Lecture 7 Renal Diseases

FOND 332: Advanced Medical Nutrition Therapy
Lecture 7: Renal Diseases
July 2021
DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Introduction
The kidney is an important organ in the body as it is involved in
homeostatic balance of fluids, electrolytes and organic solute.
The importance of nutrition in the care of patients with renal diseases is
supported by the fact that indicators of nutritional status effectively predict
morbidity and mortality in these patients.
Therefore, dietary management aims:-
 to reduce and control amount of wastes,
 treat underlying disorders,
 prevent or alleviate symptoms,
maintain optimal nutritional status and
 prevent progression of the disease
Anatomy, physiology and function of the kidney
The kidneys are a pair of organs located in the back of the abdomen.
Each kidney is about 4 or 5 inches long- about the size of a fist and
consists of approximately 1 million functioning units called nephrons
(Fig. 1). This are the working units of the kidney.
 The nephron consists of a glomerulus connected to a series of
tubules, which can be broken into functionally different segments:
the proximal convoluted tubule,
loop of Henle,
distal tubule, and
collecting duct.

Reading assignment
Prevalence and burden of renal diseases globally, SSA, Kenya
Risk factors of renal diseases in Kenya
Dialysis outcomes and practice patterns for Chronic Kidney Disease
patients
References
WHO reports
Abd ElHafeez, Samar et al. “Prevalence and burden of chronic kidney disease
among the general population and high-risk groups in Africa: a systematic
review.” BMJ open vol. 8,1 e015069. 10 Jan. 2018, doi:10.1136/bmjopen-
2016-015069

…anatomy, physiology and function of the kidney
Each nephron functions
independently in producing a
contribution to the final urine,
although all are under similar
control and thus coordinated.
Nevertheless, when one
segment of a nephron is
destroyed, that complete
nephron is no longer functional.
The functions of each of these
parts is illustrated in Fig. 2.

..physiology and function of the kidney
Functions of each part of a nephron

1. Glomerulus: The glomerulus is a spherical mass of capillaries
surrounded by a membrane, Bowman's capsule.
The function of the glomerulus is production of the large amount
of ultrafiltrate, which the following segments of the nephron then
modify.The ultra-filtrate produced in the glomerulus is very similar
in composition to blood.
Because of its barrier function, the glomerulus blocks blood cells
as well as molecules of molecular weight greater than 6500
daltons such as protein.
The production of ultrafiltrate is mainly passive and relies on the
perfusion pressure generated by the heart and supplied by the
renal artery.
The glomerular filtration rate (GFR) is the quantity of glomerular
filtrate formed per unit in all nephrons of both kidneys, an average of
125 ml/min, equivalent to 180 L/day.
Creatinine clearance is normally used as the measure of GFR.
Kidney disease decreases the creatinine clearance rate therefore
decreasing filtration of wastes out of the blood. The normal creatinine
clearance is 95-135 ml/min.
…physiology and function of the kidney
2. Tubules: The tubules reabsorb majority of the components of

the ultrafiltrate. An active process therefore requires energy.
The tubules reabsorb nutrients according to threshold level of
each substance, and excess is excreted. About 80% reabsorption
occurs in the proximal convoluted tubule.
The absorption of Na and K occurs at the distal convoluted
tubule and collecting duct.

Secretion: The tubules selectively removes substances from blood
filtrate. To help regulate blood pH, kidneys secrete H+ and re-absorbs
basic bicarbonate ions.
Most body’s metabolic processes produce excess H+ to keep pH
within normal range of 7.35-7.45. Kidneys secrete H+ from blood in
the distal convoluted tubule into the urine. Basic bicarbonate ions are
re-absorbed into the blood.
Excretion: The final urine produced is funneled into collecting ducts

Figure 2: Functions of Each Part of the Nephron
Function of the kidney
The functions of the kidney can be grouped into two major
categories:-
Excretory
Endocrine
1. Excretory
The kidney maintains homeostatic balance of fluids, electrolytes, and
organic solutes i.e. volume and composition of body fluids. The
normal kidney can perform this function over a wide range of
dietary fluctuations in sodium, water, and various solutes.
…function of the kidney
This task is accomplished by the continuous filtration of blood
and by alterations (secretion and re-absorption) in this filtered
fluid.
The kidney receives 20% of cardiac output, which allows the
filtering of approximately 1600L/day of blood.
Approximately 180 L of fluid (ultrafiltrate) is produced in
filtering this blood, and, through active processes of resorbing
certain components and secreting others, the composition of this
fluid is changed into the 1.5 L of urine excreted in an average
day.
Specific functions
Water balance: The control of excretion is regulated by an antidiuretic
hormone (ADH) secreted by the posterior pituitary. An excess of relative
body water (indicated by fall in osmolality) leads to a shut-off of ADH-for
water excretion and vice versa when osmolality rise (for water retention).
The kidney has ability to form a large concentration gradient between its
inner medulla and cortex therefore can excrete dilute urine or concentrated
urine.
Given a daily fixed solute load of about 600 mOsm (the solute load
representing the end waste products of normal metabolism), the kidney
can get rid of as little as 500 ml of concentrated urine or as much as
l2 L.

