Acute renal failure and chronic renal failure

HIBBs is a program of the Global
Health Informatics Partnership
PRESENTED BY: - NEHA BHARTI
M.SC (N) MEDICAL SURGICAL NURSING
NURSING TUTOR
SMVDCON, KAKRYAL
ACUTE RENAL FAILURE

RENAL FAILURE
 Renal failure or kidney failure (formerly
called renal insufficiency) is a situation in
which the kidneys fail to function
adequately.
 It is characterised by the reduction in
the excretory and regulatory functions of
the kidney.

 If the kidney function fails, the waste
products accumulate in the blood and
the body leading to a disruption in
endocrine and metabolic functions as
well as fluid, electrolyte, and acidbase
disturbances.
 Renal failure can be acute, with sudden
onset of symptoms, or chronic, occurring
gradually over time.

 Once renal failure occurs, it requires
immediate management and even then
prognosis is often not good unless
transplantation is done.

ACUTE RENAL FAILURE
 Acute kidney failure is
the sudden and
complete loss of the
ability of the kidneys to
remove waste.
 It occurs when the
kidneys stop working
over a period of hours,
days, or in some
cases, weeks.

Acute kidney failure a sudden decline in
renal function, usually marked by
 Decreased glomerular filtration rate (GFR),
 Increased concentrations of blood urea
nitrogen (BUN; azotemia) and creatinine;
 The urine output is less than 400 ml per
day (oliguria);
 Hyperkalemia (blood potassium level is
normally 3.6 to 5.2 millimoles per liter
(mmol/L)) and
 Sodium retention.

 Acute kidney failure is most common in
people who are already hospitalized/
particularly in Critically ill people who need
intensive care.

ETIOLOGY AND CATEGORIES OF
ACUTE RENAL FAILURE

RISK FACTORS
Acute kidney failure almost always occurs in
connection with another medical condition
or event. Conditions that increase risk of
acute kidney failure include:
 Being hospitalized, especially for a serious
condition that requires intensive care
 Advanced age

 Blockages in the blood vessels in arms
or legs (peripheral artery disease)
 Diabetes
 High blood pressure
 Heart failure
 Kidney diseases
 Liver disease

PATHOPHYSIOLOGY
In response to renal injury, there is
thought to be an increase in intra-
glomerular pressure with glomerular
hypertrophy, as the kidney attempts
to adapt to nephron loss to maintain
constant glomerular filtration
Failure of renal circulation and
glomerular or tubular dysfunction
Damaged tubules cannot conserve
sodium normally which activates
rennin angiotensin– aldosterone system
Pathogenesis of acute renal failure is not clear:

Sodium and fluid retention
which leads to edema
Reduced blood flow to
kidney due to renal
vasoconstriction
Sudden and complete loss of
kidney function

Oliguria
Increased serum creatinine, BUN
level and retention of other
metabolic waste
Increased circulatory overload
and sodium retention
ACUTE RENAL
FAILURE

1. Onset or Initiation Phase
 It marks the time from the onset of
injury till the death of a person. ARF
begins with the underlying clinical condition
leading to tubular necrosis, for example
haemorrhage, which reduces blood
volume.
 This period lasts from hours to days only
but can cause irreversible damage

2. Oliguric Phase
 This phase starts when urinary volume less
than 30 ml to 400 ml/ 24 hours. A
persistent decrease in GFR and tubular
necrosis characterizes this phase.
 This phase of acute renal failure lasts
for 7-14 days but does a lot of damage
to the walls and membranes of the
kidney.

 The period of oliguria accompanied by a
rise in the urea, creatinine, uric acid,
organic acid and intracellular cations
(potassium and magnesium).

3. Diuresis Phase
 Diuresis phase is marked by increased
urine secretion of more than 400 ml/
24 hours. Renal function of the kidney
improves quickly the fifteen to twenty five
days of this phase.
 The patient is closely monitored for
dehydration during this phase; if
dehydration occurs, the uremic symptoms
are likely to increase.

