MEDICAL NUTRITION THERAPY

FOR RENAL DISEASE

Dewi Martha Indria
Key Concepts
• Renal disease interferes with the normal capacity of nephrons to filter
waste products of body metabolism.
• Short-term renal disease requires basic nutritional support for healing
rather than dietary restriction.
Dual Role of the Kidneys
• Kidneys make urine, through which they excrete most of the waste
products of metabolism.
• Kidneys control the concentrations of most constituents of body
fluids, especially blood.
Renal Nephrons
• Basic functional unit of the kidney
• Major nephron functions
• Filtration of materials in blood
• Reabsorption of needed substances
• Secretion of hydrogen ions to maintain acid-base balance
• Excretion of waste materials
• Additional functions
• Renin secretion (for body water balance)
• Erythropoietin (EPO) secretion (for red cell production)
• Vitamin D activation
Nephron Structures
• Glomerulus
• Cluster of branching capillaries
• Cup-shaped membrane at the head of each nephron forms the Bowman’s
capsule
• Filters waste products from blood
• Glomerular filtration rate (GFR): preferred method of monitoring kidney function
• Tubules
• Proximal tubule
• Loop of Henle
• Distal tubule
• Collecting tubule
Anatomy of the Kidney
Causes of Kidney Disease
• Inflammatory and degenerative disease
• Acute glomerulonephritis
• Nephrotic syndrome
• Chronic renal failure
• Damage from other diseases
• Hypertension, diabetes mellitus
• Infection and obstruction
• Damage from other agents
• Environmental agents
• Malnutrition
• Genetic defects
Risk Factors
Nutrition Therapy
• Based on the nature of the disease process and individual responses
• Length of disease
• Long-term: more specific nutrient modifications
• Degree of impaired renal function
• Extensive: extensive nutrition therapy required
• Individual clinical symptoms
KIDNEY STONES
(NEPHROLITHIASIS)
Kidney Stones
• Frequent occurrence between the ages of
30-50, predominance in males, & high
recurrence rate
• Factors relating to urine or urinary tract
environment contribute to formation
• The most common stones:
• 10 % calcium oxalate & calcium phospate
• 5-10 % uric acid
• 5-10 % struvite
• 1 % cystine
Risk Factors
Calcium Stones
• One third to one half of patients with calcium stones  hypercalciuric
• A value of Ca > 300 mg/day in men (>250 mg/day in women)
• Causes: primary hyperparathyroidism, sarcoidosis, excess vitamin D intake,
hyperthyroidism, glucocorticoid use, renal tubular acidosis.
• Idiopathic hypercalciuria  genetic basis
• Triggered by: excessive dietary calcium intake, increased intestinal absorption
of Ca, decreased renal tubular absorption of Ca, prolonged bed rest
• Other causes:
• Excess oxalate in urine (hyperoxaluria)
• Low levels of citrate in urine (hypocitraturia)
• Infection
Calcium Stones
• Low-Ca diets recommended to reduce the hypercalciuria in these
stone formers  chronic prolonged Ca restriction, def Ca intake 
increased losses from hypercalciuria but decrease bone density at the
spine and cortical sites  increase vertebral fracture risk
• Ca supplement don’t have same protective effect as dietary Ca
(timing is important)
• Taken with meals increase urinary Ca and citrate but decrease urinary oxalate
 the increase in citrate and decrease in oxalate counterbalance the effects
of elevated urinary calcium
• If urine Ca increases  increase fluid intake
Oxalate Stones
• Hyperoxaluria  > 40 mg of oxalate in urine/day
• Causes :
• autosomal-recessive genetic defects of a hepatic enzyme  overproduction of oxalate,
• fat malabsorption e.c inflammatory bowel disease  increase bile salts & fatty acids  increase colonic permeability to
oxalate
• Excessive vit C intake in patients with CKD  increase oxalate stone formation

• Bioavailability of food oxalate & urine oxalate are affected by:

• Salt forms of oxalate
• Food processing
• Cooking methods
• Meal composition
• Presence of Oxalabacter formigenes in the GI tract
• Dietary advice
• Use of probiotic
• Reduce of dietary oxalate - simultaneous consumption of
Ca-rich food/supplement
Uric Acid Stones
• Uric acid : end product of purine metabolism from food, de novo
synthesis & tissue catabolism.
• The solubility of uric acid depends on:
• Urine volume
• Urine pH
• Causes by:
• Low urine pH
• Low intake alkali-producing foods
• Increased consumption of acid-producing foods
• GI bicarbonate loss in diarrhea predispose uric acid stones
• Diabetes mellitus
Cystine Stones
• Rare stones caused by
homozygous cystinuria
• > 250 mg cystine in urine/day
• Maintain alkaline urine pH 24
hours  use of medication
• Fluid intake > 4L/day
• Lower sodium intake
• Low-methionine diet (essentially
a low-protein diet) sometimes
recommended
Struvite Stones
• Composed of magnesium
ammonium phosphate
• Mainly caused by urinary tract
infections rather than specific
nutrient
• No diet therapy is involved
• Usually removed surgically
 Urinary pH – How does diet affect it?
• Dietary intake  influence the acidity/alkalinity of urine
High alkaline foods  low Potential Acidic Foods
potential renal acid load
Protein Meat, fish, fowl, shellfish, eggs, all types of

Alkaline Fat
cheese, peanut butter, peanuts
Bacon, butternuts, walnuts, pumpkin seeds,
foods sesame seeds, sunflower seeds, creamy salad
dressings
Acidic Carbohydrate All types of bread, oat, rice, macaroni, wheat, rice
foods bran, macaroni, wheat gluten
Sweets Gelatin desserts (dry mix with & without
aspartame), pudding (instant, dry mix)

Potential Alkaline Foods

Fat Dried chestnuts, dried beechnuts, acorn
Increased risk of chronic acidosis
Vegetables All types including lentils, but especially beets, swisschard, kale,
leeks, mustard green, spinach
Neutral Foods Fruit All types, especially currants, dates, figs, bananas, dried apricots,
Fats Butter, margarine, oils apples, prunes, raisins

Dairy Milk Spices/ All types, especially fresh dill weed, dried spices/herbs such as
herbs basil, coriander, curry powder, oregano, parsley
Vegetables Corn
Sweets Sorghum syrup, brown sugar, molasses, cocoa
Sweets White sugar, honey
Beverages Water, tea Beverages coffee
Kidney Stones: Symptoms and Treatment
• Clinical symptoms: severe pain, other urinary symptoms, general
weakness, and fever
• Several considerations for treatment
• Fluid intake to prevent accumulation of materials
• Dietary control of stone constituents
• Achievement of desired pH of urine via medication
• Use of binding agents to prevent absorption of stone elements
• Drug therapy in combination with diet therapy
 Nutrition Management
• Normalize urine excretion of stone forming solutes
• Achieve daily urine volume > 2L
• High urine flow rate  wash out any formed crystals
• Dietary Ca based on age
• Avoid high oxalate foods  add Ca to each meal to bind oxalate (about 150 mg of
Ca to bind 100 mg of oxalate)
• Lower salt intake Reduce oxalate excretion more than a traditional low
oxalate diet
• Moderate animal protein
• Vitamin C not > 500mg/day
• Citrate  inhibits urinary stone by forming a complex with Ca in urine (daily intake
> 640 mg/day)
• Mineral water (with Mg & bicarbonate content)  raise urine pH & stone inhibition
• Fructose  increase urinary excretion of Ca & oxalate  increase risk of kidney
stones
Recommendations for Diet & 24 Hrs Urine Monitoring in Nephrolitiasis
Diet Component Intake Recommendation 24-Hrs Urine
Protein Normal intake : avoid excess Monitor urinary urea
Calcium • Normal intake: < 150 mg/L
• 1000 mg (< 50 yrs old)
• 1200 mg (> 50 yrs old)
• Divide intake between 3 or more eating
sessions
Oxalate Avoid moderate to high oxalate foods  further < 20 mg/L
restrict if necessary
Fluid > 2,5 L, assess type of fluids consumed >2L
Vitamin C < 500 mg/day Monitor urine oxalate
Vitamin D, cod liver Supplements not recommended
oil
Vitamin B6 > 40 mg/day reduces risk. No recommendation
made
Sodium < 100 mmol/day Monitor urinary sodium
Low-Calcium Diet
ACUTE RENAL FAILURE
Patient with ARF:
• Uremia
• Metabolic acidosis Increase protein
• Fluid & electrolyte imbalance needs
• Physiologic stress
 Goal is to improve or maintain nutritional status

