Chronic Kidney Disease

Chronic kidney disease (CKD) is a condition characterized by a gradual loss of kidney

function over time. Chronic kidney disease includes conditions that damage your kidneys and
decrease their ability to keep you healthy by doing the jobs listed. If kidney disease gets worse,
wastes can build to high levels in your blood and make you feel sick. You may develop
complications like high blood pressure, anemia (low blood count), weak bones, poor nutritional
health and nerve damage. Also, kidney disease increases your risk of having heart and blood
vessel disease. These problems may happen slowly over a long period of time. Chronic kidney
disease may be caused by diabetes, high blood pressure and other disorders. Early detection and
treatment can often keep chronic kidney disease from getting worse. When kidney disease
progresses, it may eventually lead to kidney failure, which requires dialysis or a kidney
transplant to maintain life.

The Facts About Chronic Kidney Disease (CKD)

 30 million American adults have
CKD and millions of others are at
increased risk.
 Early detection can help prevent the
progression of kidney disease to
kidney failure.
 Heart disease is the major cause of
death for all people with CKD.
 Glomerular filtration rate (GFR) is
the best estimate of kidney function.
 Hypertension causes CKD and CKD
causes hypertension.
 Persistent proteinuria (protein in the
urine) means CKD is present.
 High risk groups include those with
diabetes, hypertension and family
history of kidney failure.
 African Americans, Hispanics,
Pacific Islanders, American Indians
and Seniors are at increased risk.
 Two simple tests can detect CKD:
blood pressure, urine albumin and
serum creatinine.

What causes CKD

The two main causes of chronic kidney disease are diabetes and high blood pressure,
which are responsible for up to two-thirds of the cases. Diabetes happens when your blood sugar
is too high, causing damage to many organs in your body, including the kidneys and heart, as
well as blood vessels, nerves and eyes. High blood pressure, or hypertension, occurs when the
pressure of your blood against the walls of your blood vessels increases. If uncontrolled, or
poorly controlled, high blood pressure can be a leading cause of heart attacks, strokes and
chronic kidney disease. Also, chronic kidney disease can cause high blood pressure.

Other conditions that affect the kidneys are:

 Glomerulonephritis, a group of diseases that cause inflammation and damage to the

kidney's filtering units. These disorders are the third most common type of kidney
disease.
 Inherited diseases, such as polycystic kidney disease, which causes large cysts to form in
the kidneys and damage the surrounding tissue.
 Malformations that occur as a baby develops in its mother's womb. For example, a
narrowing may occur that prevents normal outflow of urine and causes urine to flow back
up to the kidney. This causes infections and may damage the kidneys.
 Lupus and other diseases that affect the body's immune system.
 Obstructions caused by problems like kidney stones, tumors or an enlarged prostate gland
in men.
 Repeated urinary infections.

ANATOMY AND PHYSIOLOGY

The kidneys play three major roles:

 removing waste products from the body, keeping toxins from building up in the
bloodstream

 producing hormones that control other body functions, such as regulating blood pressure
and producing red blood cells

 regulating the levels of minerals or electrolytes (e.g., sodium, calcium, and potassium)
and fluid in the body

The two kidneys in our body possess tiny filtering units, called nephrons, each of which is made
up of a glomerulus (which acts as a kind of sieve to prevent important components such as red
blood cells from being removed), and a tubule (a tube through which fluid passes).

It's entirely possible to live a full, healthy life with only one kidney – one fully functioning
kidney can do the work of two – but it's essential to watch for signs of any problems with the
remaining kidney.
External Anatomy
The left kidney is located at about
the T12 to L3 vertebrae, whereas the right
is lower due to slight displacement by the
liver. Upper portions of the kidneys are
somewhat protected by the eleventh and
twelfth ribs. Each kidney weighs about
125–175 g in males and 115–155 g in
females. They are about 11–14 cm in
length, 6 cm wide, and 4 cm thick, and are
directly covered by a fibrous capsule
composed of dense, irregular connective
tissue that helps to hold their shape and protect them. This capsule is covered by a shock-
absorbing layer of adipose tissue called the renal fat pad, which in turn is encompassed by a
tough renal fascia. The fascia and, to a lesser extent, the overlying peritoneum serve to firmly
anchor the kidneys to the posterior abdominal wall in a retroperitoneal position. On the superior
aspect of each kidney is the adrenal gland. The adrenal cortex directly influences renal function
through the production of the hormone aldosterone to stimulate sodium reabsorption.