4. Recovery Phase
 It begins with the recovery of the tubular
function to such an extent that BUN
and serum creatinine stabilizes.
 Improvement in renal function may
continue over 3 to 12 months and
more nephrons regain function

DARK COLORED
URINE
Foamy or bubbly
urine and getting
up at night to
urinate

 Skin and mucous membrane are dry
from dehydration
 Azotemia :- is a medical condition
characterized by abnormally high levels of
nitrogen-containing compounds (such as
urea, creatinine, various body waste
compounds, and other nitrogen-rich
compounds) in the blood.
 Oliguria or anuria: Less than 30cc
(30ml) an hour urine output despite
replacement.

 Edema or Fluid retention, causing
swelling in legs, ankles or feet
 Hypertension and Rapid heart rate
 Metabolic acidosis:- is a condition that
occurs when the body produces excessive
quantities of acid or when the kidneys are not
removing enough acid from the body.

 Anemia
 Increased susceptibility to secondary infection
 Fluid and electrolyte imbalance
 Gastrointestinal System: Anorexia,
nausea, vomiting, diarrhea or constipation,
dry mucous membrane, abdominal pain and
may have the odor of urine

DIAGNOSTIC EVALUATIONS
 Blood tests: elevated blood urea nitrogen
(BUN), serum creatinine, and potassium level
(hyperkalemia); decreased bicarbonate level,
hematocrit and hemoglobin levels; and low
blood pH.
 Levels of BUN and creatinine are high in
kidney failure. This is called azotemia.
 Electrolyte levels in the blood may be
abnormally high or low because of improper
filtering.

 Urine tests: Analyzing a sample of urine, a
procedure called urinalysis, may reveal
abnormalities that suggest kidney failure.
 The amount of urine excrete in one day
may help doctor determine the cause of
kidney failure.
 Urine studies shows proteinuria,
hematuria, and decreased specific
gravity.
 Urine chemistry shows decreased amount
of sodium (below 20 mEq/L) in urine
and high potassium level.

Imaging tests:
 The diagnosis of ARF is also supported by
ultrasonography, plain films of the
abdomen, KUB radiography, renal scan,
pyelography, computerized tomography.

Kidney Biopsy:
 In certain situations, doctor may
recommend a kidney biopsy to remove a
small sample of kidney tissue for laboratory
testing.
 To remove a sample of kidney tissue, doctor
may insert a thin needle through skin and
into kidney.

MANAGEMENT
 Treatment for acute kidney failure involves
identifying the illness or injury that originally
damaged kidneys.
 Once the cause is found, the goal of
treatment is to correct or treat the cause
of kidney failure, restore kidney function and
prevent fluid and waste from building up in
the body while the kidneys heal.

A. Pharmacologic Therapy
 Drugs are used to reduce the blood pressure
(antihypertensive); diuretics (drugs that
increase urine output) are used.
 Low dose dopamine (1-3g/kg) is often used
to dilate the renal arteries through stimulation
of dopaminergic receptors.
 Diuretic therapy with furosemide or mannitol
may be used for management of fluid volume
status.

 Calcium or glucose/insulin will be given
through a vein to help avoid dangerous
increases in blood potassium levels.
 Administer intravenous sodium
bicarbonate for more severe hyperkalemic
symptoms and for the correction of acidosis
and elevated phosphate level.

 Antibiotics may be needed to treat
associated infections (predominantly only
antibiotics excreted by the liver are used if
there is no liver disease (erythromycin,
azithromycin, chloramphenicol).
 Administer anticonvulsants
(levetiracetam) for seizures (excessive and
abnormal brain cell activity), antiemetics
(drugs that prevent vomiting) for nausea,
laxatives for constipation and vitamin
supplements

B. FLUID AND ELECTROLYTE
REPLACEMENT
 Intravenous solutions must be carefully
selected according to the patient’s fluid and
electrolyte status.
 Treat hyperkalemia (high potassium) with
insulin, calcium gluconate, Sodium
polystyrene sulfonate or dialysis.

