Acute Kidney Failure

Acute Kidney Failure Overview

Acute Kidney Failure Causes
Acute Kidney Failure Symptoms
Exams and Tests
Acute Kidney Failure Treatment
Self-Care at Home
Medical Treatment
Next Steps
Follow-up
Prevention
Outlook
Support Groups and Counseling
Synonyms and Keywords
Authors and Editors
Related kidney failure articles:
Kidney Failure - on WebMD
Kidney Failure - on MedicineNet

Acute Kidney Failure Overview

The kidneys are a pair of small (about the size of your fist) bean-shaped organs that lie on either side of your spine at just below
your lowest ribs. They filter by-products and toxins from your blood and preserve the balance of bodily fluids and electrolytes.

The kidneys excrete these compounds with water to make urine.

They also eliminate excess body water while reabsorbing useful chemicals and allowing waste to pass freely into the
bladder as urine.

They allow a person to consume a variety of foods, drugs, vitamins and supplements, additives, and excess fluids
without worry that toxic by-products will build up to harmful levels.

The kidneys regulate the amount of various substances in the blood and the amount of water in the body.

Blood circulates through the kidneys for filtration.

 As the first step in filtration, the blood passes through the glomeruli, complex structures composed of tiny blood vessels
entwined together. Substances present in the blood are selectively filtered across the outer linings of the tiny blood vessels and
excreted with water as urine or reabsorbed into tube-like structures (tubules) for further filtration.

 The tubules continue filtering blood until all appropriate substances are reabsorbed into the blood and all the waste
products are excreted.

 Once urine leaves your kidney, it travels through long, thin tubular ureters to the bladder and out your urethra during
urination.

 The kidneys also help regulate blood pressure and secrete hormones that contribute to red blood cell production.

Kidney failure occurs when the kidneys partly or completely lose their ability to filter water and waste from the blood.

 The build up of toxic substances normally removed from the body by the kidneys can cause dangerous health problems.

 Acute kidney failure (also referred to as renal failure) happens rapidly.

 Mild kidney dysfunction is often called renal insufficiency.

Acute kidney failure occurs in about 5% of people who are hospitalized for any reason. It is even more common in those receiving
intensive care.

Chronic kidney failure results when a disease slowly destroys your kidneys. Destruction occurs over many years, usually with no
symptoms until the late stage of kidney failure. Progression may be so gradual that symptoms may not occur until kidney function is
less than one-tenth of normal.

Acute Kidney Failure Causes

Causes of acute kidney failure fall into one of the following categories:

Prerenal: Problems affecting the flow of blood before it reaches the kidneys

Postrenal: Problems affecting the movement of urine out of the kidneys

Renal: Problems with the kidney itself that prevent proper filtration of blood or production of
urine

Prerenal failure

Prerenal failure is the most common type of acute renal failure (60%-70% of all cases). The kidneys do
not receive enough blood to filter. Prerenal failure can be caused by the following conditions:

 Dehydration: - From vomiting, diarrhea, water pills, or blood loss

 Disruption of blood flow to the kidneys from a variety of causes:

o Drastic drop in blood pressure from major surgery with blood loss, severe injury or
burns, or infection in the bloodstream (sepsis) causing blood vessels to inappropriately relax

o Blockage or narrowing of a blood vessel carrying blood to the kidneys

o Heart failure or heart attacks causing low blood flow

o Liver failure causing changes in hormones that affect blood flow and pressure to the
kidney

There is no actual damage to the kidneys early in the process with prerenal failure. With appropriate
treatment, the dysfunction usually can be reversed. Prolonged decrease in the blood flow to the kidneys,
for whatever reason, can however cause permanent damage to the kidney tissues.

