COLLEGE OF NURSING

CIVIL HOSPITAL
AHMEDABAD

SUBJECT: NURSING
EDUCATION

TOPIC:ACUTE RENAL
FAILURE

SUBMITT
ED TO:
Ms. M. D. PATEL
LECTURER CLASS – I
SENIOR SCALE
COLLEGE OF NURSING

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 SUBMITTED BY:
RONALD THAKOR
F.Y. M.Sc NURSING
COLLEGE OF NURSING

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 RENAL FAILURE
Renal failure results when the kidneys cannot remove the body’s metabolic wastes or perform
their regulatory functions. The substances normally eliminated in the urine accumulate in the
body fluids as a result of impaired renal excretion, leading to a disruption in endocrine and
metabolic functions as well as fluid, electrolyte, and acid–base disturbances. Renal failure is a
systemic disease and is a final common pathway of many different kidney and urinary tract
diseases. Each year, the number of deaths from irreversible renal failure increases (U.S. Renal
Data System, 2001).

ACUTE RENAL FAILURE

Acute renal failure (ARF) is the sudden (hours to days) loss of the kidneys’ ability to clear waste
products and regulate fluid and electrolyte balance. There is a rapid accumulation of toxic wastes
from protein metabolism in the blood (azotemia). In azotemia, the serum urea level (measured by
BUN) and creatinine levels are elevated. Most types of acute renal failure are reversible if
diagnosed and treated early; however, ARF can lead to chronic renal failure. Acute renal failure is
often associated with a urine output of less than 30 mL/hr or 400 mL/day. It may be caused by
hypotension, vascular obstruction, glomerular disease, acute tubular necrosis (ATN) in which the
tubules are damaged after administration of diagnostic contrast media. edema (Box 37.8
Glomerulonephritis Summary). Edema may begin around the eyes (periorbital edema) and face
and progress to the abdomen (ascites), lungs (pleural effusion), and extremities. Flank pain may
be present. Blood urea nitrogen (BUN) and creatinine levels may be elevated. Urinalysis shows
red blood cells, white blood cells, albumin, and casts. The urine is dark or cola colored from old
red blood cells and may be foamy because of proteinuria.

Potential causes of intrarenal or intrinsic

PRERENAL FAILURE

• Volume depletion resulting from:

Hemorrhage Gastrointestinal losses

(vomiting, diarrhea, nasogastric
Renal losses (diuretics, osmotic suction)
diuresis)

• Impaired cardiac efficiency resulting from:

Myocardial infarction Dysrhythmias

Heart failure Cardiogenic shock

• Vasodilation resulting from:

Sepsis

Anaphylaxis Antihypertensive medications or

other medications that cause

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vasodilation

INTRARENAL FAILURE

• Prolonged renal ischemia resulting from:

-Pigment nephropathy -Myoglobinuria (trauma, crush

(associated with the breakdown injuries, burns)
of blood cells containing
pigments that in turn occlude -Hemoglobinuria (transfusion
kidney structures) reaction, hemolytic anemia)

• Nephrotoxic agents such as:

-Aminoglycoside antibiotics -Solvents and chemicals

(gentamicin, tobramycin)
-Radiopaque contrast agents
-Heavy metals (lead, mercury)
(ethylene glycol, carbon
tetrachloride, arsenic)
-Nonsteroidal anti-inflammatory
drugs (NSAIDs)

-Angiotensin-converting enzyme
inhibitors (ACE inhibitors)

• Infectious processes such as:

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-Acute pyelonephritis -Acute glomerulonephritis

POSTRENAL FAILURE

• Urinary tract obstruction, including:

-Calculi (stones) -Strictures

-Tumors -Blood clots

-Benign prostatic hyperplasia

ETIOLOGY

Acute renal failure is often classified as prerenal, intrarenal, or postrenal.

These categories relate to the causes leading to acute renal failure. Each
category is associated with the location of the cause in the kidney.
Understanding the cause can point to the direction of treatment plans
helpful to the patient.

