THE NURSING CARE AND

MANAGEMENT OF A CLIENT WITH END

STAGE RENAL FAILURE 2DEGREE TO
IGA NEPHROPATHY

PREPARED BY:
NURUL AIN BINTI ISMAIL
850704 14 6536 001
SEMESTER 3 SEPTEMBER 2014
CP 14 RENAL NURSING

INTRODUCTION
What happen in kidney failure?
Maybe acute or chronic. In both there is enough loss of nephron function to upset the
normal steady state of the bodys internal environment. Waste products of protein
metabolism accumulate.
This is termed azotemia, indicating retention of nitrogenous products( azote=nitrogen).
Azotemia is a major component of the uremic syndrome.
What is urea?
Urea is the waste product of protein metabolism and the most abundant organic waste .
Most urea is produced during the breakdown of amino acids. Its normal value in the
blood is 15- 40 mg/dL.
What is creatinine
Creatinine is a protein produced by muscle and released into the blood. The creatinine
level in the blood is determined by the rate it is being removed in the urine.
What is uremia?
Uremia, or uremic syndrome, encompasses a complex of symptoms and findings
resulting from disordered biochemical processes when kidney function fails.
Is retention of urea the cause of uremia?
Severity of the uremic symptoms roughly parallels the rise in blood urea. Urea clearly
contributes to some of the symptoms malaise, lethargy, anorexia, insomnia- but it is

not the primary toxin of uremia. Numerous other substances are retained in the body
when kidney function fails.More than 200 potential uremic toxins have been identified.
What is Chronic Kidney Disease?
The National Kidney Foundation (NKF) defines chronic kidney disease (CKD) as either
damage to the kidney or a GFR of less than 60ml/min/1.73m 2 for more than 3 months.
Kidney damage if further defined as pathologic irregularities or markers of damage such
as abnormalities in the blood, urine test or imaging studies.CKD defined according to
the presence or absence of kidney damage and level of kidney function- regardless of
type of kidney disease(diagnosis).Among individuals with CKD, the stages are defined
based on the level of kidney function. Identifying the presence and stage of CKD in an
individual is not a substitute for accurate assessment of the cause of kidney disease,
extent of kidney damage, level of kidney function, comorbid conditions, complications
of decreased kidney function, or risk foe loss of kidney function or cardiovascular
disease in that patient. Defining stages of CKD requires categorization of continuous
measure of kidney function, and the cut-off level between stages are inherently
arbitrary.
Cause of chronic kidney disease
Progressive and irreversible loss of function occurs over many months or years. As the
number of functioning nephrons decreases, each remaining unit must clear an
increasing solute load. Eventually the limit to the amount of solute that can be cleared is
reached, and the concentration in body fluids must rise. Azotemia and clinical uremia
result.

Stages Of Kidney Disease

Stages of Chronic Kidney Disease

These guidelines are adapted from the National Kidney Foundation's
Kidney Disease Outcomes Quality Initiative (KDOQI)

Stage

Description

GFR*

Signs of mild kidney disease but with normal or better

GFR

greater than 90%

Mild kidney disease with reduced GFR

60-89%

Moderate chronic renal insufficiency

30-59%

Severe chronic renal insufficiency

15-29%

End-stage renal failure

less than 15%

*GFR is given in ml/min/1.73 m2

Early chronic renal insufficiency (Stages 1 to 2)

Physical symptoms. Usually few or no physical symptoms that you can feel
(other than those you may experience if you have heavy proteinuria).

Blood work. Blood work results will show abnormalities - mainly a slightly
elevated serum creatinine. Note that there is often a time lag between
elevations of serum creatinine, and some progression of the IgAN. By the time
serum creatinine is elevated, the person may already have lost 50% of kidney
function.

Urinalysis. Urine will show abnormalities. Urine can be checked by dipstick in

the doctor's office (as an initial check), and followed up with a more complete
urinalysis. The main urine abnormality that will suggest a kidney disease is the
presence of protein and/or blood. Either will usually trigger further investigation.
However, blood and/or protein in the urine doesn't say anything about actual
kidney function.

Treatment. Treatment may involve some mild dietary changes (a lower protein
diet may in some cases be recommended), and a blood pressure medication
may be prescribed (usually of the ACE inhibitor class, the angiotensin II
receptor class, or both, even if blood pressure is not really elevated much).

Blood pressure. Some people start having high blood pressure even in early
chronic renal failure. IgAN is one kidney disease that can do this.

Anemia. Anemia may rarely occur at this stage. In this case, it is most often
caused by having heavy proteinuria rather than actual chronic renal
insufficiency.

Advanced chronic renal insufficiency (Stages 3 to 4)

Physical symptoms

You may still feel completely normal at this stage, or you may begin to experience one or
more of the following symptoms:

Serum creatinine. Serum creatinine will be higher (indicating less than

30% kidney function)

Tiredness or fatigue

Puffiness or swelling (obvious in the hands or feet and ankles, but the
puffiness will often first be seen around the eyes).

Back pain. Usually felt as a dull ache anywhere in the mid-to-lower

portion of the back, on one side or the other - this is sometimes referred
to as flank pain, or loin pain)

Appetite. Changes in appetite or eating pattern. Foods may start tasting

"funny".

Urine. Changes in urination (amount, colour, frequency). Urine may in

fact look exceptionally clear at this point, rather than abnormal. This is
because little is actually being filtered into it by your kidneys. Previously
high proteinuria and/or hematuria may actually improve.

Blood pressure. High blood pressure (also referred to as hypertension)

Digestion. Poor digestion (varying degrees of gastroparesis, which

means that digestion is slowed).

Medication

High blood pressure medications. It's common to need more than one at this stage,
and often 3 or more.

Other drugs/supplements. May be prescribed if needed, such as vitamin D analog

(calcitriol is a common one), renal vitamins (not a regular multi-vitamin, as these contain
too much vitamin A for the typical advanced renal insufficiency patient). Drugs for
controlling heavy proteinuria if necessary (note that heavier proteinuria does not
automatically follow with more advanced chronic renal insufficiency).

Phosphorus binder. You may be asked to begin taking a calcium supplement with
meals as a phosphorus binder (or a medication may be prescribed instead of or in
addition to calcium).

End-stage renal failure (or late chronic renal insufficiency)

The terms end-stage renal failure and end-stage renal disease are used
interchangeably, and the abbreviation ESRD is commonly used. Typically, patients will
have kidney function in the area of 10-15% or so. These are the common symptoms you
may experience at this stage (and some people may start experiencing some of these
earlier):

Symptoms

anemia (may begin earlier than this)

easy bleeding and bruising

headache

fatigue and drowsy feeling (more than normal or usual for you)

weakness

mental symptoms such as lowered mental alertness, trouble concentrating,

confusion, seizures

nausea, vomiting, and generally less desire to eat

thirst

muscle cramps, muscle twitching

nocturia (night-time urination)

numb sensation in the extremities

diarrhea

itchy skin, itchy eyes

skin colour changes (grayish complexion, sometimes yellowish-brownish

tone)

swelling and puffiness (more than you had while in advanced renal failure,
and most likely in the feet and/or ankles)

difficulty breathing (due to fluid in the lungs, anemia)

high blood pressure (with IgAN, you may already have had this since the
early stages)

decreased sexual interest

changes in menstrual cycle (and difficulty getting pregnant)

decreased urine output (however, you should be aware that some people
with ESRD will continue to get rid of water as urine, but not wastes therefore, the urine may be very clear and normal-looking, and some may
have increased urine output rather than decreased).

poor digestion (varying degrees of gastroparesis).