Internal Anatomy
A frontal section through
the kidney reveals an outer
region called the renal
cortex and an inner region
called the medulla. The renal
columns are connective tissue
extensions that radiate
downward from the cortex
through the medulla to separate
the most characteristic features of the medulla, the renal pyramids and renal papillae. The
papillae are bundles of collecting ducts that transport urine made by nephrons to the calyces of
the kidney for excretion. The renal columns also serve to divide the kidney into 6–8 lobes and
 provide a supportive framework for vessels that enter and exit the cortex. The pyramids and renal
columns taken together constitute the kidney lobes.

Renal Hilum

The renal hilum is the entry and exit site for structures servicing the kidneys: vessels,
nerves, lymphatics, and ureters. The medial-facing hila are tucked into the sweeping convex
outline of the cortex. Emerging from the hilum is the renal pelvis, which is formed from the
major and minor calyxes in the kidney. The smooth muscle in the renal pelvis funnels urine via
peristalsis into the ureter. The renal arteries form directly from the descending aorta, whereas the
renal veins return cleansed blood directly to the inferior vena cava. The artery, vein, and renal
pelvis are arranged in an anterior-to-posterior order.

Nephrons and Vessels

The renal artery first

divides into segmental arteries,
followed by further branching to
form interlobar arteries that pass
through the renal columns to reach
the cortex. The interlobar arteries,
in turn, branch into arcuate
arteries, cortical radiate arteries,
and then into afferent arterioles. The afferent arterioles service about 1.3 million nephrons in
each kidney.

Nephrons are the “functional

units” of the kidney; they
cleanse the blood and balance
the constituents of the

Blood Flow in the Nephron. The two

capillary beds are clearly shown in
this figure. The efferent arteriole is the
connecting vessel between the
circulation. The afferent arterioles form a tuft of high-pressure capillaries about 200 µm in
diameter, the glomerulus. The rest of the nephron consists of a continuous sophisticated tubule
whose proximal end surrounds the glomerulus in an intimate embrace—this is Bowman’s
capsule. The glomerulus and Bowman’s capsule together form the renal corpuscle. As
mentioned earlier, these glomerular capillaries filter the blood based on particle size. After
passing through the renal corpuscle, the capillaries form a second arteriole, the efferent
arteriole. These will next form a capillary network around the more distal portions of the
nephron tubule, the peritubular capillaries and vasa recta, before returning to the venous
system. As the glomerular filtrate progresses through the nephron, these capillary networks
recover most of the solutes and water, and return them to the circulation. Since a capillary bed
(the glomerulus) drains into a vessel that in turn forms a second capillary bed, the definition of a
portal system is met. This is the only portal system in which an arteriole is found between the
first and second capillary beds. (Portal systems also link the hypothalamus to the anterior
pituitary, and the blood vessels of the digestive viscera to the liver.)

Cortex

In a dissected kidney, it is easy to identify the cortex; it appears lighter in color compared
to the rest of the kidney. All of the renal corpuscles as well as both the proximal convoluted
tubules (PCTs)and distal convoluted tubules are found here. Some nephrons have a short loop
of Henle that does not dip beyond the cortex. These nephrons are called cortical nephrons.
About 15 percent of nephrons have long loops of Henle that extend deep into the medulla and are
called juxtamedullary nephrons.

Chronic Kidney Disease Stages

Chronic kidney disease (CKD) is divided into 5 stages based on the level of kidney
function. Stages are determined through certain tests performed by your doctor, including a test
used to calculate the estimated glomerular filtration rate (eGFR), which measures how well your
kidneys are cleaning your blood. Kidney disease is a progressive disease, meaning that kidney
function can continue to decline over time, eventually resulting in kidney failure.

CKD stage Description Possible signs & symptoms eGFR

Stage 1 Minimal loss of kidney function Typically, signs and symptoms 90–
of CKD do not show up until 120
Stage 2 Mild to moderate loss of kidney function later stages—if at all 60–89

Stage 3 Moderate to severe loss of kidney function 30–59

Stage 4 Severe loss of kidney function Complications such as anemia 16–29
(low blood iron), high blood
pressure (hypertension) and
abnormal blood levels of
phosphorus, calcium and
vitamin D
Stage 5 Kidney failure and need for dialysis or Fatigue associated with anemia
End stage transplant (low blood iron), decreased
renal appetite, nausea, vomiting,
disease abnormal lab values including
(ESRD) elevated potassium,
abnormalities in hormones
related to bone health, elevated
phosphorus and/or decreased
calcium, high blood pressure
(hypertension), swelling in
hands/legs/eyes/lower back
(sacrum) and shortness of
breath