PRERENAL FAILURE

Prerenal (before the kidney) failure is associated with a decrease or

interruption of blood supply to the kidneys. This type of renal failure
accounts for 55% to 60% of all cases of acute renal failure. The causes
may include a decrease in blood pressure as a result of dehydration,
blood loss, shock, or trauma to or blockage in the arteries that carry
blood to the kidneys. When the nephrons receive an inadequate blood
supply, they are unable to make urine and the waste products are not
adequately removed. The use of nonsteroidal anti-inflammatory drugs
(NSAIDs) and cyclooxygenase-2 (COX) inhibitors can also lead to
prerenal failure. These drugs impair the autoregulatory responses of the
kidney by blocking prostaglandin, which is necessary for renal perfusion.
Prerenal failure can be diagnosed by evaluating possible causes. If
dehydration is the cause, then an IV fluid challenge may be given. With
increased IV fluid, more blood flows to the kidneys for filtering, which
increases urine output and waste product filtering. An arteriogram of the
renal arteries is helpful to determine if the blood supply to the kidneys is
decreased or blocked; angioplasty may be used to open the blockage. The
serum creatinine increases and cre-atinine clearance decreases. Urinalysis
may be helpful in determining the cause as well.

INTRARENAL FAILURE

Intrarenal failure (inside the kidney) occurs when there is damage to the
nephrons inside the kidney. The most common causes are ischemia,
reduced blood flow, and toxins. Other causes are from infectious

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processes leading to glomerulonephritis, trauma to the kidney, exposure
to nephrotoxins, allergic reactions to radiographic dyes, and severe
muscle injury, which releases substances that are harmful to the kidneys
(Table 37.4).

A number of substances can be toxic to the kidneys (nephrotoxic) when

they enter the body. Kidney damage is most likely to occur when these
substances enter the body in high concentrations or when there is
preexisting kidney damage for some other reason. Environmental
nephrotoxins, such as insecticides and lead paint, may be ingested by
children.

Many commonly administered medications can be nephrotoxic.

Aminoglycosides are nephrotoxic antibiotics; when they are
administered, blood levels of the drugs are carefully monitored to avoid
toxic levels.

Contrast media used during tests such as intravenous pyelograms and CT

scans can cause kidney damage when the patient is dehydrated or has
preexisting renal damage. The medium can precipitate out in the tubules,
damaging the kidney. It is important for the patient to be adequately
hydrated before and after any diagnostic test using a contrast medium to
decrease the incidence of toxicity.

POSTRENAL FAILURE

Postrenal (after the kidney) failure is associated with an obstruction that

blocks the flow of urine out of the body. Only 5% of cases of acute renal
failure are classified as postrenal. In this case, the blood supply to the
kidneys and nephron function initially may be normal, but urine is unable
to drain out of the kidney, resulting in back-up of urine and impaired
nephron function. Common causes are kidney stones, tumors of the
ureters or bladder, and an enlarged prostate that blocks the flow of urine.

Diagnosis of causes of postrenal failure can be done with x-ray

examination of the kidneys, ureters, and bladder.

Cystoscopy will show presence of tumors, stones, or prostate

enlargement. Renal ultrasound can measure the kidney size, detect
tumors and blockages, and reveal cystic disease. Surgical intervention
may be needed to correct the problem. Therapeutic Interventions Acute
renal failure is treated by relieving the cause. Prevention of permanent
damage is the goal of treatment.

Signs and symptoms are managed as they develop and supportive care is
given. Treatment may include restoring fluid and electrolyte balance,

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discontinuing nephrotoxic drugs that may have caused the problem,
bypassing urinary tract obstructions with catheters, or short-term
continuous renal replacement therapy to filter blood and restore
potassium and other electrolytes to normal. Some symptoms such as
anemia may not have time to develop in the patient with ARF as they do
in CRF. The care of the patient with acute renal failure is similar to care
of the patient with chronic renal failure, as explained in the next section.