Treatment
The exact time that dialysis starts will vary slightly depending on various factor.
Any form of treatment that replaces the functions of the kidneys
The current available forms of RRT are:
a) Hemodialysis
b) Hemofilteration/Hemodiafiltertion
c) Peritoneal dialysis
d) Kidney transplantation
Only kidney transplantation can replace all of the functions of the kidney.

ANATOMY AND PHYSIOLOGY

The kidneys are in charge of maintaining the balance of water, salts, acids and bases,
for our whole entire body. The kidneys do that by monitoring and maintaining the chemical make-up of the blood. Kidneys are also going to regulate the volume

of blood.Another huge function is to get rid of toxin, normal metabolic wastes, excess
water and ions from the body. Our main waste products (nitrogenous, contains nitrogen) are Urea (from the normal breakdown of amino acids, Uric acid (from the normal
break down of nucleic acids aka dna), and Creatinine (from the normal breakdown of a
muscle molecule that helps manufacture ATP).

Above: The kidneys are sitting in the abdominal cavity. They are actually outside the abdominal cavity.
The peritoneum is the lining of the abdominal cavity (the white line) and the kidneys actually lie behind
that line, not inside it. Since they are behind the peritoneum and resting against the muscles of our back,
the position of the kidney is retroperitoneal.

Above:Slice of kidney and take off the front part. The outer layer is called the renal cortex. The inner layer that includes the triangle shapes (renal pyramids) is the
medulla.The triangle shapes are actually called renal pyramids. These pyramids look
like they are draining all together into the calices (major calyx). These drain into this
funnel called the renal pelvis which then drains into the ureter. Supply of blood coming
in at red vessel and blood coming out of the blue one.

Above: This structure is called the nephron. This is the structural and functional unit of
the kidney. An arteriole coming in (a very small vessel before a capillary) that is going
to branch into a capillary bed. This particular capillary bed is going to take on a special
shape that looks like a tangled up ball shape called the glomerulus. These are made
up of fenestrated capillaries. The afferent arteriole means it brings blood into the
glomerulus made up of fenestrated capillaries made of holes. Normally in a capillary
bed we have a venule but in this case, functionally we arent dealing with the exchange
of oxygen and carbon dioxide, this nephron is built specifically for filtration of our blood
to remove the nitrogenous waste and balance out the salt and what not. So, exiting this
glomerulus is not a venule but another arteriole. Because its leaving this is called an
efferent arteriole.

Above: We see they are tucked up just inside the last two ribs, so they get some protection from the last
two ribs which isnt a great deal of protection but that is why there is a lining of fat, even if someone is a
very skinny person, all around the kidney.

The cup shaped thing that surrounds the glomerulus is called the glomerular capsule
(bowmans capsule). This glomerular capsule is going to drain into the renal tubule.

Above: An extreme close up of the renal corpuscle which is just the glomerulus and
glomerular capsule. On the left we see our glomerulus with our arterioles. The one on
the right is a very detailed look at the fenestrated glomerular capillaries with the
holes. On any capillary theres a basement membrane on the outside. In the kidneys,
this basement membrane takes on a very specific structure. It looks like things are
sticking out into other things that are sticking out rather than a flat membrane. These
things sticking out are called podocytes and then we have foot processes sticking out
of these podocytes. Thats a lot of effort and complicated because the kidneys are the
most complicated stuff in physiology. The capsule is made up of simple squamous
epithelial cells and theres space in between the capillary with its specialized basement

membrane and this capsule drains away into a proximal convoluted tubule where the
cells become cuboidal.

This is a similar idea where two surfaces come together and create a specialized membrane where gases are exchanged. In this structure an incredible amount of volume to
pass through this membrane very quickly. The fluid in the blood called the plasma and
the holes in this picture are the pores of the fenestrated capillary. Theres a little strip of
basement membrane and the yellow things sticking out are the podocytes that are cut
into a cross section.
Because of these podocytes, more spaces for things to pass through. Its a series of
spaces for letting plasma pass through. The stuff that will be able to fit through the
holes are water, ions, glucose, amino acids and urea. The things that are going to be

too big to pass through are mostly proteins (things in the blood like albumin, globulins,
etc). The renal tubule (the collection tube from the globular capsule) is going to accept
all the fluid from that membrane and once it goes in the tubule its called filtrate. Then
were going to have a bunch of different sections to this tubule.

Above: We take a slice of a kidney and blow it up to this level. We go in to the globerulus collecting the filtrate and direct it into the tubule. As you could see in this picture the
tubule is very, very long. Theres different sections to it that take on different arrangements or shapes to it. Proximal to the whole (proximal meaning close) section is very
curvy, so its called the proximal convoluted tubule.Medulla (meaning deep) and this

forms a loop. This loop is conveniently called the nephron loop thats made up of the
descending limb and ascending limb. Up to the cortex and more convoluted stuff its
called the distal convoluted tubule. Then this distal convoluted tubule is going to
dump into the collecting duct which will eventually drain into the calices and into the
ureters.
Above (right side): On the right a bunch of cells that show what each section is made up
of. The proximal convoluted tubule cells contain microvilli that increase surface area.
The nephron loop contains microvilli but are more squashed than the convoluted cells.
The distal convoluted tubule cells are similar to the proximal in their cuboidal shape
except there are far less microvilli.
These difference in cell types are a representation of their function. When blood enters
into this glomerulus which is a capillary bed, its entering it at a very high pressure and
because of the shape of this specialized ball-shaped capillary bed, it has that end that
juts out so when the blood needs to turn the corner, it forces the fluid out. Conveniently
we have the fenestrations so the pressure can quickly press the fluid out so you end up
capturing a ton of fluid in that capsule. As that plasma has a bunch of stuff in it, it has to
make its way through the tubule and the kidney needs to figure out what to keep and let
go. In the proximal portion especially, because of all the microvilli, those cells can reabsorb a lot of water. So when a person is very dehydrated: As the kidney is taking in
blood, it tries to conserve the water and this proximal convoluted tubule takes back a lot
of water. Thats what happens in these tubules: They keep, take back, return whatever
the body needs. If the situation was the other way around, such as if we were bloated

or over-hydrated and you wanted to get rid of water, we dont have to absorb that water.
The kidney monitors the water and salt balance and just lets the water to keep going
and that water will work its way down eventually into the urinary bladder.

Above: The loop is pretty short in the cortical nephrons. The juxtamedullary tubules
have super long loops that go deep down into the medulla. A very large collecting duct
(white) accepting fluid from the different nephrons (all the cut off branches are getting fluid).
Blood vessels associated with nephrons: We have not covered peritubular capillaries
and the vasa recta, yet. The purple thing is sort of like another set of capillaries. We

have our afferent arteriole leading into the glomerulus and our efferent arteriole exiting
the capsule so now we are free of the capsule but if we follow this efferent arteriole, this
efferent arteriole is leading yet into another capillary bed. This one on the left is sort of
tangling itself in and among the convoluted tubules. We cant follow it perfectly but
eventually that capillary bed is going to exit and dump into. a vein!
So, isnt it interesting that we have a capillary bed wrapping around those tubules?
What were the tubules doing? They could take back some filtrate (meaning absorb
back into the body) and those cells that have the microvilli made up of the tubules. If
we have capillaries against those tubules, we can let things go outside the tubules for
the capillaries to pick them up which then lead to the veins. So the peritbular capillaries keep the stuff that were absorbed by the tubules. The vasa recta (vasa=vessel,
recta=straight) are the purple capillaries that happen to surround the very long loop in
the juxtamedullary nephron. They are both low-pressure capillaries while the glomeruli
deal with high pressure.
Fun fact: The filtrate that is produced by the glomeruli that isnt kept becomes urine. We
produce a liter of this fluid every 8 minutes. 99% of the filtrate ends up getting reabsorbed by the tubules.