Excretion of waste products (renal solute load): Kidneys excrete
mainly nitrogenous products of protein metabolism i.e urea, uric acid,
creatinine and ammonia. If not eliminated appropriately they collect
in abnormal quantities in the blood.
Electrolyte and acid-base balance : Kidney controls amount of
electrolyte Na, K, chloride, bicarbonate, P, Ca etc. pH is regulated by
excreting acids or bases when there is excess in the blood.
Excretion of foreign substances e.g. medication, food additives

2. Endocrine function
The kidney also produces the hormone erythropoietin (EPO), a critical
determinant of erythroid activity in the bone marrow. Deficiency of
EPO is a factor in the severe anemia present in chronic renal disease.
Maintenance of calcium-phosphorus homeostasis involves the complex
interactions of parathyroid hormone (PDH); calcitonin; active vitamin
D; and three effector organs: the gut, kidney, and bone.
The role of the kidney includes production of the active form of
vitaminD-1,25-(OFI)2D3-as well as elimination of both calcium and
phosphorus.
The kidney also performs functions unrelated to excretion. One of these
involves the renin-angiotensin mechanism, a major control of blood pressure.
Decreased blood volume causes cells of the glomerulus (the juxtaglomerular

apparatus) to react by secreting renin, a proteolytic enzyme.
Renin acts on angiotensinogen in the plasma to form angiotensin I, which is

converted to angiotensin II, a powerful vasoconstrictor and a potent
stimulus of aldosterone secretion by the adrenal gland. As a consequence,
sodium and fluid are resorbed, and blood pressure is returned to normal

Pathophysiology of chronic kidney disease
The manifestations of renal disease are direct consequences of
the portions of the urinary tract system most affected.
These manifestations include:-
 glomerular diseases, acute renal failure (ARF),
 tubular defects, end-stage renal disease (ESRD) and renal
stones.
The main objectives of nutritional care depend on the abnormality
being treated.

1. Nephritic syndrome
Pathophysiology
Nephritic incorporates the clinical manifestations of a group of
diseases characterized by inflammation of the capillary loops of
the glomerulus.
The primary manifestation of these diseases is hematuria (blood
in the urine), a consequence of the capillary inflammation that
damages the glomerular barrier to blood cells.
The syndrome is also characterized by hypertension and mild loss of
renal function.
…pathophysiology
The most common presentation follows a streptococcal infection and is
usually, although not always, self-limiting.
 Other causes include:

 primary kidney diseases such as immunoglobulin A nephropathy;
hereditary nephritis; and
 secondary diseases such as systemic lupus erythematosus, vasculitis,
and glomerulonephritis associated with endocarditis, abscesses, or
infected ventriculoperitoneal shunts.

Dietary management
The treatment of acute glomerulonephritis attempts to maintain
good nutrition status while allowing time for the disease to
resolve spontaneously.
In patients in whom an underlying disease is responsible, treatment of
that disease predominates and largely determines outcome.
Restricting protein or potassium intake is of no benefit unless
significant uremia or hyperkalemia develops.
When hypertension is present, it is related mainly to extracellular
volume excess and should be treated with sodium restriction.
2. Nephrotic Syndrome
Pathophysiology
Nephrotic syndrome comprises a heterogeneous group of diseases,
the common manifestations of which derive from a loss of the
glomerular barrier to protein.
Large protein losses in the urine lead to :-
hypoalbuminemia with consequent edema
hypercholesterolemia hence risk for cardiovascular diseases
Hypercoagulability
abnormal bone metabolism.

…pathophysiology
Causes
Damage to the kidneys from infections
Blood clots in the renal veins
Metabolic disorders such as diabetes mellitus
Some drugs and toxins
Nephrotic syndrome is sometimes an early sign of renal failure
especially in those with diabetes mellitus.
In other cases treatment of underlying condition can correct the
disorders before renal failure develops.
Major consequences
Figure 3 illustrates the major consequences of nephrotic syndrome which
include:-
protein energy malnutrition (PEM),
 increased risk of infection,
blood coagulation disorders,
accelerated atherosclerosis,
occlusion of blood vessels from clots in lungs and
legs and rickets (lack of vitamin D and calcium bonding proteins).

Treatment: Involves diet and
drugs
Drugs: Diuretics to decrease
edema, lipid lowering drugs
e.g. statins, angiotensin I
inhibitors, antibiotics, anti-
inflammatory drugs etc
Figure 3: Consequence of Protein Loss

Dietary management
Aim: The primary objectives of medical nutrition therapy 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

Protein
In the past, a high protein (up to 1.5 g/kg/day) were used in an
attempt to increase serum albumin and prevent protein malnutrition.
However, studies have shown that a reduction of protein intake to
as low as 0.8 mg/kg/day can decrease proteinuria without
adversely affecting serum albumin.
To allow for optimal protein use, 50-60% of the protein should
be from sources of high biologic value (HBV), and energy intake
should be about 35 kcal/kg/day for adults and 100 to 150
kcal/kg/day for children.