Symptoms of Chronic Kidney Disease

Most people may not have any severe symptoms until their kidney disease is advanced.
However, you may notice that you:

 feel more tired and have less energy  fatigue

 have trouble concentrating  shortness of breath
 have a poor appetite  loss of appetite
 have trouble sleeping  nausea and vomiting (this is a
 have muscle cramping at night common symptom)
 have swollen feet and ankles  thirst
 have puffiness around your eyes,  bad taste in the mouth or bad breath
especially in the morning  weight loss
 have dry, itchy skin  generalized, persistent itchy skin
 need to urinate more often,  muscle twitching or cramping
especially at night.  a yellowish-brown tint to the skin
 high blood pressure
 Risk factors of Chronic Kidney Disease

Anyone can get chronic kidney disease at any age. However, some people are more likely than
others to develop kidney disease. You may have an increased risk for kidney disease if you:

 have diabetes
 have high blood pressure
 have a family history of kidney failure
 are older
 belong to a population group that has a high rate of diabetes or high blood pressure, such
as African Americans, Hispanic Americans, Asian, Pacific Islanders, and American
Indians.

Complications of Chronic Kidney Disease

Being diagnosed with chronic renal failure can be very frightening.The future of the
condition, however, depends on the medical problem that caused the kidney failure, how much
kidney damage has occurred, and what, if any, complications are present.

Some of these complications may include:

 anemia

 high blood pressure (hypertension)  mineral abnormalities

(e.g., hypercalcemia [high levels of
 increased risk of bleeding calcium in the blood]
or hyperphosphatemia [high levels of
 increased risk of infection
phosphorus in the blood])
 fluid overload (called edema)
 brittle bones
 dehydration
 malnutrition
 electrolyte abnormalities
 seizures
(e.g., hyperkalemia, high levels of
potassium in the blood)

Pathophysiology of Chronic Kidney Disease

There are many diseases that cause chronic renal disease; each has its own pathophysiology.
However, there are common mechanisms for disease progression.

1. Pathologic features include fibrosis, loss of renal cells, and infiltration of renal tissue
by monocytes and macrophages.
 2. Proteinuria, hypoxia, and extensive angiotensin II production all contribute to the
pathophysiology. In an attempt to maintain GFR, the glomerular hyperfiltration; this
results in endothelial injury.
3. Proteinuria results from increased glomerular permeability and increased capillary
pressure.
4. Hypoxia also contributes to disease progression. Angiotensin II increases
glomerular hypertension, which further damages the kidney.

Predisposing Factors

 Diabetes, which is the most common risk factor for chronic kidney failure in the
United States
 Age 60 or older
 Kidney disease present at birth (congenital)
 Family history of kidney disease
 Autoimmune Disorder (Lupus erythematosus)
 Bladder outlet obstruction (BPH and Prostatitis)
 Race (Sickle cell disease)

Precipitating Factors

 Occupational Hazard (overexposure to toxins and to some medications)

 Sedentary Lifestyle (hypertension, atherosclerosis)
 Diet (High residue diet)

Schematic Diagram
 Prognosis
The prognosis of patients with chronic kidney disease is guarded asepidemiological
data has shown that all cause mortality(the overall death rate) increases as kidneyfunction
decreases. The leading cause of death in patients with chronic kidney disease is cardiovascular
disease, regardless of whether there is progression to stage 5.While renal replacement
therapies can maintain patients indefinitely and prolong life, the quality of life is severely
affected.
Renal transplantation increases thesurvival of patients with stage 5 CKD significantly
when compared to other therapeutic options; however, it is associated with an increased short-
term mortality (due tocomplications of the surgery). Transplantation aside, high intensity home
hemodialysis appears to be associated with improved survival and a greater quality of life ,when
compared to the conventional three times a week hemodialysis and peritoneal dialysis.
 Assessment and Diagnostic Findings
Laboratory studies required to establish the diagnosis of CRF include:

 Glomerular filtration rate. GFR and creatinine clearance decrease while serum
creatinine (more sensitive indicator of renal function) and BUN levels increase.
 Sodium and water retention. Some patients retain sodium and water, increasing the
risk for edema, heart failure, and hypertension.
 Acidosis. Metabolic acidosis occurs in ESRD because the kidneys are unable to
excrete increased loads of acid.
 Anemia. In ESRD, erythropoietin production decreases and profound anemia results,
producing fatigue, angina, and shortness of breath.
 Urine
o Volume: Usually less than 400 mL/24 hr (oliguria) or urine is absent
(anuria).
o Color: Abnormally cloudy urine may be caused by pus, bacteria, fat,
colloidal particles, phosphates, or urates. Dirty, brown sediment indicates
presence of RBCs, hemoglobin, myoglobin, porphyrins.
o Specific gravity: Less than 1.015 (fixed at 1.010 reflects severe renal
damage).
o Osmolality: Less than 350 mOsm/kg is indicative of tubular damage, and
urine/serum ratio is often 1:1.
o Creatinine clearance: May be significantly decreased (less than 80
mL/min in early failure; less than 10 mL/min in ESRD).
o Sodium: More than 40 mEq/L because kidney is not able to reabsorb
sodium.
o Protein: High-grade proteinuria (3–4+) strongly indicates glomerular
damage when RBCs and casts are also present.
 Blood
o BUN/Cr: Elevated, usually in proportion. Creatinine level of 12 mg/dL
suggests ESRD. A BUN of >25 mg/dL is indicative of renal damage.
o CBC: Hb decreased because of anemia, usually less than 7–8 g/dL.
 o RBCs: Life span decreased because of erythropoietin deficiency, and
azotemia.
o ABGs: pH decreased. Metabolic acidosis (less than 7.2) occurs because of
loss of renal ability to excrete hydrogen and ammonia or end products of
protein catabolism. Bicarbonate and PCO2 Decreased.
o Serum sodium: May be low (if kidney “wastes sodium”) or normal
(reflecting dilutional state of hypernatremia).
o Potassium: Elevated related to retention and cellular shifts (acidosis) or
tissue release (RBC hemolysis). In ESRD, ECG changes may not occur
until potassium is 6.5 mEq or higher. Potassium may also be decreased if
patient is on potassium-wasting diuretics or when patient is receiving
dialysis treatment.
o Magnesium, phosphorus: Elevated.
o Calcium/phosphorus: Decreased.
 Proteins (especially albumin): Decreased serum level may reflect protein loss via
urine, fluid shifts, decreased intake, or decreased synthesis because of lack of essential
amino acids.
 Serum osmolality: Higher than 285 mOsm/kg; often equal to urine.
 KUB x-rays: Demonstrates size of kidneys/ureters/bladder and presence of
obstruction (stones).
 Retrograde pyelogram: Outlines abnormalities of renal pelvis and ureters.
 Renal arteriogram: Assesses renal circulation and identifies extravascularities,
masses.
 Voiding cystourethrogram: Shows bladder size, reflux into ureters, retention.
 Renal ultrasound: Determines kidney size and presence of masses, cysts, obstruction
in upper urinary tract.
 Renal biopsy: May be done endoscopically to examine tissue cells for histological
diagnosis.
 Renal endoscopy, nephroscopy: Done to examine renal pelvis; flush out
calculi, hematuria; and remove selected tumors.
 ECG: May be abnormal, reflecting electrolyte and acid-base imbalances.
 X-ray of feet, skull, spinal column, and hands: May reveal
demineralization/calcifications resulting from electrolyte shifts associated with CRF.
 Medical Management
The patient with ESRD requires astute nursing care to avoid the complications of reduced renal
function and the stresses and anxieties of dealing with a life-threatening illness.

Nursing Assessment

Assessment of a patient with ESRD includes the following:

 Assess fluid status (daily weight, intake and output, skin turgor, distention of neck
veins, vital signs, and respiratory effort).
 Assess nutritional dietary patterns (diet history, food preference, and calorie counts).
 Assess nutritional status (weight changes, laboratory values).
 Assess understanding of cause of renal failure, its consequences and its treatment.
 Assess patient’s and family’s responses and reactions to illness and treatment.
 Assess for signs of hyperkalemia.

Diagnosis

For kidney disease diagnosis, you may also need certain tests and procedures, such as:

 Blood tests. Kidney function tests look for the level of waste products, such as creatinine
and urea, in your blood.

 Urine tests. Analyzing a sample of your urine may reveal abnormalities that point to
chronic kidney failure and help identify the cause of chronic kidney disease.

 Imaging tests. Your doctor may use ultrasound to assess your kidneys' structure and size.
Other imaging tests may be used in some cases.