In the early stage of ARF  often unable to eat 

malnourished  high mortality

Individualized therapy based on renal function (indicated by

GFR).
• At the onset of AKI, depending on severity, some
patients can be treated with medical management,
other patients require renal replacement therapy
(RRT) with standard haemodialysis (HD) or
peritoneal dialysis (PD)
• Parenteral nutrition therapy may be required
Protein
• The amount of protein is influenced by the underlying cause & the
presence of other conditions.
Nondialysis patient 0,5 – 0,8 g/kg
Dialyzed patient 1 – 2 g/kg
• Patient’s overall medical status stabilizes & improves  metabolic
requirements decrease  minimum protein intake 0,8 – 1 g/kg
(during stable period)
Energy
• Energy requirements are determined by the underlying cause of ARF
& comorbidity.
• 25 – 40 kcal/kg of upper end IBW (Ideal Body Weight) or adjusted
IBW per day.
• Excessive calorie intake can lead to excess CO2 production  depressing
respiration
• Large intakes of carbohydrate & fat are needed to prevent the use of
protein for energy production.
• For patients who receive parenteral nutrition  high concentrations of
carbohydrate and lipid can be administered to fulfil these needs as long as
respiratory status is monitored.
Fluid & Sodium
• Fluid & electrolyte intake should balance the net output.
• Replace output fluid from the previous day (vomitus, diarrhea, urine) + 500
mL
• Sodium is restricted  based on decreased urinary production.
• In the oliguric phase  sodium output is very low  intake should be low as well (20
– 40 mEq/day)
• Limiting sodium is often impossible because of the requirement for many
IV solutions (including IV antibiotics, medications for blood pressure, and
PN). The administration of these solutions in electrolyte-free water in the
face of oliguria quickly leads to water intoxication (hyponatremia).
• All fluid above the daily calculated water loss should be given in a balanced salt
solution.
Potassium
• Potassium intake needs to be individualized according to serum level.
• Potassium removal during AKI  dialysis
• Control of serum potassium levels between dialysis administrations relies
mainly on IV infusions of glucose, insulin, and bicarbonate, all of which drive
potassium into cells.
• Exchange resins, such as sodium polystyrene sulfonate (Kayexalate), which
exchange potassium for sodium in the GI tract, can be used to treat high
potassium concentrations;
CHRONIC KIDNEY DISEASE
Stages of Chronic Kidney Disease
Medical Nutrition Therapy
• Primary objectives:
• Manage the symptoms associated with the syndrome (oedema,
hypoalbuminemia, and hyperlipidaemia),
• Decrease the risk of progression to renal failure,
• Decrease inflammation,
• Maintain nutritional stores.
• The diet should attempt to provide sufficient protein and energy to
maintain a positive nitrogen balance and to support tissue synthesis
while not overtaxing the kidneys.
• In most cases, sufficient intake from carbohydrate and fats is needed
to spare protein for anabolism.
Protein
 The RDA for protein is 0.8 g/kg/day
 may decrease proteinuria without adversely affecting serum albumin
 Role for protein restriction in the management of patients with mild
to moderate renal insufficiency  preserve renal function.
 To allow for optimal protein use  50-60 % of the protein should be from
sources of high biologic value (HBV)  meaning that the body is easily able to
digest and use the amino acids.
• The NKF’s Kidney Dialysis Outcome Quality Initiative (KDOQI) panel:
• GFR < 25 ml/min (not yet begun dialysis)  should be maintained on 0.6
g/kg/day of protein and 35 kcal/kg/day.
• If patients cannot maintain an adequate caloric intake on this protein
recommendation  protein intake should be increased to 0.75 g/kg/day.
• In both cases approximately 50% of the protein should be of HBV.
• Progressive renal failure
• 0,8 g/kg/day with 60 % HBV (GFR > 55 mL/min)
• 0,6 g/kg/day with 60 % HBV (GFR 25 – 55 mL/min)
(The National Institute of Diabetes & Digestive & Kidney Diseases (NIDDKD))