Energy
Adequate energy intake is important in sparing protein and
maintaining a desirable weight.
Malnourished patients should be encouraged to consume a minimum
of 35 kcal (146 KJ)/kg IBW.
Obese patients should lose weight therefore decreases in energy
intake to help in control of lipid levels.
Children should be given 100-500 kcal/day.

Fat and sodium
Fat: A low fat diet is recommended to control elevated lipids
therefore fats should contribute <30% of total energy, with a decrease
in saturated fat.
Sodium
Sodium should be restricted due to edema and Na retention. Early

treatment uses low Na, approximately 250 mg, then progresses to
modest restriction of 3 g/ day, non-amine salts as condition improves.

3. Acute glomerulonephritis
This is the inflammation of the glomeruli capillary loops as a result
of streptococcal infection as a result of shock, drugs, surgery in other
parts of the body.
 This results to damages of the glomerular barrier (membrane)
allowing large molecules such as red blood cells and proteins to be
filtered out of the blood.
 It occurs mainly in children and adults.

Symptoms
Nausea and vomiting Oliguria (decreasing urine output, less
than 500 ml/day- it is impossible for
Hematuria (blood in urine)
such a small urine volume to eliminate
Proteinuria especially albumin all of the daily waste.
Edema due to loss of protein (lack Increasing blood urea nitrogen (BUN)
of oncotic pressure)
Hypertension because of decrease in
blood flow

Dietary management
Salt and fluid restriction depends on the level of fluid retention. In
oliguria, restrict fluid to 500 ml + volume of previous day urine
output.
Salt 80-100 mmol
Protein is restricted in uremic patients

4. Chronic glomerulonephritis
Occurs due to repeated episodes of acute phase leading to loss of

nephrons and kidney function.
 It is characterized by increased loss of protein, accumulation of urea

and creatinine.
Dietary management is as for acute glomerulonephritis

5. Renal failure
This is the condition in which the kidneys are no longer able to
maintain the normal composition of the blood i.e. inability to excrete
daily load of waste.
a) Acute Renal failure (ARF)
Pathophysiology: This is a condition whereby the nephrons suddenly
lose function and are unable to maintain homeostasis.
ARF is characterized by a sudden reduction in GFR, or the
amount of filtrate per unit in the nephrons, and an alteration in
the ability of the kidney to excrete the daily production of
metabolic waste.
…acute renal failure
It can occur in association with oliguria or normal urine. Typically occurs
in previously healthy kidneys. Its duration varies from a few days to
several weeks.
The degree varies from mild to severe. With prompt treatment ARF is
reversible.
Causes
Intrinsic ARF can result from toxic drug exposure, a local allergic
reaction to drugs, rapidly progressive glomerulonephritis, or a
prolonged episode of ischemia leading to ischemic acute tubular
necrosis. Of these causes the latter is the most devastating.

…causes of ARF
Fluid loss (dehydration) due to diarrhea, vomiting, burns, excessive
diuresis
Blood loss due to GIT bleeding, surgery, accidents (external
bleeding)
Hypotensive state from cardiogenic shock, hear failure, sepsis or
aortic aneurysms
Obstruction e.g. prostatic enlargement, cancer of bladder, prostate
gland, cervix, renal calculi

Consequences
Sudden reduction in GFR and urine output

Accumulation of waste products i.e. blood urea, creatinine, uric acid
Hyperkalemia (excessive K levels). Blood K+ rises in the oliguric
phase as the kidney cannot excrete it. Severe stress causes cell break
down and intercellular fluids release K+. Hyperkalemia can lead to
sudden heart failure.
Blood volume changes. In early stages, kidney fails to excrete fluids
leading to pulmonary edema especially among older persons.
Clinical symptoms-uraemic syndrome observed as toxic wastes rise
Acidosis may occur as H+ are not excreted

Treatment
The primary goal is to treat the underlying disorder therefore:-
Rehydration in dehydration (IV fluids)
Blood transfusion to restore blood volume
Dialysis (renal replacement therapy) for restoring fluid and

electrolyte balance, and removal of toxic substances.
Diet therapy

Dietary management
Nutritional care in ARF is particularly important because the
patient not only has uremia, metabolic acidosis, and fluid and
electrolyte imbalance but also usually suffers from physiologic
stress (e.g., infection or tissue destruction) that increases protein
needs.
The problem of balancing protein and energy needs with
treatment of acidosis and excessive nitrogenous waste is
complicated and delicate.
In the early stages, the patient is usually moribund and is unable to
eat hence total parenteral nutrition (TPN) plus dialysis is normally
used, and positively affects patient survival.

…dietary management
Replacement of renal function during ARF can be carried out as
standard hemodialysis; peritoneal dialysis (PD); or
 continuous arteriovenous hemofiltration (CAVH) or continuous
venovenous hemofiltration (CVVH), which use a small
ultrafiltration membrane powered by the patient's own blood or a
pump to produce an ultrafiltrate that can be replaced by
parenteral nutrition fluids.
This allows parenteral feeding without fluid overload. Patients are
usually in three categories: non-catabolic, moderate and catabolic.

Energy
Initially, in diarrhea and vomiting, TPN may be used (especially
moderate and catabolic patients) to reduce protein catabolism.
Glucose and essential amino acids decrease catabolism more than

glucose alone.
When oral intake is permitted a high energy intake 35-50 kcal; is

given for non-catabolic while catabolic patients are given 50 kcal.