 Removing a sample of kidney tissue for testing. Your doctor may recommend a kidney
biopsy to remove a sample of kidney tissue. Kidney biopsy is often done with local
anesthesia using a long, thin needle that's inserted through your skin and into your kidney.
The biopsy sample is sent to a lab for testing to help determine what's causing your kidney
problem.
 Treatment

Kidney transplant
Depending on the underlying cause, some types of kidney disease can be treated. Often, though,
chronic kidney disease has no cure.

Treatment usually consists of measures to help control signs and symptoms, reduce
complications, and slow progression of the disease. If your kidneys become severely damaged,
you may need treatment for end-stage kidney disease.

Treating the cause

Your doctor will work to slow or control the cause of your kidney disease. Treatment options
vary, depending on the cause. But kidney damage can continue to worsen even when an
underlying condition, such as high blood pressure, has been controlled.

Treating complications

Kidney disease complications can be controlled to make you more comfortable. Treatments may
include:

 High blood pressure medications. People with kidney disease may experience worsening
high blood pressure. Your doctor may recommend medications to lower your blood
pressure — commonly angiotensin-converting enzyme (ACE) inhibitors or angiotensin II
receptor blockers — and to preserve kidney function. High blood pressure medications can
initially decrease kidney function and change electrolyte levels, so you may need frequent
blood tests to monitor your condition. Your doctor will likely also recommend a water pill
(diuretic) and a low-salt diet.

 Medications to lower cholesterol levels. Your doctor may recommend medications called
statins to lower your cholesterol. People with chronic kidney disease often experience high
levels of bad cholesterol, which can increase the risk of heart disease.

 Medications to treat anemia. In certain situations, your doctor may recommend

supplements of the hormone erythropoietin (uh-rith-roe-POI-uh-tin), sometimes with added
iron. Erythropoietin supplements aid in production of more red blood cells, which may
relieve fatigue and weakness associated with anemia.
  Medications to relieve swelling. People with chronic kidney disease may retain fluids.
This can lead to swelling in the legs, as well as high blood pressure. Medications called
diuretics can help maintain the balance of fluids in your body.

 Medications to protect your bones. Your doctor may prescribe calcium and vitamin D
supplements to prevent weak bones and lower your risk of fracture. You may also take
medication known as a phosphate binder to lower the amount of phosphate in your blood,
and protect your blood vessels from damage by calcium deposits (calcification).

 A lower protein diet to minimize waste products in your blood. As your body processes
protein from foods, it creates waste products that your kidneys must filter from your blood.
To reduce the amount of work your kidneys must do, your doctor may recommend eating
less protein. Your doctor may also ask you to meet with a dietitian who can suggest ways
to lower your protein intake while still eating a healthy diet.

Your doctor may recommend follow-up testing at regular intervals to see whether your kidney
disease remains stable or progresses.

Treatment for end-stage kidney disease

If your kidneys can't keep up with waste and fluid clearance on their own and you develop
complete or near-complete kidney failure, you have end-stage kidney disease. At that point, you
need dialysis or a kidney transplant.

 Dialysis. Dialysis artificially removes waste products and extra fluid from your blood when
your kidneys can no longer do this. In hemodialysis, a machine filters waste and excess
fluids from your blood. In peritoneal dialysis, a thin tube (catheter) inserted into your
abdomen fills your abdominal cavity with a dialysis solution that absorbs waste and excess
fluids. After a period of time, the dialysis solution drains from your body, carrying the
waste with it.

 Kidney transplant. A kidney transplant involves surgically placing a healthy kidney from
a donor into your body. Transplanted kidneys can come from deceased or living donors.
You'll need to take medications for the rest of your life to keep your body from rejecting
the new organ. You don't need to be on dialysis to have a kidney transplant.

For some who choose not to have dialysis or a kidney transplant, a third option is to treat kidney
failure with conservative measures. However, once you have complete kidney failure, your life
expectancy generally would be only a few months.
Potential future treatments

Regenerative medicine holds the potential to fully heal damaged tissues and organs, offering
solutions and hope for people who have conditions that today are beyond repair.

Regenerative medicine approaches include:

 Boosting the body's natural ability to heal itself

 Using healthy cells, tissues or organs from a living or deceased donor to replace damaged
ones

 Delivering specific types of cells or cell products to diseased tissues or organs to restore
tissue and organ function

For people with chronic kidney disease, regenerative medicine approaches may be developed in
the future to help slow progression of the disease.