IgA Nephropathy (Berger's Disease)

Introduction
This is a form of glomerulonephritis that was first described by Berger and Hinglais in
1968
Berger's disease is often the name attached to the mildest form of this IgA nephropathy.
It is caused by immune complexes of IgA that become lodged in the glomeruli followed
by complement fixation. This is unusual because IgA tends to be associated with
immunity on mucosal surfaces and normally IgA is unable to activate complement. The
alternative complement fixation pathway is apparently used. Pathology shows a
spectrum of glomerular lesions but mesangial proliferation with prominent IgA deposition
is present in most biopsies. Galactose deficiency of IgA molecules has been identified
as being the most likely pathological mechanism

Classificationsi
1. Acute IgAN. often a child, teenager or young adult, first presents with an
acuteglomerulonephritis or nephritic syndrome, which eventually turns out to be
IgAN
2. Chronic IgAN
typical, slowly-progressive type of IgAN that may be relatively stable for years
(basically the common IgAN that adults usually have). Approximately 30 percent of
these patients will progress to end-stage renal failure in 10 to 25 years.
3. Rapidly-progressive IgAN.

Sometimes referred to as crescenticIgAN. This pattern is a more aggressive form

which progresses to end-stage renal failure within months or more commonly, a
few years (5 years or less).

Oxford classification system

A new classification system has been developed by an international consensus working
group, based on specific pathological features. Four variables detected on renal biopsy
have been found to be independent prognostic factors for progression to renal disease.
These are:

The mesangialhypercellularity score (an estimate of the density of the mesangial

cells around renal blood vessels)

Segmental glomerulosclerosis (a reflection of scar tissue developing in glomeruli)

Endocapillaryhypercellularity (an increase in the number of cells within the

glomerular capillary lumina)

Tubular atrophy/interstitial fibrosis (interstitial fibrosis reflects and increase in

supporting connective tissue in the renal parenchyma; tubular atrophy implies the
presence of tubules with thick redundant basement membranes or a reduction in
tubular diameter)

Epidemiology
Although not described until 1968, this is the most common form of acute
glomerulonephritis. As it represents a spectrum of severity it is possible that the mildest
cases are not diagnosed. It is more common in people of European or Asian ancestry
than those of African descent. It is about twice as common in males as in females. Of
biopsies performed for glomerular disease, IgA nephropathy is found in about 40% in
Asia, 20% in Europe and 10% in North America. Prevalence is high in Singapore,
Japan, Australia, Hong Kong, Finland and southern Europe but low in the United
Kingdom, Canada and the United States.

It is uncommon below the age of 10 and 80% of cases are diagnosed between the ages
of 16 and 35.

Causes:
1.
2.
3.
4.
5.

Idiopathics
Antigen exposures: virus, bacteria, toxin, allergen
Genes : family, ethnic groups
Cirrhosis or liver diseases
Celiac disease (Gluten enteropathy)

Associated diseases
It is associated with a number of other diseases including Henoch-Schnleinpurpura.
IgA deposits are also found in systemic lupus erythematosis (SLE), hepatitis, dermatitis
herpetiformis and ankylosing spondylitis. It may also be associated with cirrhosis and
coeliac disease and it has occasionally been linked to HIV infection. A familial form of
IgA nephropathy, inherited as an autosomal dominant condition, has also been
described.

One study reported IgA nephropathy in three elderly patients with renal cell carcinoma.

Presentation
The disease can be highly variable, ranging from microscopic haematuria to rapidly
progressive glomerulonephritis. The majority of cases run a benign course.

Symptoms and findings

In 40 to 50% of patients there is gross haematuria, usually with an upper respiratory
tract infection or, less often, gastroenteritis.

In 30 to 40% of patients there are no symptoms but urine shows erythrocytes,

casts and proteinuria.

Much less often the presentation may be in acute renal failure that usually
reverses spontaneously or chronic renal failure.

In around 80% of patients there is an upper respiratory tract infection and, either
at the onset or within the first 24 to 48 hours, there is gross haematuria that lasts
for less than 3 days. The urine is red or brown and in a third of patients there is
loin pain, presumably due to swelling of the renal capsule.

Gross haematuria is not usually accompanied by clots. It tends to occur in the

younger patients whilst microscopic haematuria tends to occur with the older age
range.

Illnesses that can precipitate haematuria include urinary tract infection,

pneumonia, staphylococcal infection, acute gastroenteritis, influenza and
glandular fever.

Between episodes of macroscopic haematuria there may be persistent

microscopic haematuria. The National Institute for Health and Clinical Excellence
(NICE) has found that IgA nephropathy is the most common cause of isolated
persistent microscopic haematuria.

Of those that do not remit, there is a slow progression to end-stage renal failure
(ESRF) in 1 to 2% per year.

Signs
Usually there is no abnormality to find although occasionally there may be hypertension.
This is uncommon at presentation but may occur if renal function fails. If
glomerulonephritis leads to nephrotic syndrome there will be oedema.

Other finding
Microscopic haematuria is usually accompanied by a light albuminuria. Heavy
proteinuria to cause hypoalbuminaemia and oedema is an uncommon presentation that
occurs in about 5%. It may remit or persist.

Investigations

Urine testing by dipstick will probably show light to moderate albumin and blood.

Urine microscopy is required for red blood cells, leukocytes and casts.

Measurement of 24 hours' protein excretion should be undertaken. A semiquantitative estimate from a spot urine and extrapolation based on creatinine
content is less satisfactory. If the patient is over 50, protein electrophoresis
should be undertaken to exclude myeloma.

Assess renal function with urea and electrolytes, creatinine and a 24 hours'
creatinine clearance testing.

Plasma levels of IgA are raised in about half of cases but it also occurs in other
conditions and the predictive value of this test is poor.

Serum undergalactosylated IgA is being investigated as a diagnostic test and

may lead to further elucidation of the pathogenesis of the condition.

The current gold-standard diagnostic test of IgA nephropathy is by renal biopsy.

Light microscopy, electron microscopy and immunofluoresence are required.

Light microscopy of a glomerulus from a patient with immunoglobulinnephropathy showing

increased mesangial matrix and cellularity.

Management

In the majority this is a benign disease but chronic renal failure (CRF) and endstage renal failure (ESRF) may eventually appear in 20 to 40% of patients. This
is a significant number with a serious adverse outcome and a benign course is
usually a retrospective diagnosis. There is no cure but treatment can delay the
need for dialysis or transplantation.

Patients with haematuria but no albuminuria need monitoring by urinalysis, renal

function and checking blood pressure.

Hypertension needs early and aggressive treatment. Angiotensin-converting

enzyme (ACE) inhibitors are the drugs of choice with angiotensin receptor
blockers (ARBs) in reserve. They protect renal function and may even be
beneficial with normal blood pressure.

A combination of an ACE inhibitor and the ARB losartan may lower urinary
protein excretion compared with higher doses of ACE inhibitor monotherapy but
patients need to be closely monitored for hyperkalaemia. Such a combination
should be avoided in patients with advanced renal failure.