Protein
The requirements depend on renal fixation, metabolic state and
nutritional status.
Patients who are not on dialysis-0.6-0.7 g/kg IBW/day to reduce
nitrogenous wastes, and 70-75% HBV
Patients on dialysis-more liberal intake as some is lost in the
procedure, 1.2-2.5 g/kg IBW/day.
NB: It is important to consider complicating factors such as
infections, muscle wasting, negative nitrogen balance etc.

Fluid
This should be regulated according to urinary output and any additional
losses from vomiting and diarrhea, or fever plus insensible water losses
from skin, lungs and perspiration.
 In oliguric phase, little fluid of approximately 500 ml/day is required. In
the diuretic (recovery phase) stage little urine volume increases therefore
allow more fluid.
Table 1 provides an example of a calculation of fluid requirements.
Because of the numerous IV drugs and blood and blood products
necessitated by the underlying disease the challenge in managing
patients at this point becomes how to cut fluid intake as much as
possible while providing adequate protein and energy.
Table 1: Sample Calculation of Fluid Requirements in Acute Renal Failure
Source: Mahan LK and Escott-Stump S. Krause’s Food & Nutrition therapy, International Edition. Saunders, an
imprint of Elsevier Inc. I1830 Wesdine Industrial Drive. St. Louis, Missouri 6314. Page 927.

Electrolytes
Sodium should be restricted to 500-1000mg in oliguric phase but
intake increased in the diuretic phase.
Potassium requirements depend on serum levels and whether the

patient is on dialysis. Normally restrict to <2 g/day in oliguric phase,
supplementation in the diuretic phase.
NB: Monitor weight, electrolytes and fluid balance.

b. Chronic renal failure (CRF)
This is a gradual and irreversible damage of the kidney tissue i.e.
insufficiency of renal excretory and regulatory function.
Causes
Nephritis-inflammation of the kidney
Hypertension
Diabetic nephropathy
Obstruction (stone, prostate enlargement)
Myeloma, atherosclerosis

Stages of CRF
1. Reduced renal reserve; > 50% of renal fixation lost, creatinine normal,
asymptomatic
2. More than 75% damage (renal insufficiency, 40 ml/min creatinine
clearance, creatinine 120-250 mmol/L
3. Renal failure; creatinine clearance 20 ml/min, creatinine levels >300
mmol/L
4. End stage renal failure (ESRF): >90% of tissue damaged (nephrons),
GFR 10-20 ml/min (normal 95-135 ml/min), uremic symptoms present-
lethagy, itch, tiredness, morning nausea, decreased mental alertness
…stages of CRF
Table 2 shows the stages of chronic renal disease. The kidney undergoes a
series of adaptations to prevent the decrease in GFR.
Although in the short term this leads to improvement in filtration
rate, in the long term it leads to an accelerated loss of nephrons and
progressive renal insufficiency.
The nature of these adaptations involves a change in the hemodynamic
characteristics of the remaining glomeruli, specifically leading to
increased glomerular pressure.
 Factors that increase glomerular pressure tend to accelerate this
process, whereas factors that decrease glomerular pressure tend to
alleviate it.

Table 2: Stages of chronic renal disease
Stage of disease Description GFR (ml/min per 1.73 m2)
1 Kidney damage with normal or ≥90

increased GFR
2 Kidney damage with mildly 60-89
decreased GFR
3 Moderately decrease GFR 30-59
4 Severely decreased GFR 15-29
5 Kidney failure <15 (undergoing dialysis)

Consequences
Bone diseases-renal osteodystophy as the kidney is unable to excrete
phosphorus therefore its levels in the blood rises. Excess phosphorus
forms salts with calcium which are deposited in soft tissues, skin,
eyes, lungs, heart, blood vessels therefore levels falls. In addition, the
diseased kidney is unable to effectively activate vitamin D which
increases calcium absorption from GIT as well as low calcium diet.
Hypocalcemia

…consequences
Hypophosphatemia
Hyperkalemia
Sodium and fluid retention
Elevated lipids
Anaemia due to insufficient EPO production
Growth failure in children and wasting in both children and adults
Nitrogen retention-urea and creatinine
Treatment
Conservative management (prior to needing replacement)
Diet and medical therapy
Dialysis
Transplant

Conservative management
The diet aims to:
retard progression to renal failure
reduce and control the amount of waste produced which accumulates in
the body. Some conditions such as hyperkalemia are life threatening
prevent or improve symptoms of uremia e.g. decreased appetite,
vomiting, nausea, lethargy etc.
maintain optimal nutritional status
provide dietary freedom to lead a near normal life.

…conservative management
The important nutrients in diet therapy in CRF are protein, energy
sources (carbohydrates and fats), protein, sodium and fluid,
potassium, phosphorus, other minerals and vitamins.
Protein
An important nutrient for repair and maintenance of tissue and for
growth in children.
Restrict to 0.6 g/kg IBW (quantity and quality is important in renal

failure)
…protein
Quantity: Levels of restriction should suffice to maintain vital body
functions. The amounts should not be too high as excess protein increases
urea levels and other nitrogen related waste products. The ailing kidney is
unable to eliminate urea and other waste products in sufficient quantities
therefore levels of protein should be adapted to a level the kidney can
cope with.
Quality: Consideration is necessary to ensure positive nitrogen balance.