 Replace lost fluids, such as water, blood, and
plasma, and restore blood flow to the kidneys
in cases of prerenal ARF caused by
dehydration or blood loss, for example,
kidney function may quickly return to
normal after fluid and blood levels are
corrected.

C. Nutritional Therapy
 Proper nutrition is crucial in the management
of acute renal failure. A high calorie diet
that’s low in protein, sodium and potassium is
usually prescribed to meet the metabolic
needs of patient in renal failure.
 Potassium intake is usually restricted to
40 to 60mEq/day and sodium is usually
restricted to 2g/day.
 Low-potassium foods include apples,
cabbage, carrots, green beans, grapes and
strawberries.

NURSING MANAGEMENT
 ASSESSMENT:-

NURSING DIAGNOSIS
1. Fluid volume excess related to decreased
glomerular filtration rate, decreased urine
output and sodium retention as evidenced
by weight gain, edema, intake greater than
output, changes in urine specific gravity,
jugular vein distention and shortness of
breath; orthopnea.
2. Risk for decreased cardiac output related to
fluid overload, fluid shifts, fluid deficit
(excessive losses), and electrolyte imbalance
(potassium, calcium),severe acidosis.

3. Imbalanced Nutrition: Less Than Body
Requirements related to protein catabolism;
dietary restrictions to reduce nitrogenous
waste products, increased metabolic needs,
anorexia, nausea, vomiting, dietary restriction
and malnutrition associated with renal failure
as evidenced by weakness and weight
changes.
4. Risk for infection related to depression of
immunologic defenses (secondary to uremia),
invasive procedures/ devices and changes in
dietary intake/malnutrition

5. Risk for deficient fluid volume related to
excessive loss of fluid (diuretic phase of ARF,
with rising urinary volume and delayed return
of tubular re- absorption capabilities)

Chronic kidney disease (CKD), also
known as chronic renal disease, is a
rapidly progressive deterioration or loss
of renal function in which the body’s
ability to maintain metabolic and fluid
and electrolyte balance fails, resulting in
uremia or azotemia over a period of
months or years.

This is characterized by a slow, insidious,
and irreversible impairment of renal
excretory and regulatory function.
The final stage of chronic kidney disease
is called endstage renal disease (ESRD).

Chronic glomerulonephritis (inflammation of
the glomeruli)
Long term infection such as chronic pyelo-
nephritis, and tuberculosis
Nephrotoxic agents: Long term aminoglycoside
therapy
Autoimmune disorders (such as systemic lupus
erythematosus and scleroderma)
Kidney stones and infection

Due to any etiological factors renal
functions declines
Nephron damage is progressive;
damage nephron cannot function and do
not recover
Decreased GFR
Remaining nephrons undergo changes
to compensate for those damaged
nephrons

Compensatory excretion
continues as GFR diminishes
Filtration of more concentrated blood
by the remaining nephrons
Damage of nephron results in
hypertrophy
Urine may contain abnormal
amount of protein, RBCs, WBCs

Increased serum creatinine,
BUN, urea and other
nitrogenous waste in blood
Further, damage of nephron
80-90%
CHRONIC RENAL
FAILURE

1. REDUCED RENAL RESERVE:
Chronic renal failure is a progressive
disease process.In the early,or silent,
stage the patient is usually without
symptoms,even though up to 50
percent of nephron function may have
been lost.This stage is often not
diagnosed.

2. RENAL INSUFFICIENCY:
 The renal insufficiency stage occurs when
the patient has lost 75 percent of nephron
function and some signs of mild renal failure
are present.
 Anemia and the inability to concentrate
urine may occur. The BUN and creatinine
levels are slightly elevated. These patients
are at risk for further damage caused by
infection,dehydration, drugs,etc.