Lifestyle and home remedies

Depending on your situation, kidney function and overall health, your dietitian may recommend
that you:

 Avoid products with added salt. Lower the amount of sodium you eat each day by
avoiding products with added salt, including many convenience foods, such as frozen
dinners, canned soups and fast foods. Other foods with added salt include salty snack
foods, canned vegetables, and processed meats and cheeses.

 Choose lower potassium foods. Your dietitian may recommend that you choose lower
potassium foods at each meal. High-potassium foods include bananas, oranges, potatoes,
spinach and tomatoes. Examples of low-potassium foods include apples, cabbage, carrots,
green beans, grapes and strawberries. Be aware that many salt substitutes contain
potassium, so you generally should avoid them if you have kidney failure.

 Limit the amount of protein you eat. Your dietitian will estimate the appropriate number
of grams of protein you need each day and make recommendations based on that amount.
High-protein foods include lean meats, eggs, milk, cheese and beans. Low-protein foods
include vegetables, fruits, breads and cereals.
 Monitoring
Monitoring patients with CKD requires regular blood and urine testing. The frequency
and type of bloods that are required changes throughout the stages and it is important to get this
right (see Table 1). When testing blood, it is important to remember that prior to the test, patients
should be asked not to exercise or eat meat for 12 hours beforehand.1 It is also recommended
that blood samples should be processed no longer than 12 hours from venepuncture. When
testing for microalbuminuria, an early morning urine sample is preferable, and testing should be
avoided in an acute illness or menstruation.2

Controlling blood pressure in renal disease is thought to be beneficial in protecting

long-term kidney function and slowing of progression. People are often unaware of the link
between kidney disease and hypertension, and as such require education in understanding how
lowering blood pressure can protect their kidneys from further damage. The National Institute for
Health and Care Excellence (NICE) recommend a systolic blood pressure of 120-139mmHg and
a diastolic pressure less than 90mmHg. However, a different target is required if the patient is
either diabetic and/or has significant albuminuria.1

Microalbuminuria, quantified by urinary albumin creatinine ratio (uACR) is known to

be significant from a cardiovascular point of view in people without diabetes at a level of
2.5mg/mmol (male) or 3.5mg/mmol (female). However in the presence of diabetes it becomes
significant at this level from both a cardiovascular and renal perspective and blood pressure
should range from 120-129mmHg systolic and 70mg/mmol.1 Similarly, eGFR classification of
microalbuminuria requires two samples separated by at least two weeks.2 Again samples should
not be included in diagnosis of microalbuminuria in the presence of infection.

In addition achieving good glycaemic control, managing any cardiovascular risk factors
will contribute to the preservation of kidney function and should play an integral part of an
individual's treatment plan if applicable.

Despite best intentions, a proportion of people with CKD will see their condition progress
and as a result will need specialist assessment. Following discussion, people with the following
should be considered for referral into secondary care specialist renal services:

CKD stage 4 and 5 (with or without diabetes).

Heavy proteinuria (ACR >70mg/mmol) unless already known to be due to diabetes and being
treated accordingly.

Proteinuria (>30mg/mmol) together with haematuria.

Progressive CKD (>5ml/min/1.73m² in one year or 10ml/min/1.73m² within five

years).

Resistant hypertension: if using at least four anti-hypertensive drugs without success.

People with or suspected of having rare or genetic causes of CKD.

Suspected renal artery stenosis.

Role of primary care nurses

 Primary care nurses play a pivotal role in the management of patients with CKD. Helping

and enabling people to be aware of their condition, and educating them to make informed

decisions about long-term treatment is thought to be beneficial. Enhancing self-

management can be achieved by:

 Educating patients on the importance of blood pressure control ensuring they are aware

that reducing raised blood pressure is a key factor in preventing progression of CKD.

 Encourage home blood pressure monitoring where appropriate.

 Education on maintaining a good glycaemic control to slow progression of CKD.

 Advice on healthy eating and exercise.