Corticosteroids should be given for 6 months to patients with preserved renal

function, nephrotic syndrome and few histological changes on light microscopy. A
typical regime is 1 g of intravenous methylprednisolone for three consecutive
days at the beginning of months 1, 3 and 5, with low-dose oral steroids every
other day for 6 months. There may be benefit in extending beyond the 6-month
period.

Introduction of corticosteroids at an early stage in patients with proliferative IgA

nephropathy slows the development of pathological histological changes and
reduces proteinuria. In patients with modest proteinuria (1.5-3.5 g/day)
corticosteroids slows deterioration of renal function.

One study found that a combination of steroids with an ACE inhibitor was better
than an ACE inhibitor alone in reducing the progression of renal disease.

A combination of methylprednisolone and cyclophosphamide has been found to

improve renal function and reduce haematuria and proteinuria in children with IgA
nephropathy.

One study has reported benefits with lisinopril in children with mild IgA
nephropathy.

The value of fish oil (omega-3 fatty acids) at a dose of 12 g a day is controversial
with conflicting results but is frequently used in patients with declining renal
function.

Dietary restriction of gluten, meat and dairy produce has been suggestive but its
value is unproven. If gluten sensitivity is demonstrated it must be excluded.

Protein restriction is of value in advanced renal impairment.

Amongst other evidence-based interventions, it is suggested that if recurrent

tonsillitis causes recurrent disease there is benefit from tonsillectomy.

End-stage renal failure requires dialysis or transplantation. IgA complexes may

form again in the transplanted kidney and this occurs with variation from 20 to
60%. The rate is higher in transplants from live related donors, suggesting a
possible genetic vulnerability. However, the disease continues to progress slowly
with loss of graft function in only 10%.

Prognosis

In the majority, the disease is benign but end- stage renal failure (ESRF) occurs by 10
years in 15 to 20% and by 20 years in around 30%.These figures are based on those
who have had renal biopsies and so those with milder disease presumably do better
than this. Those with microscopic haematuria seem to fare worse than those with
macroscopic disease. This could be because they present later.

Other features of poor prognosis are sustained hypertension, impaired renal function,
persistent haematuria and proteinuria in excess of 1 g a day. Histological findings of
interstitial fibrosis, tubular atrophy and glomerular scarring give a worse outcome. As
with other glomerular diseases, the risk of progression is more closely correlated with
tubulointerstitial pathology than with glomerular disease.
Pregnancy is usually uneventful unless there is poorly controlled blood pressure, a bad
histological picture or poor renal function with a creatinine clearance of less than 70 ml
a minute. ACE inhibitors and angiotensin-II receptor antagonists must be stopped
before trying to conceive as they are markedly teratogenic.

Prevention
The value of a screening programme to detect microscopic haematuria in school
children in Korea has been demonstrated but its benefits in the UK with a much lower
prevalence may be doubted.Although not described until 1968, this is the most common
form of acute glomerulonephritis. As it represents a spectrum of severity it is possible
that the mildest cases are not diagnosed. It is more common in people of European or
Asian ancestry than those of African descent. It is about twice as common in males as

in females. Of biopsies performed for glomerular disease, IgA nephropathy is found in

about 40% in Asia, 20% in Europe and 10% in North America. Prevalence is high in
Singapore, Japan, Australia, Hong Kong, Finland and southern Europe but low in the
United Kingdom, Canada and the United States.It is uncommon below the age of 10
and 80% of cases are diagnosed between the ages of 16 and 35.

Associated diseases
It is associated with a number of other diseases including Henoch-Schnleinpurpura.
IgA deposits are also found in systemic lupus erythematosis (SLE), hepatitis, dermatitis
herpetiformis and ankylosing spondylitis. It may also be associated with cirrhosis and
coeliac disease and it has occasionally been linked to HIV infection. A familial form of
IgA nephropathy, inherited as an autosomal dominant condition, has also been
described.

PRESENTATION OF THE CASE

PATIENTS BIODATA
Name

: Madam Norul Hasnah Husin

Age

: 36 years old

Gender

: Female

Race

: Malay

Religion

: Muslim

Marital status

: Married, no children, stays with husband

Occupation

: Secretaries

Address

: No xx, TamanPanchor Jaya, Seremban Negeri Sembilan

Register Number

: 678910

Consultant

: Dr M

HISTORY
Presented to emergency department of Hospital Tunku Jaafar, Seremban on 5/3/2012
with complaint of shortness of breath on and off for 5 days and bilateral lower limbs
pitting oedema..
Seen by Dr M (nephrologist), direct admit to ward a for stat haemodialysis. Patient is
diagnosed for Chronic Renal Disease- End stage renal failure secondary to IgA
nephropathy.
Underwent renal biopsy done on 11/10/2010 with finding as Focal Proliferative IGA
Nephropathy With Acute Tubular Necrosis changes.She is under regular follow up with
Dr M and were treated for hypertension and hyperlipidemia. Her progress is monitored
until she is diagnosed for Advanced Chronic Renal Failurein December 2011. On left
radiocephalic fistula (Left AVF) which was created on 28/1/2012 by Dr N (Vascular
Surgeon).Her first dialysis is commenced on 5/3/2011 via right Intrajugular catheter
(IJC) which inserted on same day of admission with complication of blood clots. Trial of
fistula was done on 10/3/12 but failed with result of haematoma and ordered by Dr N to
rest for 2 weeks.Patient is discharged on 13/3/2012 after 9 days admitted with IJC

intact, medications and follow up at nephrology clinic and commenced for regular
dialysis 3 x/week at Unit Dialisis, Hospital Tunku Jaafar, Seremban.

Copy from dietician referral form;

ESRD on dialysis, ESRD 2o to IgA Nephropathy.
Low salt, low K+, low PO4, other fluid
restriction.
Date / time
5/3/12
Respond date
6/3/12
Date seen
6/3/12
Seen
Dietician G
by
Biochemical Data (3/3/12)
Urea
26.1 ()
Na
138()
K
6.2 ()
Creat
830()
Uric
675()
acid
HB
8.9()
Antropometry Data
Weigt
71.2
Heigh
1.56
BMI
29.2 kg/ m2
Recommended weight
45- 61 kg
Clinical Assessment - No obvious abnormality
Physical assessment - No obvious abnormality
Dietary assessment
Current mode oral
Therapeutic - Low salt diet
Other relevant information - patients is doing dialysis, cant get diet history
Nutritional Assessment

Patient36 years old, female, admitted for ESRD 2o to IgA Nephropathy, started HD,
BMI 29.2 kg/m2 (pre obese)
Nutritional Diagnosis
Excessive Na, Po4, K intake related to ESRD as evidence by blood test result
Nutritional intervention
1)Advised patient and husband about high protein diet(1.2 gm/kg),low Na, K and Po4
diet
2) Emphasied on diet modification and explained about fluid restriction.
3) Give guidelines for high protein, low salt, low K,low PO4 diet.
Monitor and evaluation
Follow up counselling after dialysis

ASSESSMENT
Patients Assessment On 14/3/12

Ward : Haemodialysis Unit

Date

: 14 March 2012

Time of Admission

: 1200 hours

Reason for Admission

: Regular Dialysis 3 times /week

Mode of arrival

: Walking

Consultant : Dr. M

Vital Sign : Normal Range

Temperature
Pulse
Respiration
Blood Pressure

: 36.5 C

36.5 37.3 C

: 99bpm60 80 beats / minutes

: 20bpm16 20 breath / minutes
: 172/99mmHg

Diastolic : 60 90 mmHg
Systolic : 90 130 mmHg

Oxygen saturation rate : 100% (room air)

Weight

: 70.8 kg

Height

: 156 cm

Medical History

: - Hypertension>4years(2008)
-Hyperlipidemia

Surgical History

: Apendicectomy (14/2/ 2011)

Left Radiocephalic Fistula (28/1/12)

Family Medical History

: Mother hypertension on medications

CurrentMedication

: - Tablet IberetFolic 1 tabletdaily

-Tablet calcium carbonate 1 tablet/ twice daily
-Tablet lasix 80 mg on morning
- Tablet Rocaltriol 1 tablet every alternate day ( post dialysis)
- Tablet Norvasc 5 mg daily

Allergies

: NIL

Skin condition

: Clean.