Majority of the protein should be HBV proteins e.g. eggs, milk and
products as they have a higher percentage of essential amino acids.
Ideally, HBV proteins should contribute 70-75% of protein requirements.

Energy
Amounts required for maintenance is important as the quantity and quality of
protein itself. Insufficient energy from non-protein sources (carbohydrates and
fats) will lead to negative nitrogen balance and PEM.
Also, the body will use its own tissue to meet energy requirements with a
corresponding rise in urea and creatinine levels. Excess energy is undesirable as
it will be stored in fatty tissue, which is a future problem with access to
haemodialysis or transplant.
Hence, energy should be 35-40 kcal/kg body weight. For satisfactory energy
intake, low protein foods with a high carbohydrate and fat content is used.

Carbohydrates and fat
Carbohydrates: Ideally, 50% of energy, and majority from starches.

They contain some protein, K and P and it may be difficult to
incorporate them in sufficient quantities.
Fat: Fat should contribute 40% of energy, a percentage higher than

general recommendation due to dietary protein restrictions. A
concentrated form of energy makes the food palatable.

…fat
Remember, hyperlipidemia is a common feature of CRF (though not
to be associated with refined carbohydrates and saturated fats but
with kidney disease and starts long before).
There is no conclusive evidence to prove that changing the type of

carbohydrate and fat alters hyperlipidemia in CRF.
It may be wise though to restrict saturated fats.

Sodium and fluids, potassium
Sodium and fluids: Individual needs depend on blood electrolyte
levels, blood pressure, urine output and oedema. Restrict in the
presence of oedema or hypertension. Sodium, 60-100 mg/day. Fluid,
previous day’s urine + 500 ml/day.
Potassium: Generally not restricted in non-oliguric patient i.e. >1000

ml urine output and serum K+ <5.5 mmol/L. When serum K+ > 5.5
mmol/L, and urine output is < 100 ml restrict to 50-60 mmol/day.

Phosphorus: Phosphorus is retained in renal failure hence restrict to 1-1.3
g/day or 10-12 mg/g protein. Limit high potassium foods such as eggs to
1/day.
Vitamins: Water soluble vitamins, vitamin B6, folic acid, and vitamin D may
need supplementation as deficiency may occur due to poor appetite, altered
metabolism, uremia, restricted diet.
Calcium: Oral calcium supplementation of 1000-1500 mg elemental

calcium/day. It is important to note that serum phosphate levels should be
under control before calcium supplementation as hypophosphatemia leads to
CaPO4 deposition in soft tissues.
Dietary challenges
Achieving adequate energy intake because of protein restriction

therefore glucose polymers may be used.
A lot of nutrient restrictions e.g. K+, Na, fluid, phosphorus etch
therefore compliances to the diet may not be easy.
Ways of reducing potassium intake
Avoid foods high in potassium-generally fruits and vegetables,
potatoes, fruit juices, bananas
Reduce potassium content by cutting and boiling twice to discard
water
Ways of boosting energy (calorie intake)
Spread margarine/jam thickly
Add margarine to vegetables, cream to mashed vegetables
Fry meat and vegetables
Add sugar to cereals, desserts, tea/coffee
Drink soft drink, squash not water
Include lollies (no toffee or chocolate-high in potassium)

Monitoring dietary treatment and renal function
1. Monitor serum biochemistry, urea, creatinine, K+, P
2. Renal function-creatinine clearance
3. GFR
NB: Serum creatinine levels remains normal till 50% of renal function is
lost. In ESRF > 1000 μmol/L. Serum urea is not a good marker of renal
function as it is affected by diet, drugs e.g. steroids, catabolism, blood
transfusions etc.
Progression to end stage renal disease: Chronic renal failure can progress
to end stage renal disease (ESRD) which requires replacement therapy.

c. End stage renal disease
Pathophysiology: ESRD can result from a wide variety of different
kidney diseases.
Currently 90% of patients reaching ESRD have chronic (1)
diabetes mellitus; (2) hypertension; or (3) glomerulonephritis.
With (ESRD come a myriad of problems related to 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.
Replacement therapy in chronic renal failure
Treatment chronic renal failure requires either transplantation
or dialysis.
1. Transplantation
Transplantation involves the surgical implantation of a
kidney from a living related donor, a living nonrelated
donor, or a deceased (cadaveric) donor.
Rejection of the foreign tissue or infection secondary to
immunosuppressive therapy are major complications.

Dietary management
The nutritional care of the adult patient who has received a
transplanted kidney is based mainly on the metabolic effects of the
required immunosuppressive therapy.
Medications typically used for the long term include glucocorticol

steroids, prednisone, cyclosporine, azathioprine, and mycophenolate
mofetil, Thcrolimus, Sirolimus, Thymoglobulin, and Atgam are also
used.