• If protein is restricted  careful monitoring & anthropometric studies

periodically
 The 70-kg reference man needs 0.8 g/kg or 56 grams protein per day.
 If we use 50% HBV to estimate his needs, he needs about 28 grams.
− [(.50)(56 grams) = 28 grams]

 If we use 75% HBV to estimate his needs, he needs about 42 grams.

− [(.75)(56 grams) = 42 grams]
How much protein remains for
other food groups?
50% HBV 75% HBV

56 g protein total 56 g protein total

− 28 g HBV protein − 42 g HBV protein
28 g other protein 14 g other protein
Lower Protein Pro (g)
Grains (1 oz.) 2.2–2.4
Vegetables (1/2 cup) 0.7–1.7
Fruits (1/2 cup) 0.7
Fats and oils 0
Sugars 0
Divide the remaining protein between the
other food groups
Protein remaining 6g
50% HBV ½ cup milk (4 g) −4 g
Protein remaining 28 g 2g
9 grains (2 g) −18 g
10 g

Protein remaining 2g
Protein remaining 10 g 3 fruit (0–1 g) −2 g
4 vegetables (1 g) −4 g 0g
6g
Energy
• Energy intake should be approximately about 35 kcal/kg/day for
adults to spare protein for tissue repair & maintenance

Lipid
• Lowering protein intake in adult patients may also lower fat &
cholesterol intake from animal sources.
 Sodium
• Total body sodium overload  edema
• Control of oedema in this group of diseases should be with dietary
intake of 1500 g/day
INTERMAP: Salt is the leading source of
sodium in middle-aged Americans