Slightly bilateral lower limb pitting oedema

Mobility

: Ambulate

Personal Hygiene

: Independent

Hobbies

: Watching TV program, listening radio

Level of Conscious

: Conscious

Emotional Status

: Anxious

Communication:
Speech

: Malay, English

Vision

: On eye aids ( spectacles)

Hearing

: Normal

Laboratory results as out patient

TEST

DATE
29/4/10

Haematology
HB
Red cell
Haematocrit / PCV
MCV
MCH
RDW
Platelet
ESR
WBC
Glucose
Renal Function Test
Uric acid
Creatinine
Urea
Sodium
Potassium
Chloride
Calcium
Phosphate
Lipid Profile
Total Cholesterol
Triglyceride
HDL
LDL

8/10/10

15/10/10

3/11/10

12.3
4.1
36
88
31
10.9
384
40
9.6
5.6
548
193
10.7
139
4.1
102
2.26
1.45
7.3
2.63
1.12
5.0

REFERRENCE
RANGE
11.5-16 g/dL
4.0- 5.2 1012 /L
36-46 %
76- 103/L
26- 36 pg
8.0 -14.6 %
150- 500( 103/ul)
0.25mml/Hr
4.3- 10.5 (103 /uL)
3.9-6.1 mmol/L

462
173
9.4
138
4.0
102

467
186
8.6
139
4.2
105

455
172
8.7
139
4.4
103

143-405 umol/L
43- 115 umol/L
2.0-6.0 mmol/l
135- 155 mmol/L
3.5- 5.5 mmol/L
95- 111 mmol/L
2.09- 2.55 mmol/L
0.78- 1.5 mmol/L

5.0
2.47
1.26
3.6

<5.2
<1.71
>1.68
<2.6

% HDL
Liver Function Test
Protein
Albumin
Globulin
A/G Ratio
Total Bilirubin
Direct Bilirubin
Indirect Bilirubin
SGOT/AST

15

25

>25%

73
40
33
1.2
4.5
1.5
3.0
11

70
41
29
1.4
7.6
2.2
5.3
12

63- 83 g/l
35- 50 gm/l
25-40 g/l
1.0-2.0
2.0- 28.0 umol/l
< 6.8 umol/l
<20.5 umol/l
7-44 u/l

Renal biopsy result (done on 11/10/10)

Specimen
Renal tru cut biopsy cores.
Gross
Specimen of renal trucut biopsy tissue received in two pieces and submitted entirely in a
single block
Histology
3 strips of renal corticol tissue containing 23 glomeruli out of which 4 are globally
sclerosed.3 fibrocellular crescents seen. Several glomeruli show segmental lesion with
proliferation and sclerosis with capsular adhesion. The rest of other glomeruli show mild
mesangial widening due to increase in matrix and mesangial cell proliferation. No
endocapillary proliferation, hyalinosis or thickening of the glomerular basement
membrane seen. The tubules show ATN changes with dilatation and sloughing. Very
mild interstitial fibrosis and tubular atrophy noted. No interstitial inflammatory infiltration
present. Arteries and arterioles show mild to moderate hypertensive changes.

IMMUNOFLOURESCENCE STUDIES
C3 1 + Segmental within mesangium
C4 Negative
IgG negative
IgA 2+ diffuse within mesangium
IgM- negative
Fibrin- 1+ at mesangium and around capillary loops

INTERPRETATION
FOCAL PROLIFERATIVE IGA NEPHROPATHY WITH ATN CHANGES.
17% GLOBAL SCLEROSIS + 13% CRESCENT

MANAGEMENT FOR ESRD

1. MEDICATIONS
2. RENAL REPLACEMENT THERAPY
3. RENAL TRANSPLANT

Drug Prescriptions and RRT

In critical care medicine, drug prescription can be challenging because many of the
drugs are critical to patient survival and many have narrow therapeutic windows. Both
underdosage and overdosage are serious problems for critically ill patients. RRT
contributes to the elimination of many drugs, including the active ones, with a possibility
of increasing the removal of some drugs, thereby leading to underdosages. Conversely,
RRT is usually much less efficient in drug clearance than the native kidney (which may
also metabolize certain drugs), and thus drug overdosage is equally of concern.
Therefore, altered pharmacokinetics of many drugs must be taken into account by the

physician when prescribing drugs, and a modification of these prescriptions is usually

necessary.
In a critically ill patient, different organ failures are responsible for some important
pharmacokinetic modifications of distribution volume, the protein binding, clearance,
and elimination half-life.45 RRT also induces by itself a modification of the distribution
volume with the removal of plasma water. Furthermore, it has been shown that there is
a strong interindividual variability of these pharmacokinetic parameters, even in the
healthy volunteer. During RRT, different factors influence the elimination of drugs and
other compounds, including solubility, protein binding, interaction with the
dialyzer/hemofilter membrane, size, and charge. Variation in these properties across
various drugs makes it necessary to consider each drug individually and consult
appropriate dosing recommendations. A complete discussion is beyond the scope of
this review. Precise knowledge of drug pharmacokinetics and pharmacokinetic
modifications linked to both the state of the patient and the RRT is indispensable for
proper drug administration.

Medications That Patient is on:

Medications

Group

Dose

Frequency

Route

Tablet Iberet Folic

Hematinic

1 tab

Daily

Oral

1 tab

Twice daily

Oral

Tablet Calcium Carbonate Phosphate Binder

(CaCO3)

Tablet Lasix

Anti Diuretic

80 mg

On morning

Tablet Rocaltriol

Vitamin D

1 tab

3x/ week (post Oral

dialysis)
Daily

Tablet Norvasc

Anti Hypertensive

5 mg

Injection Eprex

Erythropoiten

2000 units 4000/ week

Oral

Oral
Intravenous

NURSING CARE PLAN

1.Alteration In Emotional Status, Anxiety related to new environment and
therapy.2.Knowledge deficit related unfamiliarity with disease process and
treatment.
3.Excess Fluid volume related to excess intake of sodium and fluid.
4. Risk of Infection Related To Internal Jugular Catheter insertion.
5. Alteration in Breathing Pattern, SOB Related To Fluid Overload.
6. Risk for Situational Low Self- Esteem related to dependence on outpatient
dialysis, body image changes.

1.Alteration In Emotional Status, Anxiety related to new environment and therapy.

Date & Time:14/3/2012@1200 pm
Supporting data:
1) Patient facial expression present anxious and keep on asking questions about
the disease and therapy.
2) Patient blood pressure on admission is 180/100mmHg, pulse:72bpm.