Nursing Diagnosis

1. Risk for Decreased Cardiac Output

2. Risk for Ineffective Protection
3. Disturbed Thought Process
4. Risk for Impaired Skin Integrity
 5. Risk for Impaired Oral Mucous Membrane
6. Deficient Knowledge
7. Excess Fluid Volume
8. Acute Pain
9. Impaired Renal Tissue Perfusion
10. Impaired Urinary Elimination
11. Imbalanced Nutrition: Less than Body Requirements

Planning and Goals

1. The patient will have negative or equal intake and output during hospitalization.
2. The patient will have decreased peripheral edema of 1+ or less within 48 hours.
3. The patient will have 30 cc or greater of urinary output during a 24 hour period.
4. The patients BUN and creatinine will be within normal range within 36 hours.
5. The patient will weigh 165lbs or less by discharge.
6. The patient will verbalized the importance of daily weights and limiting salt intake by
discharge.
7. The patient will name 5 foods that contain high salt intake to avoid by discharge.
8. The patient will verbalize understanding about how hemodialysis works before dialysis.

5 Possible Diagnosis
1. Decreased Cardiac Output.
2. Fluid and Electrolyte imbalances.
3. Imbalanced Nutrition.
4. Ineffective Breathing Pattern.
5. Impaired Skin Integrity.

Nursing Interventions

Decreased Cardiac Output related to increased cardiac load.

Goal:

 Decreased cardiac output does not occur with the outcome criteria:
 maintain cardiac output and blood pressure with evidence of cardiac frequency in the
normal range, strong peripheral pulses, and the same with capillary refill time.

Intervention:
1 Auscultation of heart and lung sounds.
R: The presence of tachycardia, irregular heart rate.

2 Assess for hypertension.

R: Hypertension may occur due to interference with the system of the renin-angiotensin-
aldosterone system (caused by renal dysfunction).

3 Investigate complaints of chest pain, note the location, radiation, severity (0-10 scale).
R: HT and CRF can cause pain.

4 Assess activity level, response to activity.

R: Fatigue can also accompany CRF anemia.

Fluid and Electrolyte imbalances related to secondary edema (fluid volume unbalanced
because of the retention of Na and H2O).

Goal:
Maintain ideal body weight without excess fluid with outcome criteria: no edema, the balance
between inputs and outputs.

Intervention:
1 Assess fluid status with daily weigh, balance input and output, skin turgor, vital signs.

2 Limit your fluid intake.

R: fluid restriction akn determine ideal body weight, urine output, and response to therapy.

3 Explain to the patient and family about the liquid restrictions.

R: Understanding to increase cooperation of patients and families in the fluid restriction.
4. Instruct the patient / teach the patient to record the use of fluid intake and output mainly.
R: To determine the balance of inputs and outputs.

Imbalanced Nutrition, Less Than Body Requirements related to anorexia, nausea, vomiting.

Goal:
Maintain adequate nutrient inputs to the outcome criteria: demonstrate stable weight.

Intervention:

1 Monitor the consumption of foods / liquids.

R: Identifying nutritional deficiencies.

2 Notice of nausea and vomiting.

R: Symptoms that accompany the accumulation of endogenous toxins that can alter or lower
income and require intervention.

3 Give food a little but often.

R: The portion of a smaller can increase food intake.

4 Increase visits by people nearby during meals.

R: Provides transfer and improve the social aspects.

5. Provide frequent mouth care.

R: Lowering stomatitis oral discomfort and unwelcome taste in the mouth that can affect food
intake.

Ineffective Breathing Pattern related to hyperventilation secondary: compensation via

respiratory alkalosis.

Goal:
Breathing pattern back to normal / stable.

Intervention:

1 Auscultation of breath sounds, note the presence of crakles.

R: To declare the existence of the collection of secretions.

2 Teach patient effective coughing and deep breathing.

R: Cleaning the airway and facilitate the flow O2.

3 Adjust the position as comfortable as possible.

R: Preventing the occurrence of shortness of breath.

4 Limit to move.
R: Reduce workload and prevent tightness or hypoxia.

Impaired Skin Integrity related to pruritis

Goal:
The integrity of the skin can be maintained with the outcome criteria: Maintain intact
skin, Shows behaviors / techniques to prevent damage to the skin.
Intervention:

1 Inspection of the skin to change color, turgor, vascular, note the presence of redness.
R: Indicates area of poor circulation or damage that may lead to the formation of pressure sores /
infections.

2 Monitor fluid intake and hydration of the skin and mucous membranes.
R: Detecting the presence of dehydration or overhydration affecting circulation and tissue
integrity.

3 Inspection of the area depends on edema

R: Tissue edema is more likely to be damaged / torn.

4 Change positions as often as possible.

R: Reduce pressure on edema, poorly perfused tissue to reduce ischemia.