The goal of care is to prevent further
damage if possible by good control of
blood sugar levels and blood pressure.

3. END-STAGE RENAL DISEASE:
 ESRD occurs when 90 percent of the nephrons are lost.
Patients at this stage experience chronic and persistent
abnormal kidney function. The BUN and creatinine
levels are always elevated.
 These patients may make urine but not filter out the
waste products, or urine production may cease.
Dialysis or a kidney transplant is required to survive.
Uremia (urea in the blood) is present in chronic renal
failure.

Patients eventually develop problems in
all body systems.If left untreated,the
patient with uremia dies,often within
weeks

Uremic symptoms can affect every organ
system, most noticeably the following:
NEUROLOGICAL SYSTEM:
 Cognitive impairment,
 Personality change,
 Asterixis ( (tremer) motor disturbance that
affects groups of muscles), seizures (rare),
confusion,
 Inability to concentrate, disorientation,
 Burning of soles of feet

GASTROINTESTINAL SYSTEM –
Nausea,vomiting,
Food distaste,
Ammonia odor to breath,
Mouth ulcerations and bleeding,
Constipation or diarrhea and
Bleeding from gastrointestinal tract.

BLOOD-FORMING SYSTEM :-
Anemia due to erythropoietin deficiency
PULMONARY SYSTEM:-
Fluid in the lungs with breathing
difficulties,
Thick sputum,
Uremic pneumonitis (inflammation of lung
tissue),
Pleuritic pain; shortness of breath

CARDIOVASCULAR SYSTEM:-
Chest pain due to inflammation of the sac
surrounding the heart (pericarditis) and
pericardial effusion (fluid accumulation
around the heart),
Hypertension,
Pitting edema,
Hyperkalemia and hyperlipidemia.

SKIN:-
Generalized itching (pruritus),
Dry,
Thin,brittle nails, and thin hairs.

Other Symptoms –
General ill feeling and fatigue
Weakness
Oliguria
Headache
Bone pain
Low level of sexual interest

CBC
IMAGING STUDIES:-
 Imaging tests (such as CT or ultrasound) may be
recommended to determine if there are any
obstructions (blockages) of the urinary tract,
kidney stones, or other abnormalities.
RENAL BIOPSY:-
 In a renal biopsy, a small piece of kidney tissue is
removed and analyzed. The biopsy helps to
identify abnormalities in kidney tissue that may
be the cause of renal failure

Treatment of chronic renal failure may
include dietary therapy such as a low
protein diet to limit the accumulation of
end products of protein metabolism that
the kidneys cannot excrete.
For patients on continuous peritoneal
dialysis, however a high protein diet is
recommended,

 For some patients, dietary restrictions are
also implemented. Sodium, potassium and
phosphate restrictions, for example, prevent
elevated levels of these minerals and fluid
restrictions help maintain fluid balance.
 Other measures include balanced fluid
intake, and monitoring weight changes, vital
signs, electrolyte balance, and cardiac and
mental status.

To treat hyperkalemia and fluid
imbalances dialysis may be performed.

 Drug therapy is commonly implemented as
well.
 To mobilize fluids that cause edema, loop
diuretics such as furosemide (Lasix) and
cardiac glycosides such as digoxin are used.
 Phosphate binders such as calcium carbonate
(caltrate) or calcium acetate (Phoslo) is
prescribed to treat renal osteodystrophy
(defective bone development) by binding
phosphate and supplementing calcium.

Blood pressure and edema are controlled
with antihypertensive agents.
Antiemetic are used to relieve nausea
and vomiting, ranitidine decrease gastric
irritation.

 Kidney transplant surgery is a procedure of
curing the patient with endstage of renal
disease.
 A kidney transplant is a surgical procedure in
which a kidney is removed from one person
(donor) and placed into the body of a person
suffering from renal failure (recipient), in whom
the transplanted kidney can perform all the
functions which the patient’s own kidneys are
not able to perform.