3) Patient isolate from others

Goal:
Patient facial expression show more cheerful after 1 hour nursing intervention carry
out and during haemodialysis.
Nursing interventions:
1) Assess patient level of anxiety and level of understanding about the disease and
treatment will be carry out. For example: facial expression, vital sign especially
blood pressure and pulse.
Act as baseline data and to plan appropriate nursing care.
2) Monitor vital sign every hourly especially blood pressure and pulse.
High level of anxiety patient may present tachycardia and hypertension.

3) Reinforce doctors explanation to patient via using simple word and avoid
medical jargon.
To make patient more easy to understand about her disease and treatment to
reduce the anxiety level.
4) Inform and explain to patient about procedure before carry out. For example:
Dressing of Internal Jugular Catheter, commence haemodialysis.
To reduce anxiety and gain co-operation for every procedure.
5) Encourage patient to ask questions about her disease or treatment if have any
doubt.
To clarify her curious.
6) Encourage patient family members spend time to accompany patient.
To provide emotional support and reduce level of anxiety.
7) Re-explain to patient if she still has any doubt.
To clarify his doubt and to ensure patient understand about the disease or
treatment.
8) Provide health education for patient. For example: IJC care and diet restriction.
Understanding will reduce the level of anxious.
9) Introduce patient to unit staffs and other patients , facilities provided. To let
patient feels more comfortable with new environment.
10)Inform doctor if patient still present high level of anxiety after nursing intervention
carry out.Patient may need further explanation from doctor to reduce anxiety.
Evaluation:
Date &Time: 14/3/2012@1300pm
Patient verbalize that his anxiety is reduce and have better understanding about the
disease and treatment will be carry out.
Supporting data:
-Patient present more cheerful.
-Patient start to socialize with staffs and other patients
-Her Blood pressure was reduce to158/89mmHg, pulse: 68bpm.
Re-evaluation:
Date &Time: 14/3/2012@16pm
During goes home patient present cheerful and calm.
Supporting data:
Patient facial expression present happy andBlood pressure is 128/84mmHg.

2.Knowledge deficit related unfamiliarity with disease process and treatment.

DATE : 14/3/2012 @ 12pm
Supporting data
-

Patient verbalized confusion about treatment.

Patient request for information and keep on asking regarding disease and
treatment.

Goal :
- Patient verbalized understands of condition or disease process and treatment after
nursing
intervention given within 1- 2 hours.
-Patient able to reexplain about her disease and treatment process.
Nursing intervention :
1.Assess patient level of understanding regarding disease and treatment by asking the
patient what she understand about the disease.
: An understanding of ESRD will help with compliance with the needed treatment.
2.Begin with information that patient already known and more to what the patient does
not know the disease.
: Progressing from simple to complex information can make patient easy to understand.

3.Use simple words, report and summarize as needed in Malay language.

: To promote and easy for patient to understanding regarding topics.
4.Provide written information or guideline such as pamphlet, journal or magazine that
related to disease.
: Written information can support and re inforce learning.

5.Discuss one topic at a time and avoid giving too much information in one session.
: To avoid patient confuse from overload information.
6.Encourge patient to ask the question what is patient does not know or not understand
about the disease.
: To provide better understanding according patient needs.
7.Discuss end-stage renal failure with the patient, including the need for dialysis or renal
transplantation for survival.
: Patient needs information about treatment options in order to make informed
decisions.
8.Instruct the patient in dietary and fluid restrictions
: Diet needs to be individualized according to the renal impairment of renal function.
Actual daily requirement depend on dialysis treatment type ( haemodialysis versus
peritoneal dialysis)

9.Discuss the need for reading food labels for sodium, potassium and other mineral
content before
:Many processed foods contain high levels of sodium. The sodium may be in forms
other than salt or sodium chloride.
10.Discuss the importance of taking prescribed medications. Discuss thoroughly dosage
and side effect.

Date &Time: 14/3/2012@1400pm

Evaluation :
-

Patient verbalized more understand regarding disease procedure within 12hours after nursing intervention given.

Supporting data :
-Patient verbalized that she is more understand about the End Stage Renal Disease
and need adequate treatment.

3.Excess Fluid volume related to excess intake of sodium and fluid.

Date & Time: 14/3/12 @ 1200 pm
Supporting data:
1) On arrival, patients Blood pressure is 172/99 mmHg.
2) Patients legs present pitting edema.
3) Patients face looks puffy
Goal:
1) Patient experiences optimal fluid balance is evidenced by normotensive BP,
weight gain less than 2-3 pounds between haemodialysis treatments.

Nursing interventions:
1) Assess patient for signs of fluid volume access: elevated BP, tachycardia,
edema, weight gain, and distended neck veins.
:The sign of fluid volume excess are the result of sodium retention and increased
intracellular fluid volume.
2) Asses respiratory pattern and work of breathing.
: Kussmauls respiration and dypnea may be evident.
3) Assess the amount of peripheral edema by palpating area over the tibia, ankles,
sacrum and back; and by assessing appearance of the face.
: Dependent areas often exibit signs of edema formation.
4) Assess the patients compliance with dietary and fluid restriction at home.

:Assess weight at every visit before and after dialysis (weight gain not exceed 2-3
pounds between visits)
5) Instruct in administration of antihypertensive medications if prescribed.
: As a rule, hypertension management can be difficult in this population.
6) Instruct the patient regarding restricting dietary sodium.
: Sodium intake produces a feeling of thirst. By restricting sodium intake, the amount
of fluid a patient drinks can be reduced.
7) Instruct the patient in methods to relieve dry mouth and maintain fluid restriction:
Suggest keeping sugar-free hard candy on hand
- This alleviates dry mouth( stimulate secretion of saliva)
Suggest taking ice chip, as needed
- One cup of ice equals only cup of water. Sucking a cup of ice takes
much longer than drinking a cup of water; patient can attain more

satisfaction.
Suggest frequent mouth rinses using cup of mouth- wash( nonalcohol)
Mixed with cup of ice water.
-Rinses can produce freshness in mouth and temporary alleviate
thirst.Non alcohol base mouth- wash may avoid of dry mouth.

8) Monitor vital signs especially Blood pressure hourly.

- To monitor the effectiveness of interventions and to detect early changes of
patient condition.
9) Restrict patient fluids intake. Eg.: 500mls +previous day output.
- Fluid overload will cause stress to the heart and blood pressure also will be
increase.

10)Administer medications eg. Calcium Antagonists (Norvasc 5mg OD) and Loop
diuretic (oral Lasix 8mg daily) as prescribed by doctor.
-To promote urine output and stabilize the haemodynamic status.
11) Commence haemodialysis as prescribed by doctor.
- By osmosis, diffusion and convection process able to remove excessive fluids
and balance the electrolyte, directly the blood pressure also can be stabilized.
Evaluation:
Date & Time: 14/3/12@ 14pm
After 2hours nursing intervention carry out, patient blood pressure reduce to
158/89mmHg, pulse 78bpm.
Re-evaluation:
Date & Time: 16/3/12@ 12pm
Recheck blood pressure: 142/85mmHg, pulse: 66bpm
Re-evaluation:
Date & Time: 20/3/12@ 1600pm
Recheck blood pressure: 138/80mmHg, pulse: 65bpm
Re-evaluation:
Date & Time: 22/3/12@ 1600pm
Patient blood pressure upon discharge was 128/84mmHg, pulse: 71bpm

4. Risk of Infection Related To Internal Jugular Catheter insertion.

Date & Time: 14/3/12 @12 pm
Supporting data:
1) Patient had inserted Right Internal Jugular Catheter on 5/3/12 @ 12 pm.