5. Give skin care.

R: Reduce drying, skin tears.

6 Maintain a dry linen.

R: Lowering dermal irritation and the risk of skin damage.

7 Instruct the patient to use a damp and cold compresses to put pressure on the area pruritis.
R: Eliminate the discomfort and reduce the risk of injury.

8 Encourage wear loose cotton clothes.

R: Preventing direct dermal irritation and improve skin moisture evaporation.
 PATIENT DATA
Patient’s name: XxX Age: 81 Sex: Male
Birthdate: December 18, 1936 Rendered Date: August 28, 2018
Patient ID: 08-07172 Released Date: August 28, 2018
Chief Complaint: Dizziness, Loss of appetite Weight: 54kg

LABORATORY RESULT

COMPLETE BLOOD COUNT

TEST Result Ref. Value (SI)
CBC
White Blood Cells 5.96 4.50-10.00 x 10^9/L
Red Blood Cells 4.76 4.60-6.20 x
10^12/L
Hemoglobin 12.1 (H) 13.50-18.00 g/dL
Hematocrit 0.40 0.40-0.54
MCV 84.5 80.00-100.00 fL
Platelete 196 150.00-450.00 x 10^9/L

DIFFERENTIAL COUNT
Neutrophil 0.55 0.50-0.70
Lymphocyte 0.15 (L) 0.20-0.40
Monocyte 0.11 (H) 0.03-0.08
Eosinophils 0.17 (H) 0.01-0.04
Basophils 0.02 (H) 0.00-0.01

CLINICAL CHEMISTRY FORM 1

 TEST RESULT NORMAL
VALUES
Conventional SI
Conventional
Potassium 4.14 meq/L 3.60-5.50 3.60-
5.50 meq/L

Creatinine 10.25 mg/dL 53.00-123.70 0.60-

1.40 mg/Dl

Calcium 1.13 mmol/L 1.13-1.31

mmol/L

DRUG STUDY
Patient’s name: XxX.
Diagnosis: Chronic Kidney Disease
Generic Name: Mechanisms of Side Effects/ Adverse Nursing
Erythropoietin Action Reaction Responsibilities
(EPO)
CNS: Before starting
Brand Name: Mimics effects of asthenia, dizziness, therapy, evaluate
Epogen erythropoietin. fatigue, headache, patient’s iron status.
Functions as a paresthesia, seizures. Patient should
Dosage: growth factor and as CV: receive adequate
4TU 2 x a week SQ a differentiating edema, hypertension, iron supplementation
factor, enhancing increased clotting of beginning no later
RBC production arteriovenous grafts. than when epoetin
GI: alfa treatment starts
Indications: abdominal pain and and continuing
constipation (in children) throughout therapy.
Anemia caused by diarrhea, nausea, vomiting. Patient may need
Chronic renal Classification MUSCKULOSKELETAL: vitamin B 12 and
failure. arthralgia folic acid .
Haematopoietic RESPIRATORY:
Cough, shortness of Monitor BP before
breath. therapy. Blood
SKIN: pressure may
infection site reactions, increase, especially
rash, urticaria. when hematocrit
increases in the early
part of therapy.

Monitor blood
counts; elevated
hematocrit may
cause excessive
clotting

Inform patient that

pain in limbs and
long may occur after
injection (usually
within 2 hours.)

Patient may need

additional heparin to
prevent clotting
during dialysis
treatment.

Tell patient to
monitor blood
pressure athome and
to adhere to dietar
REFERENCE:

https://www.scribd.com/doc/19675249/Chronic-Kidney-Disease

https://www.scribd.com/doc/136233844/Chronic-Kidney-Disease-Pathophysiology-Schematic-
Diagram

https://www.fairview.org/patient-education/86310

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0103-21002014000100009

https://www.uptodate.com/contents/chronic-kidney-disease-beyond-the-basics

http://www.registerednursern.com/nursing-care-plan-and-diagnosis-for-renal-failure/

http://www.scielo.br/scielo.php?pid=S010321002016000500486&script=sci_arttext&tlng=en

https://journals.rcni.com/nursing-standard/chronic-kidney-disease-risk-factors-assessment-and-
nursing-care-ns2006.11.21.10.48.c6381

https://www.niddk.nih.gov/health-information/kidney-disease/chronic-kidney-disease-ckd/tests-
diagnosis

https://www.mayoclinic.org/diseases-conditions/chronic-kidney-disease/diagnosis-treatment/drc-
20354527