PATHOPHYSIOLOGY

In acute renal failure, rapid damage to the kidney causes waste products
to accumulate in the bloodstream, resulting in the symptoms of renal
failure. The patient becomes oliguric, with urine output decreasing to less
than 20 mL/h. Treatment is directed toward correcting the cause,
supporting the patient with dialysis, and prevention of complications that
may lead to permanent damage. Many patients with acute renal failure
recover completely. Approximately 50% of patients with intrarenal ARF
die as a result of complications of infection, pneumonia, or septicemia.
ARF can progress through four stages, with an intrarenal cause taking a
longer recovery time frame since there is actual renal damage. Once an
event causes ARF in the initial phase, symptoms occur in hours to days.

OLIGURIC PHASE.

In the oliguric phase, less than 400 mL of urine in 24 hours is produced.

Fifty percent of those with ARF experience this phase, which occurs

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from 24 hours to 7 days after the initial phase. This phase can last up to 2
weeks to several months. Prognosis for renal recovery is decreased the
longer this phase lasts.

In the oliguric phase, fluid is retained, electrolytes become imbalanced,

and waste products are not excreted as urine output decreases. Signs of
fluid overload are seen. Serum potassium rises while sodium is lost in the
urine, creating a normal or low serum sodium level. The longer thisphase
lasts, the more effects are seen. These may include metabolic acidosis
from reduced hydrogen ion excretion and sodium bicarbonate levels,
increased phosphate and decreased calcium levels, abnormal blood cells
(RBC, WBC, platelets), neurological effects ranging from confusion,
seizures to coma, and finally effects on all body systems as is seen in
CRF (discussed later).

DIURETIC PHASE

As the kidneys begin to be able to again excrete waste products, 1 to 3

L/day of urine is produced. The osmotic diuresis occurs from the
elevated waste products (urea) which the body is attempting to eliminate.
The kidneys are not yet able to concentrate urine and so dehydration and
hypotension are a concern. It is important for the nurse to monitor for
hypovolemia, hyponatremia, and hypotension in this phase. Serum BUN
and creatinine levels are high until the end of this phase, at which time
they begin to return to normal. This phase may last from 1 to 3 weeks.

RECOVERY PHASE. In this final phase, recovery begins as the

glomerular filtration rate rises. Waste product levels (BUN, creatinine
levels) decrease greatly within the first 2 weeks of this phase. However,
recovery can take up to 1 year. Those who do recover usually do so
without complications. Older adults are more at risk for reduced recovery
of renal function. In those who do not recover renal function, chronic
renal failure occurs.

CONTINUOUS RENAL REPLACEMENT THERAPY

(CRRT). CRRT is a therapy to remove fluid and solutes in a controlled,

continuous manner in unstable patients with acute renal failure. Unstable
patients may not be able to tolerate rapid fluid shifts as occurs in
hemodialysis so CRRT provides an alternative therapy that results in less
dramatic fluid shifting. CRRT can be used along with hemodialysis,
which is necessary if severe symptoms of uremia (hyperkalemia) are
present. CRRT is not as complex as hemodialysis and can be done for
more than a month if needed. Temporary vascular access is used with
CRRT.

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During CRRT, a permeable hemofilter is attached to the vascular access.
Blood flows through the hemofilter and excess fluids and solutes move
into a collection bag. The remaining blood returns to the patient via the
venous access.

If desired, replacement fluid and electrolytes can be given through the

vascular access. Monitoring intake and output, fluid and electrolytes,
daily weights, hourly vital signs, and vascular access is important.