Goal:

Patients body temperature will be maintain within normal range and no sign and
symptoms of infection will be noted during dialysis procedure.
Nursing interventions:
1) Assess patients IJC site for early sign and symptoms of infection. Eg.: redness,
discharge,hygiene.
: To act as baseline data and for comparison purposes.
2) Monitor vital sign especially Temperature every 4 hourly..
: Hyperthermia is one of the indicator of infection.
3) Perform daily dressing with aseptic technique and when necessary. Eg.: if the
dressing is wet or dirty.
: To prevent from infectionandmaintain the hygiene.
4) Advice patient do not touch the dressing site if unnecessary.
: Touch the dressing site frequently will cause cross infection.
5) Teach patient about sign and symptoms of infection. Eg.: discharge, smelly,
itchiness.
: Early detection may prevent further complication.
6) Advice patient and family members do not apply any ointment/powder around
the IJC site.
: Moist will enhance the growth of bacteria.
7) Administer antibiotic cream eg. Bactroban cream as prescribed by doctor.
:Act as prophylaxis treatment to prevent further complications associated with
infection.
8) Inform doctor if patient present of any sign and symptoms of infection.
: Early detection to plan for further intervention and prevent complication.
Evaluation:
Date & Time: 14/3/12 @ 16am
1) During goes home, patient free from any sign and symptoms of infection.
During dialysis procedure patient afebrile

5.Risk for situational Low Self-esteem related to dependence on outpatient

dialysis and body image changes.

Supporting Data
- Patient verbalized has bad feeling about herself
- Patient verbalized doesnt like to have socialized with family members and
friends.
Goal:
-Patient manifests more positive self-esteem evidenced by verbalization of positive
feelings about self.
Intervention:
1. Assess for sign of low self-esteem; self negative verbalization, depression, expressed
anger, withdrawal, expression of shame or guilt, or evaluation of self as unable to deal
with events.
: The long-term dialysis patient is faced with long-term changes in lifestyle, occupation,
and financial status. The patients future depends on medications, dietary restrictions
and dialysis.
2. Assist patient in identifying the major areas of concern related to alteredself esteem.
Use a problem solving technique with the patient.

: The nurse-patient relation can provide a strong basis for implementing other strategies
to assist the patient anf family with adaption
3. Assist the patient incorporating changes in health status into activities of daily living
(ADLs), and occupational activities.
: As the patients condition worsens with ESRD, it is more difficult to engage in even
routine activities.
4. Talk with the patient, husband and friends if possible, about expectations regarding
chronic outpatient dialysis.
: Survival depends on such treatment. The patient may resent such dependence.
5. Allow the patient time to voice concerns and express anger related to having a
chronic condition.
: Denial and anger are anticipated responses to the diagnosis of a chronic illness.
6. Encourage an attitude of realistic hope.
: Hope provides a way of dealing with negative feelings.
7. Provide or encourage discussions with other patients with ESRD
: Such patient can share their responsesto illness.
8. Refer to psychiatric consultant as necessary.

: Most dialysis patients experience some degree of emotional imbalance. With

professional psychiatric consultation, most patients can gradually accept changed selfesteem.

6. Alteration in Breathing Pattern, SOB Related To Fluid Overload.

Date & Time: 30/3/12@17pm

Supporting data:
1) Verbalize by care giver, patients present SOB since midnight 5am and worsen
when exertion.
2)Patients respiration rate was 30bpm and Spo was 96% without oxygen.
3) Patients unable to complete a sentences when talking
Goal:
Patient breathing pattern will be maintain normal within 2hours after nursing
interventions carry out and during hospitalization.

Nursing interventions

1.Assess patients general condition (eg.: Cyanosis, confusion), breathing pattern

(eg. :respiration rate, depth, regular) and Spo.
: Act as baseline data and to plan further interventions.
2.Monitor vital signs hourly to 4hourly especially pulse rate, respiration rate, Spo.
: To detect further deterioration of patient condition and effectiveness of treatment.
3.Position patient in Fowlers position.
: To promote lungs expansion and better gas exchange.
4.Administer oxygen 5L/min via nasal prong as order by doctor.
: To supply adequate oxygen for body requirement.

5.Restrict fluids intake. (500mls+previous day output)

: To prevent further fluids overload.
6. Restrict patient sodium intake.
:Salt intake will enhance patient thirsty and retention of fluids as well.
7. Advice patient to RIB.
: Aggressive activity will cause more consumption of oxygen .
8.Administer medications eg. Loop diuretic (IV Lasix 80mg stat) as prescribed by doctor.
: To promote urine output and reduce the fluidoverload.
9. Commence haemodialysis as prescribed bydoctor.
: To correct the imbalance of electrolytes and remove excessive fluids.

Evaluation:

Date & Time: 30/3/12@ 1900 pm

After 2hours nursing intervention carry out, patient present less SOB and more
comfortable. Patient able to complete a sentences.
Supporting data:
1.Patient Spo increased to 98% with oxygen 5L/min via nasal prong.
2. Patient respiration rate 21bpm and present more regular.

HEALTH EDUCATION

MEDICATIONS
Compliance to medications as prescribed by doctor to avoid complications.

DIET
What is a hemodialysis diet?
The hemodialysis diet is an eating plan tailored to patients who are in stage 5 of chronic
kidney disease (CKD), also known as end stage renal disease (ESRD). These patients
have very little or no kidney function and must undergo dialysis to clean their blood of
waste and excess fluids.
Hemodialysis is one type of dialysis. The procedure is done several times a week,
usually for 3 to 4 hours at a time. The hemodialysis diet is designed to reduce the
amount of fluid and waste that builds up between hemodialysis treatments so that you
can feel your best.
What can I eat?
In addition to enjoying a variety of nutritious foods, the hemodialysis diet will introduce a
higher amount of protein into your eating plan. The exact amount will be determined by
your dietitian. You will be encouraged to get protein from high quality sources such as

lean meat, poultry, fish and egg whites. These high protein foods provide all the
essential amino acids your body needs.
What cant I eat?
The hemodialysis diet will restrict foods that contain high amounts of sodium,
phosphorus and potassium. Your dietitian will provide you with a diet guide and food
lists that indicate which foods are allowed and which ones you should avoid or limit. You
will also limit your fluid intake.
Why do I have to eat this way?
Your dietitian and doctor will strongly recommend you follow the hemodialysis diet, so
your dialysis treatments will be effective and you can feel your best. You will also reduce
the risk of other health complications associated with kidney disease and dialysis.
How does the hemodialysis diet help?
Potassiumbuilds up in the blood between dialysis treatments. The amount of
potassium that accumulates is determined by the amounts and types of foods eaten, as
well as how much kidney function remains. Too much potassium is very dangerous. It
can cause muscle weakness and make your heart stop beating. Potassium is easily
removed by dialysis. Certain fruits, vegetables, dairy products and other foods that are
very high in potassium will need to be restricted on your hemodialysis diet.
Phosphorus is difficult for hemodialysis to filter from the blood. This mineral can build
to high levels in the bloodstream and cause complications to your health, such as weak