Corticosteroids are associated with:
Accelerated protein catabolism
Hyperlipidemia
sodium retention
weight gain
glucose intolerance
inhibition of normal calcium, phosphorus, and vitamin D
metabolism.
Cyclosporine and tacrolimus are associated with:
Hyperkalemia
Hypertension
hyperlipidemia.
Therefore, dietary modifications for the renal transplant patient are
designed to provide adequate calories and proteins to counteract the
catabolic effects of surgery during the early post-transplant period
and to manage nutritional side effects of the immunosuppressive
drugs.

The dietary modifications following kidney transplantation can be
divide into the following stages:-
a) Up to 1 month post-transplant
 A diet containing solid food is implemented according to patient
tolerance. The initial diet prescription is often dependent on
function of the transplanted kidney.
 Kidney function can be assessed by examining urine volume,
urine specific gravity, and serum creatinine levels.

Protein and energy intake
Protein hypercatabolism resulting from usage of high dosage steroids
together with surgical stress and pre-existing malnutrition requires
increased protein intake.
During the first month after transplantation, a high protein diet
(1.3 to 1.5 g/kg body weight) with an energy intake of 30 to 35
kcal/kg (weight adjusted for obesity) is recommended to prevent
negative nitrogen balance.
 Higher amounts of protein, 1.6 to 2 g/kg, are required in cases
of increased need such as fever, infection, and increased surgical
or traumatic stresses.
…protein and energy intake
For patients with nonfunctional transplanted kidney requiring
haemodialysis, protein requirements remain the same, but peritoneal
dialysis patients actually may need greater than 1.5 g protein/kg body
weight.
A high-protein, low-carbohydrate (1 g carbohydrate/kg body weight) has
been shown to reduce cushingoid side effects (thinning of the skin,
weakness, weight gain, bruising, hypertension, diabetes, thin weak bones
(osteoporosis), facial puffiness and, in women, cessation of menstrual
periods).
As this diet requires a relatively high fat intake, it should not be used
beyond 3-4 weeks post transplantation.
 During this acute period, fat restriction is not warranted.
Tissue weight gain and resultant obesity is a common problem
after transplantation due to medication side effects, fewer dietary
restrictions, and the lack of physical exercise.
Thus management counseling is indicated to promote a healthy

lifestyle and thereby contribute to the longevity of the
transplanted kidney.
In addition, majority of transplant recipients have elevated serum

triglycerides or cholesterol or both. The etiology of this
hyperlipidemia is multifactorial.

Intervention consists of calorie restriction for those who are
overweight, cholesterol intake limited to less than 300 mg/day,
and limited total fat.
Patients with glucose intolerance, limiting carbohydrates and

maintaining a regular moderate exercise regimen are appropriate.
Patients with diabetes mellitus should resume diabetic plan, although

calorie needs for appropriate weight maintenance may need to be
reevaluated.

Fluids and sodium
Hydration must also be monitored closely after transplantation.
Typically patients are encouraged to drink 2 L/day, but their
overall needs will depend on their increased urine output.
A moderate sodium restriction (80 to 100 mEq/day) during this
period minimizes fluid retention and helps to control blood
pressure.
This may be indicated by a decrease in urine output and weight gain.
After this time protein intake can be decreased to 1 g/kg, and
calorie intake should be at a level sufficient to achieve and
maintain an appropriate weight for height. Sodium intakes are
individualized based on fluid retention and blood pressure. It is
prudent that patients with hypertension resume sodium-controlled
diets.
Potassium, phosphorus, calcium and vitamin D
Potassium: Hyperkalemia (above 6.0 mEq per liter), commonly
associated with cyclosporine therapy warrants dietary potassium
restriction, although this is usually only temporary.
Phosphorus, calcium and vitamin D: Following transplantation,

many patients exhibit hypophosphatemia and mild hypercalcemia
caused by bone resorption associated with persistent
hyperparathyroidism and the effects of steroids on calcium,
phosphorus, and vitamin D metabolism.

…phosphorus, calcium and vitamin D
Antacids used to minimize steroid induced gastritis and ulcers may
also potentiate hypophosphatemia.
The diet should contain adequate amounts of calcium and
phosphorus (1200 mg of each daily), and serum levels should be
monitored periodically.
Supplemental phosphorus may be necessary to correct
hypophosphatemia and antacids must be used with medical
supervision.

b) After 1 month post- transplant
Nutrition care plan after first month following transplant involves
managing the nutritional side effects of immunosuppressive therapy
and individualizing die modifications based on kidney function.
Immunosuppressive therapy generally consists of treatment
combinations of pharmacological agents including prednisone,
cyclosporine (CSA), azathioprine, antithymocyte globin (ATG), and
muromonatab-CD3 (Orthoclone OKT3).
Thus the nutrition care procedures should coincide with the side
effects occurring in the individual patient.