Assessment:-
 Nurses may find some sign and symptom of
acute renal failure.
 There are many complain from patient related to
his / her condition such as; Anorexia, Nausea,
Vomiting,, Headache, diarrhea or constipation,
Irritability, Restlessness, Lethargy,, Thick
tenaciouse sputum, Urine output less than 400
ml/day for 1 to 2 weeks and then followed by
diuresis (3 to 5 L/day) for 2 to 3 weeks, Weight
gain

Determine if there is a history of cardiac
disease, malignancy, sepsis, or
intercurrent illness.
Determine if patient has been exposed to
potentially nephrotoxic drugs
(antibiotics, N SAIDs, contrast agents,
solvents).

Conduct an ongoing physical
examination for tissue turgor, pallor, and
alteration in mucous membranes, blood
pressure, heart rate changes, pulmonary
edema,and peripheral edema.
Monitor intake and output

 Fluid volume excess related to decreased
glomerular filtration rate or decreased urine
output or sodium retention as evidenced by
weight gain, edema, intake greater than
output,changes in urine specific gravity.
 GOAL:- Maintenance of normal fluid and
electrolyte level and proper body weight
without excess fluid and absence of edema.

Monitor weight daily at time; report gain
of greater than 2 pounds.
Record accurate intake and output. and
sodium levels Include hidden fluids, such
as IV antibiotic additives, liquid
medications, ice chips, and frozen treats.
Measure GI losses and estimate
insensible losses,such as diaphoresis

 Assess skin, face, and dependent areas for
edema. Evaluate degree of edema.
 Administer and restrict fluids, as indicated.
Maintain sodium and fluid restrictions as
ordered.
 Prepare for dialysis as indicated, such as
hemodialysis, peritoneal dialysis (PD), or
continuous renal replacement therapy
(CRRT)

Risk for infection related to depression of
immunologic defenses (secondary to
uraemia), invasive procedures/ devices
and changes in dietary intake /
malnutrition.
GOAL:- Preventing infection

Monitor for signs and symptoms of
infection and report promptly to
physician.
Protect patient from any source of
infection, including infected roommates,
visitors, or nursing staff.
Promote good hand washing by Client
and staff

 Avoid invasive procedures, instrumentation,
and manipulation of indwelling catheters. Use
aseptic technique When caring for IV and
invasive lines. Change site & dressings per
protocol.
 Provide routine catheter care and promote
meticulous perineal care. Keep urinary drainage
system closed and remove indwelling catheter as
soon as possible.
 Encourage deep breathing, coughing, and
frequent position changes

Teach patient and family signs and
symptoms of infection to report to
physician.
Administer antibiotic medications as
prescribed by the physician.
Obtain specimen(s) for culture and
sensitivity and administer appropriate
antibiotics as indicated.

Risk for decreased cardiac output related
to fluid overload, fluid shifts, fluid deficit
(excessive losses), and electrolyte
imbalance (potassium, calcium), severe
acidosis.
GOAL:- Maintaining adequate c a r d i a c
output

 Monitor blood pressure and adequate
cardiac output heart rate at regular
intervals.
 Observe electrocardiogram (ECG) or
telemetry for changes in rhythm;
 Assess colour of skin, mucous
membranes, and nail beds. Note capillary
refill time.
 Maintain bed rest or encourage adequate
rest and provide assistance with care and
desired activities.
 Provide supplemental oxygen if indicated.

 Note occurrence of slow pulse, hypotension,
flushing, nausea/vomiting, and depressed level
of consciousness.
 Investigate reports of muscle cramps,
numbness/ tingling of fingers, with muscle
twitching, hyperreflexia.
 Administer medications as indicated: Inotropic
agents; e.g digoxin (Lanoxin); Calcium
gluconate; Aluminum hydroxide gels
(Amphojel, Basalgel); Sodium bicarbonate or
sodium citrate; Sodium polystyrene sulfonate
(Kayexalate).

Acute renal failure and chronic renal failure

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