bones, heart problems, joint pain, or skin ulcers. By limiting foods that contain
phosphorus, you lessen the risk of developing other health problems. In addition to a
low phosphorus diet, your doctor may prescribe a medicine called a phosphorus binder
to help keep phosphorus levels normal.
Sodium causes your body to hold onto more fluid and raises your blood pressure. You
may feel uncomfortable and short of breath if you consume too much sodium and fluid.
When excess fluid is removed during dialysis, you can get muscle cramps and feel
dizzy and weak during or after treatment. Eating less sodium and drinking less fluid can
help you feel comfortable before and after your dialysis sessions.
Your hemodialysis diet will also include a balance of nutrients to help keep your body
healthy and strong, while allowing the amount of potassium, phosphorus and sodium
your body can safely handle.
What about fluid intake?
You will be given specific instructions on the amount of fluid you can have. Fluid intake
is not limited to what you can drink; fluid is also hidden in some foods you eat. Being
aware of the fluid in foods such as gelatin, ice, sherbet, watermelon, sauces, gravies
and other high liquid foods is important. Your dietitian will give you guidelines to help
you monitor your fluid intake.
Too much fluid gain between hemodialysis sessions can cause discomfort. You may
experience swelling, shortness of breath or high blood pressure. Fluid gain can also
make your hemodialysis session uncomfortable due to muscle cramping and drops in

blood pressure during dialysis. Following your recommended fluid intake is an important
part of feeling better before and after a dialysis session.
How long do I have to follow the hemodialysis diet?
You will need to follow the hemodialysis diet as long as you need hemodialysis. Your
dietitian may make some changes to the diet in order to adjust to your current condition
and activity levels.
How do I know if the hemodialysis diet is working?
There are a variety of ways to know if the hemodialysis diet is working. One way is by
how you feel before and after dialysis.
Your body will continue to store waste and fluid between dialysis sessions. By following
the hemodialysis diet, sticking to your fluid allowance and taking your prescribed
medicines, the build up will be minimal and you wont feel ill. Your dialysis treatments
wont have to pull too much fluid from your body and you can avoid feeling weak or
dizzy afterwards. Also, you may experience fewer health complications caused by too
much phosphorus, sodium and potassium.
Another way to tell that the hemodialysis diet is working is by your target, or dry,
weight. Your target weight is the weight your doctor thinks you would be when all the
extra fluid is removed from your body. You can compare it to the stable day-to-day
weight maintained when you did not have kidney disease. Damaged kidneys cannot
remove the excess fluid from the blood, and this leads to fluid weight gain between

dialysis treatments. You will be weighed before and after your treatment to see how
close you are to your target weight. This is one way your healthcare team decides how
much fluid to remove during the dialysis treatment. Following your recommended fluid
intake will keep you from going too high above your target weight.

DIALYSIS TREATMENT
Dialysis helps people with renal failure, or kidney failure, to survive. The body must filter
out its extra fluid and waste products in order to be healthy. If the kidneys are failing,
this filtering cannot take place and the body becomes overwhelmed with both too much
fluid and too many wastes, which may be dangerous in high amounts.

Dialysis filters the body for the kidneys either by removing blood little by little to be
filtered directly (hemodialysis) or by putting fluid into the abdominal cavity and pulling
out excess waste with it (peritoneal dialysis).
People with severe kidney failure cannot survive long without dialysis. Dialysis cannot
curekidney failure; it can only keep a person alive long enough for their kidneys to heal
themselves (if it is acute kidney failure) or to receive a kidney transplant.

IJC CARE
Instruct patient to:

1.Keep dressing dry and clean

2. Apply new dressing when necessary.
3. Do not sleep on IJC site to avoid pressure or kink of the catheter.
4. Report any signs of infection such as discharge or pus from exit site
5. Report any bleeding around catheter immediately.
6. Apply direct pressure and go to emergency room if catheter becomes dislodged
accidently.

FISTULA CARE
New Fistula
There are certain precautions that have to be taken with the "Fistula Hand" especially if
it has been recently created.
1. Make sure that blood pressure is not taken on the fistula arm.
2. Regular exercise should be done. Take a small rubber ball in your fistula hand and try
to squeeze the ball every 5 minutes for an hour.
3. The fistula hand should be kept at a higher level, for example on pillows, especially
when freshly created.
4. The fistula hand should not be kept below the level of the head when sleeping.

Cleanliness

Cleanliness is one way someone on hemodialysis can keep their fistula uninfected.
Keep an eye out for infections, which can often be detected when there is pain,
tenderness, swelling or redness around the access area. If notice fever, doctor may
prescribe antibiotics for an infection, which should likely go away easily with early
diagnosis.
Unrestricted blood flow
Any restriction of blood flow can cause clotting. Here are some tips to help keep blood
flowing without restriction:

1.

Avoid tight clothing or jewelry that could put pressure on your access area

2.

Do not carry bags, purses or any type of heavy item over your access area

3.

Dont let anyone put a blood pressure cuff on your access arm have your
blood pressure taken from your non-access arm

4.

Request that blood being drawn is taken from your non-access arm

5.

Dont sleep with your access arm under your head or pillow

6.

Check the pulse in your access daily

The vibration of blood going through your arm is called the thrill. You should check this
several times a day. If the thrill changes or stops a blood clot may have formed. By
immediately contacting your doctor or dialysis health care team the clot may be quickly
dissolved or removed.

SUMMARY

5/3/2012 :Presented to emergency department ofHospital Tunku Jaafar onwith

complaint of shortness of breath on and off for 5 days and bilateral lower limbs
pitting oedema.
Seen by Dr M (nephrologist), direct to admit to ward a for stat haemodialysis.
Patient is diagnosed for Chronic Renal Disease- End stage renal failure
secondary to IgA nephropathy.
First dialysis commenced on same day via intrajugular catheter.
6/3/12 : Received blood transfusion 2 pints pack cells during dialysis (at second day)
10/3/12: Trial of fistula done but failed with result of haematoma and advised to rest for
2
weeks.
13/3/12: Discharge from ward after 9 days in ward with medications and follow up and
haemodialysis treatment continue at Unit Dialisis HTTJ.
14/3/12: First day dialysis started at Unit Dialisis HTTJ.

Past History:
11/10/2010: Renal biopsy; result Focal Proliferative IGA Nephropathy With Acute
Tubular
Necrosis changes.17% Global sclerosis and 13% Cresent.
28/1/2012 : Left radiocephalic fistula (Left AVF) created by Dr N (Vascular Surgeon).

REFERRENCES
BOOK
Anna Core Curriculum for Nephrology Nursing, Third Edition retrieved on 10/4/2012
NicolaThomas, Renal Nursing, 3rd Edition retrieved on 15/3/12
Renal Replacement Therapy, Clinical Practice Guidelines( 2 nd Edition)

INTERNET

http://www.kidney.org.uk/Medical-Info/Calcium-Phosphate/levels.html#Calcium retrieved on
30/3/12
Medindiahttp://www.medindia.net/patients/patientinfo/Dialysis_fistula.retrieved on1/4/12
htm#ixzz1poqZPfpwhttp://www.patient.co.uk/doctor/IgA-Nephropathy-%28Berger%27sDisease%29.htm retrieved on 1/4/2012

http://www.medicinenet.com/hemodialysis/page6.htm retrieved on 2/4/12

http://www.uptodate.com/contents/kt-v-and-the-adequacy-of-hemodialysisretrieved on 2/4/12
http://www.davita.com/kidney-disease/diet-and-nutrition/diet-basics/the-hemodialysisdiet/e/5314.

FACULTY OF NURSING AND ALLIED HEALTH

SCIENCES

NBNC 2407
CLINICAL PRACTICE 14
(RENAL NURSING)
PREPARED BY :
NURUL AIN BINTI ISMAIL
850704 14 6536 001
SEMESTER 3
SEPTEMBER 2014