Clinical Manifestations

Almost every system of the body is affected when there is failure of the
normal renal regulatory mechanisms. The patient may appear critically ill
and lethargic, with persistent nausea, vomiting, and diarrhea. The skin
and mucous membranes are dry from dehydration, and the breath may
have the odor of urine (uremic fetor). Central nervous system signs and
symptoms include drowsiness, headache, muscle twitching, and seizures.
The effect of ARF are widespread. The major consequences include the
following:

- Fluid and electrolyte imbalances (fluid overload or depletion,

hyperkalemia, hyponatremia, hyperkalemia, hyponatremia,
hypocalcemia and hypermagnesemia)

- Increased susceptibility to secondary infections

- Anemia

- Platelet dysfunction

- Gastrointestinal complications (anorexia, Nausea, Vomiting,

Diarrhoea or constipation, and stomatitis)

- Increased incidence of Pericarditis

- Uremic encephalopathy

- Impaired wound healing

Assessment and Diagnostic Findings

Diagnostic Evaluation for Acute Renal Failure

• Arterial blood gas (ABG) analysis shows metabolic acidosis.

• Blood chemistry shows increased potassium, phosphorus,

magnesium, blood urea nitrogen (BUN) creatinine, and uric acid
levels. Also decreased of calcium, carbon dioxide, and sodium
levels.

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 • Creatinine clearance is low

• Excretory urography shows decreased renal perfusion and

function.

• Glomerular filtration rate (GFR) is 20 - 40 ml/minute (renal

insufficiency), 10 - 20 ml/minute (renal failure), or less than 10
ml/minute (end-stage renal disease).

• Hematology shows decreased hemoglobin (Hb) level, hematocrit

(HCT), and erythrocytes. Also increase of prothrombin time (PT)
and partial thromboplastin time (PTT).

• Urine chemistry shows albuminuria, proteinuria, increase sodium

levels {casts, red blood cells (RBCs), and white blood cells
(WBCs)}, and urine specific gravity greater than 1.025 which
continue fixed at less than 1.010.

CHANGES IN URINE

Urine output varies (scanty to normal volume), hematuria may be

present, and the urine has a low specific gravity (1.010 or less, compared
with a normal value of 1.015 to 1.025). Patients with prerenal azotemia
have a decreased amount of sodium in the

urine (below 20 mEq/L) and normal urinary sediment. Patients with

intrarenal azotemia usually have urinary sodium levels greater than 40
mEq/L with casts and other cellular debris. Urinary casts are
mucoproteins secreted by the renal tubules whenever inflammation is
present.

NURSING MANAGEMENT

Nursing Diagnosis:

1. Deficient fluid volume or Excess fluid volume

2. Imbalanced Nutrition less than body requirements

3. Risk for impaired skin integrity

4. Risk for infection

5. Anxiety

The nurse has an important role in caring for the patient with ARF. In
addition to directing attention to the patient’s primary disorder (which
may be a factor in the development of ARF), the nurse monitors for
complications, participates in emergency treatment of fluid and

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electrolyte imbalances, assesses progress and response to treatment, and
provides physical and emotional support. Additionally, the nurse keeps
family members informed about the patient’s condition, helps them
understand the treatments, and provides psychological support. Although
the development of ARF may be the most serious problem, the nurse
must continue to include in the plan of care those nursing measures
indicated for the primary disorder (eg, burns, shock, trauma, obstruction
of the urinary tract).

MONITORING FLUID AND ELECTROLYTE BALANCE

Because of the serious fluid and electrolyte imbalances that can occur
with ARF, the nurse monitors the patient’s serum electrolyte levels and
physical indicators of these complications during all phases of the
disorder. Hyperkalemia is the most immediate lifethreatening imbalance
seen in ARF. Parenteral fluids, all oral intake, and all medications are
screened carefully to ensure that hidden sources of potassium are not
inadvertently administered or consumed. Intravenous solutions must be
carefully selected according to the patient’s fluid and electrolyte status.
The patient’s cardiac function and musculoskeletal status are monitored
closely for signs of hyperkalemia. The nurse monitors fluid status by
paying careful attention to fluid intake (intravenous medications should
be administered in the smallest volume possible), urine output, apparent
edema, distention of the jugular veins, alterations in heart sounds and
breath sounds, and increasing difficulty in breathing. Accurate daily
weights, as well as intake and output records, are essential. Indicators of
deteriorating fluid and electrolyte status are reported immediately to the
physician, and preparation is made for emergency treatment.
Hyperkalemia is treated with glucose and insulin, calcium gluconate,
cation-exchange resins (Kayexalate), or dialysis. Fluid and other
electrolyte disturbances are often treated with hemodialysis, peritoneal
dialysis, or other continuous renal replacement therapies.

