentrated (2 kcallmL)
formulas contain only approximately 70% water by
volume.
• All sources of fluid being given to a patient receiving EN,
including feeding tube flushes, medications, and
intravenous fluids, should be considered when
determining and calculating a patient's intake. Additional
water can be provided through the feeding tube as
needed
Energy, protein requirements
• Metabolic basal:1 kcal/kg/h (for men), 0.9
kcal/kg/h (for women)
• Extra energy is required for activity (3001000 kcal)
• Protein 0.8 g/kg/B/weight
Traditional & formulated foods
Whole Milk or yogurt, 240 ml=150 kcal,12g CHO,8g protein
Fresh Fruit juice (apple), 240 ml= 120 kcal
Filtered Soup, 240 = 100 kcal
Canned fruit, 240 = 150 kcal
Coconut oil, 1 g = 9 kcal, MCT
Ensure (gluten free, lactose free),
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400 g Can = 1724 kcal, 62 g protein, 64 g fat
100 g = 431 kcal, 15.5 g protein, 14 g fat
54.5 g (6 spoon+190ml=230ml) =230 kcal,1 ml=1 kcal
400 g (1 Can) = 7 and half meals of 230 ml