Dietary management
A diet containing about 1 g protein/kg body weight/day is suggested to
promote nitrogen balance while preventing possible damage to the graft
tissue caused by excessive amounts of dietary protein.
 Weight control should be stressed due to tendency for increased appetite
caused by immunosuppressive therapy.
Given the high incidence of CVD in these patients at the time of
transplantation, and well known hyperlipidemic effects of corticosteroid
and cyclosporine therapy, measures to reduce hyperlipidemia are in order
The goals of nutrition intervention over the long term are to prevent excess
weight gain, restore nitrogen balance, minimize muscle wasting, and
minimize post-transplant glucose intolerance and hyperlipidemia.
Rejection
Acute or chronic rejection of the kidney may occur following kidney
transplantation.
During periods of acute rejection, protein and calorie needs increase
as doses of catabolic steroids are increased.
The same guidelines for calculating calorie and protein needs during
postplant period should be used during periods of acute rejection
Chronic rejection is the most common cause of late renal renal
allograft failure. Because no specific therapy exists, it leads to
progressive loss of the transplanted kidney.

…rejection
It is becoming an increasingly common cause of end stage renal failure. A
low-protein diet should be reserved for patients with progressive chronic
rejection and proteinuria, and in conjuction with blood pressure control.
 Levels of protein should probably be lower than 0.7 g/kg with adequate
calories.
Monitoring the nutritional status of these patients is important as they may
require higher protein levels.
Sodium and/or fluid restriction may also be warranted if hypertension or
fluid retention worsens.

2. Dialysis
 This is the removal of waste products from blood using the

principle of simple diffusion and osmosis through a semi-
permeable membrane (of an artificial kidney).
 Dialysis can be accomplished either by hemodialysis or by

peritoneal dialysis, the former being commonly used.

a) Haemodialysis
 Hemodialysis (HD) requires permanent access to the bloodstream
through a fistula created by surgery to connect an artery and a vein.
Fistulas are often made near the wrist, which greatly enlarges the
forearm veins (Fig. 4a).
 If the patient's blood vessels are fragile, an artificial vessel called a
graft may be surgically implanted. The person’s arterial blood rich in
nitrogenous waste is circulated from the body into a dialyzer (machine).
 The blood passes through semi-permeable dialysis membrane that are
bathed in a dialysate fluid. Sheets of membrane or hollow fibre separate
blood and dialysate.
…haemodialysis
The dialysate is similar
to plasma in
composition. As blood
circulates in the
dialyzer, wastes,
electrolytes and water
are exchanged into the
dialysate by osmosis
and diffusion, and
removed from blood by
ultrafiltration (Fig. 4b).
The purified blood is
returned into the vein.
The entire process
requires 4-6 hours, three
times a week. Figure 4a: Haemodialysis machine. © 2007 Thomson-Wadsworth2007

Figure 4b: Exchange of wastes, electrolytes and water from blood into the dialysate by
osmosis and diffusion and removal by ultrafiltration. © 2007 Thomson-Wadsworth
…haemodialysis
Disadvantages
Loss of protein (amino acids), 9-12 g/6 hours treatment
It is costly
Complications: infections, blood clotting, hypotension, muscle

cramping, headaches, fatigue, altered taste, anorexia, agitation,
nausea and vomiting after dialysis

b) Peritoneal dialysis
Peritoneal dialysis (PD) makes use of the semi permeable membrane of the
peritoneum. A catheter is surgically implanted in the abdomen and into the
peritoneal cavity (Fig. 5 a & b).
 Dialysate containing a high-dextrose concentration is instilled into the

peritoneum, where diffusion carries waste products from the blood through the
peritoneal membrane and into the dialysate; water moves by osmosis.
This fluid is then withdrawn and discarded, and new solution is added. Treatment lasts
10-12 hrs/day three times per week. In acute conditions 30-72 hrs. Types of peritoneal
dialysis include continuous ambulatory peritoneal dialysis (CAPD) and continuous
cyclical peritoneal dialysis (CCPD).

Continuous ambulatory peritoneal dialysis (CAPD)
It is similar to standard peritoneal dialysis, except that the dialysate
is left in the peritoneum and exchanged manually so no machine
is required.
Exchanges of dialysis fluid are done four to five times daily,
making it a 24-hour a day treatment.
Protein losses are higher than the regular peritoneal dialysis.

Continuous cyclical peritoneal dialysis (CCPD)
In this therapy, patients' treatments are done at night by a
machine that does the exchanges.
During the day, these patients may keep a single dialysate
exchange in the peritoneal cavity for extended periods of time
(called a long dwell),perhaps the entire day.
Several combinations of CAPD and CCPD are possible and will
be referred to as PD.
Patients who choose PD have higher protein needs (about 1.2 to
1.5 g of protein per kilogram) because of greater protein losses.
Figure 5a: Peritoneal dialysis exchange diagram
Figure 5b: Peritoneal dialysis. © 2007 Thomson-Wadsworth
Advantages of PD
Most people on PD do not have to limit potassium in their
diet. Many need to add high-potassium foods to keep blood levels
from getting too low; a typical intake is 3 to 4 g/day.
Avoidance of large fluctuations in blood chemistry, longer
residual renal function, and the ability of the patient to achieve a
more normal lifestyle.
Patients choosing PD have more liberal fluid, sodium, and
potassium allowances because the therapy is continuous and more
of these products are removed. The loss of sodium can be as
much as 6 g/day; thus these patients may need higher sodium
intakes as shown in Table 3.