REDUCING METABOLIC RATE

The nurse also directs attention to reducing the patient’s metabolic rate
during the acute stage of renal failure to reduce catabolism and the
subsequent release of potassium and accumulation of endogenous waste
products (urea and creatinine). Bed rest may be indicated to reduce
exertion and the metabolic rate during the most acute stage of the
disorder. Fever and infection, both of which increase the metabolic rate
and catabolism, are prevented or treated promptly.

PROMOTING PULMONARY FUNCTION

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Attention is given to pulmonary function, and the patient is assisted to
turn, cough, and take deep breaths frequently to prevent atelectasis and
respiratory tract infection. Drowsiness and lethargy may prevent the
patient from moving and turning without encouragement and assistance.

PREVENTING INFECTION

Asepsis is essential with invasive lines and catheters to minimize the risk
of infection and increased metabolism. An indwelling urinary catheter is
avoided whenever possible because of the high risk for UTI associated
with its use.

PROVIDING SKIN CARE

The skin may be dry or susceptible to breakdown as a result of edema;

therefore, meticulous skin care is important. Additionally, excoriation
and itching of the skin may result from the deposit of irritating toxins in
the patient’s tissues. Massaging bony prominences, turning the patient
frequently, and bathing the patient with cool water are often comforting
and prevent skin breakdown.

PROVIDING SUPPORT

The patient with ARF requires treatment with hemodialysis, peritoneal

dialysis, or continuous renal replacement therapies to prevent serious
complications (see Chap. 44); the length of time that these treatments are
necessary varies with the cause and extent of damage to the kidneys. The
patient and family need assistance, explanation, and support during this
time. The purpose and rationale of the treatments are explained to the
patient and family by the physician. High levels of anxiety and fear,
however, may necessitate repeated explanation and clarification by the
nurse. The family members may initially be afraid to touch and talk to
the patient during the procedure but should be encouraged and assisted to
do so.

Although many of the nurse’s functions are devoted to the technical

aspects of the procedure, the psychological needs and concerns of the
patient and family cannot be ignored. Continued assessment of the
patient for complications of ARF and of its precipitating cause is
essential.

PREVENTION OF ACUTE RENAL FAILURE:

1. Provide adequate hydration to patients at risk for dehydration: Surgical

patients before, during, and after surgery Patients undergoing intensive
diagnostic studies requiring fluid restriction and contrast agents (eg,
barium enema, intravenous pyelograms), especially elderly patients who

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may not have adequate renal reserve Patients with neoplastic disorders or
disorders of metabolism (ie, gout) and those receiving chemotherapy

2. Prevent and treat shock promptly with blood and fluid replacement.

3. Monitor central venous and arterial pressures and hourly urine output
of critically ill patients to detect the onset of renal failure as early as
possible.

4. Treat hypotension promptly

5. Continually assess renal function (urine output, laboratory values)

when appropriate.

6. Take precautions to ensure that the appropriate blood is administered

to the correct patient in order to avoid severe transfusion reactions, which
can precipitate renal failure.

7. Prevent and treat infections promptly. Infections can produce

progressive renal damage.

8. Pay special attention to wounds, burns, and other precursors of sepsis.

9. Give meticulous care to patients with indwelling catheters to prevent

infections from ascending in the urinary tract. Remove catheters as soon
as possible.

10. To prevent toxic drug effects, closely monitor dosage, duration of

use, and blood levels of all medications metabolized or excreted by the
kidneys.

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