Sodium intake is higher than recommended

Reference: http://www.iom.edu/Reports/2010/Strategies-to-Reduce-Sodium-Intake-in-the-United-States.aspx Reference: Adapted from Anderson et al. J Am Diet Assoc 2010; 110(5):736–745.
Potassium
• Variability in disease states, individual intakes, & use of medications
that may decrease potassium.
• Early stage CKD take potassium-wasting diuretics  require
supplementation
• When urine output drops below 1 L/day  may require a potassium
restriction as the kidney is no longer able to excrete all potassium
ingested (CKD stage 4)  based on serum level examination
• The reference range is 3,5 – 5 mEq/L
Numerous sources contribute to potassium levels
in CKD
 Potassium-rich foods  Medications:
 Salt substitutes – K supplements
 KCl, K citrate
– Low-sodium products may
have added KCl. – Impair excretion
 ACEi
 Herbs and dietary  ARBs
supplement (examples)  K+-sparing diuretics
 Nonsteroidal anti-
– Noni juice (56 mmol/L)
inflammatory drugs
– Alfalfa
– Dandelion  Potassium food additives
– Horsetail
– Nettle • References: Palmer, N Eng J Med 2004;351(6):585–92;
• Hollander-Rodriguez & Calvert, Am Fam Physician.
2006;73(2):283–90.
Phosphorus
• Serum phosphorus levels elevate at the same rate as eGFR (estimated
GFR) decreases.
• Early initiation of phosphate reduction therapies is advantageous for delaying
hyperparathyroidism and bone disease  often asymptomatic during the
early phase of hyperparathyroidism and hyperphosphatemia  not attend to
their modified diets or understand the need to take phosphate binders with
meals.
• No more than 1000 mg/day  a limit that allows approximately 1 – 2
dairy foods/day
• Patients who are in later stages of CKD and intolerant of red meats
because of uremic taste alterations often are able to substitute milk
foods for meat and still maintain a limited phosphate intake.
Vitamin
• Restrictions may cause the diet to be inadequate  CKD patients are
routinely recommended a water-soluble renal customized vitamin
supplement
END STAGE RENAL DISEASE
End-Stage Renal Disease
• 90 % ESRD patients have chronic:
• Diabetes mellitus
• Hypertension
• Glomerulonephritis
• Dialysis or transplant are only options
Goals of MNT in ESRD
• Prevent deficiency & maintain good nutrition status through adequate
protein, energy, vitamin, & mineral intake.
• Control edema & electrolyte imbalance by controlling sodium, potassium,
& fluid intake.
• Prevent/slow the development of renal osteodystrophy by controlling Ca, P,
Vit D & PTH (Pituitary Hormone).
• Enable the patient to eat a palatable, attractive diet that fits their lifestyle
as much as possible.
• Coordinate patient care with families, dietitians, nurses, & physicians in
acute care, outpatient facilities.
• Provide initial nutrition education, periodic counseling & long term
monitoring of patients with the goal of patients receiving enough
education to direct their own care and diet.
Protein
• Dialysis  drain on body protein  protein intake must be increased.
• Protein losses of 20 to 30 g can occur during a 24-hour PD, with an average of
1 g/hr.
• Peritoneal Dialysis:
• Daily protein intake of 1.2 to 1.5 g/kg of body weight (At least 50% should be HBV
protein)
• Receive Haemodialysis 3x/week
• Daily protein intake of 1.2 g/kg of body weight
• Serum BUN and serum Cr levels, uremic symptoms, and weight should be
monitored, and the diet should be adjusted accordingly.
Energy
• Adequate to spare protein for tissue protein synthesis and to prevent
its metabolism for energy (Therrien, 2015)  depending on the
patient’s nutrition status and degree of stress (between 25 and 40
kcal/kg of body weight)
Lipid
• The patient with ESRD typically has an elevated triglyceride level with
or without an increase in cholesterol.
• Lipid-lowering drugs, including most statins, may have a significant
effect on better management.
• Use of lipid-lowering drugs should be monitored and cut back if
necessary in these patients, particularly if they are underweight or
suffering from malnutrition.
Fluid & 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,
• resultant hypertension.
• Haemodialysis
• Sodium and fluid intake are regulated to allow for a weight gain of 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 65 to 87 mEq (1500 to 2000 mg) daily
• A limit on fluid intake (usually about 750 ml/day plus the amount equal to the urine
output) is usually sufficient to meet these guidelines.
Potassium
• Potassium usually requires restriction, depending on:
• the serum potassium level,
• urine output,
• medications, and
• the frequency of HD.
• Reduced to 60 - 80 mEq (2.3 - 3.1 g) per day
• Anuria patient on dialysis  reduce to to 51 mEq (2 g) per day.
• Cose monitoring of the patient’s laboratory values, potassium content
of the dialysate, and dietary intake is essential.
• Some low-sodium foods contain potassium chloride as a salt
substitute rather than so- dium chloride.
Phosporus
• Phosphate intake is lowered by restricting dietary sources to 1200
mg/day or less.
• The difficulty in implementing the phosphorus restriction comes from
the necessity for a high-protein diet.
• Thus high-phosphorus foods cannot be eliminated without restricting protein,
creating a challenge to balance intake with dietary intervention alone.
• Require phosphate-binding medications (calcium carbonate, calcium
acetate, sevelamer carbonate, sucroferric oxyhydroxide, ferric citrate,
and lanthanum carbonate)
• used routinely with each meal or snack to bind to phosphorus in the gut.