Disadvantages of PD
Risk of infection e.g. peritonitis
Weight gain (absorb 600-800 Kcalories from glucose dialysate
Protein loss

Dietary management in HD and CAPD
Proteins
HD: 1-1.2 g/kg IBW 70% HBV CAPD: 1.2-1.54 g/kg IBW
Energy
HD: 30-35 Kcal/kg IBW CAPD: 25-35 Kcal/kg IBW
Sodium
Restrict to control thirst and hypertension
HD: 2-3 g/day PD: 2-4 g/day

..dietary management in HD and CAPD
Fluid
HD: Restrict to prevent edema and hypertension 500-700 ml plus daily urine
output
PD-in CAPD ≥ 2000 ML, monitor weight and blood pressure, restrict if oliguric.
Potassium
HD: 2-3 g/day CAPD: 3-4 g/day
Phosphorus
HD: 1-1.2 g/day CAPD: 1.5-2 g/day
NB: Dialysis cannot substitute for healthy normally functioning kidney
therefore patients should observe dietary restrictions.
Table 3: Nutrient requirements for adults
with renal disease based on type of
therapy
Source: Mahan LK and Escott-Stump S.

Krause’s Food & Nutrition therapy,
International Edition. Saunders, an imprint
of Elsevier Inc. I1830 Wesdine Industrial
Drive. St. Louis, Missouri 6314. pp. 933
6. Nephrolithiasis (kidney stones)
Pathophyology
Kidney stone formation is a complex process that consists of
saturation, supersaturation; nucleation; crystal growth or
aggregation; crystal retention; and stone formation in the presence
of promoters, inhibitors, and complexors in urine.
Calcium stones are the most common: calcium oxalate (60%),
calcium oxalate and calcium phosphate (10%), calcium phosphate
(l0%), and uric acid (5% to 10%), struvite (5% to 10%), and
cystine (1%).
Low urine volume is the single most important risk factor for
urolithiasis.
Calcium stones
a) Hyperoxaluria: It is caused by over production of oxalic acid (>40 mg of
oxalate in urine/day) , a rare inherited disorder-Calcium oxalate stones.
Treatment
Decreased dietary oxalate, rhubarb, spinach, strawberry, chocolate, wheat bran,
nuts, tea
Calcium intake 800-1200 to bind oxalate
Increase fluid intake as a low urine volume is the the most common
abnormality noted on metabolic evaluation of stone formers,
NB: Changes in urinary oxalate excretion exerts more influence on the formation
of calcium stones than changes in urinary calcium.

…calcium stones
b) Hypercalciuria is defined as a mean value of calcium in
excess of 300 mg (7.5 mmol)/day in men or 250 mg (6.25
mmol)/day in women, or 4 mg (0.1 mmol)/kg/day for either in
random urine collections of out patients on unrestricted diets.
Thirty to 40% of patients with calcium stones are hypercalciuric.
Results from increased calcium absorption from GIT/impaired renal
calcium absorption /excessive resorption of calcium from bone due to
primary hyperthyroidism (treated with surgery).
Low protein diet increases as high calcium excretion. Increase fluid
intake. Mild salt restrictiom to 4-5 g/day.
…calcium stones
c) Hyperuricosuria is the formation of calcium oxalate rather than
uric acid stones.
 Uric acid encourages formation of calcium oxalate stones by binding

calcium oxalate inhibitors.
Dietary animal protein for excretion of uric acid and calcium and
decreased urinary citrate excretion.

Case studies and Practicals
Renal diets: Controlled protein, potassium and sodium diet

Next lecture
Cancer

Lecture 7 Renal Diseases

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Lecture 7 Renal Diseases

Uploaded by

Copyright:

Available Formats

FOND 332: Advanced Medical Nutrition Therapy

Lecture 7: Renal Diseases

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Functions of each part of a nephron

2. Tubules: The tubules reabsorb majority of the components of

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Decreased blood volume causes cells of the glomerulus (the juxtaglomerular

Renin acts on angiotensinogen in the plasma to form angiotensin I, which is

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

 Other causes include:

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Figure 3: Consequence of Protein Loss

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

 manage the symptoms associated with the syndrome (edema,

decrease the risk of progression to renal failure, and

 maintain nutritional stores

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Sodium should be restricted due to edema and Na retention. Early

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Salt 80-100 mmol

Protein is restricted in uremic patients

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Occurs due to repeated episodes of acute phase leading to loss of

 It is characterized by increased loss of protein, accumulation of urea

Dietary management is as for acute glomerulonephritis

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Sudden reduction in GFR and urine output

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Rehydration in dehydration (IV fluids)

Blood transfusion to restore blood volume

Dialysis (renal replacement therapy) for restoring fluid and

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Glucose and essential amino acids decrease catabolism more than

When oral intake is permitted a high energy intake 35-50 kcal; is

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

Potassium requirements depend on serum levels and whether the

NB: Monitor weight, electrolytes and fluid balance.

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY

1 Kidney damage with normal or ≥90

4 Severely decreased GFR 15-29

5 Kidney failure <15 (undergoing dialysis)

DR. M. CHESEREK, DEPARTMENT OF HUMAN NUTRITION, EGERTON UNIVERSITY