Postrenal failure

Postrenal failure is sometimes referred to as obstructive renal failure, since it is often caused by
something blocking elimination of urine produced by the kidneys. It is the rarest cause of acute kidney
failure (5%-10% of all cases). This problem can be reversed, unless the obstruction is present long
enough to cause damage to kidney tissue.
 Obstruction of one or both ureters can be caused by the following:

 Kidney stone: usually only on one side

 Cancer of the urinary tract organs or structures near the urinary tract that may obstruct the
outflow of urine

 Medications

Obstruction at the bladder level can be caused by the following:

 Bladder stone

 Enlarged prostate (the most common cause in men)

 Blood clot

 Bladder cancer

 Neurologic disorders of the bladder impairing its ability to contract

Treatment consists of relieving the obstruction. Once the blockage is removed, the kidneys usually
recover in one to two weeks if there is no infection or other problem.

Renal damage

Primary renal damage is the most complicated cause of renal failure (accounts for 25%-40% of cases).
Renal causes of acute kidney failure include those affecting the filtering function of the kidney, those
affecting the blood supply within the kidney, and those affecting the kidney tissue that handles salt and
water processing.

Some kidney problems that can cause kidney failure include:

 Blood vessel diseases

 Blood clot in a vessel in the kidneys

 Injury to kidney tissue and cells

 Glomerulonephritis

 Acute interstitial nephritis

 Acute tubular necrosis

Glomerulonephritis: The glomeruli, the initial filtration system in the kidney, can be damaged by a
variety of diseases, including infections. The resulting inflammation impairs kidney function.

 A common example is strep throat. Streptococcal bacterial infections may damage the glomeruli.
 Glomerular disorder symptoms may include dark-colored urine (like cola or tea) and back pain.

 Other symptoms include producing less urine than usual, blood in the urine, high blood pressure,
and body swelling (retaining water).

 Treatment usually consists of medications and, if kidney function fails significantly, dialysis may
be needed to remove life-threatening waste products that cannot be excreted.

Acute interstitial nephritis: This is a sudden decline in kidney function caused by inflammation of
interstitial kidney tissue which primarily handles salt and water balance rather than the filtering of wastes.

 Medications such as antibiotics, anti-inflammatory medicines (for example, aspirin, ibuprofen),

and water pills (diuretics) are the most common causes.

 Other causes include infections and immune-related diseases such as lupus, leukemia,
lymphoma, and sarcoidosis.

 It is usually reversible if the kidney damage is not severe.

 Treatment consists of withdrawal of offending drugs, treatment of infection, and dialysis in cases
of very low kidney function.

Acute tubular necrosis: The kidney tubules are damaged and do not function normally. Tubular necrosis
is usually the end result from the other causes of acute renal failure. The tubules are delicate structures
that handle much of the kidney's filtration function. When there is necrosis, the cells that form the tubules
become dysfunctional and "die".

 This condition accounts for 90% of cases of primary acute kidney failure.

 Causes include shock (decreased blood supply to the kidneys), drugs (especially antibiotics) and
chemotherapy agents, toxins and poisons, and dyes used in certain kinds of x-rays.

 Some people produce much less urine than usual. Other symptoms of acute tubular necrosis
include tiredness, swelling, lethargy, nausea, vomiting, abdominal pain, loss of appetite, and rash.
Sometimes there are no symptoms.

 Treatment depends on the cause of the damage and may consist of discontinuing problem
medications, replenishing body fluids, and improving blood flow to the kidney. A diuretic may be given
to increase urine production if the total body water level is too high. Medications may be given to
correct blood chemistry imbalances.

 If there is no recovery of the patient's kidneys and these treatments do not sufficiently substitute
for the lost kidney function, the patient will need regular dialysis or may be a candidate for kidney
transplantation.

Acute Kidney Failure Symptoms

The following symptoms may occur with acute kidney failure. Some people have no symptoms, at least in the early stages. The
symptoms may be very subtle.
 Decreased urine production

 Body swelling

 Problems concentrating

 Confusion

 Fatigue

 Lethargy

 Nausea, vomiting

 Diarrhea

 Abdominal pain

 Metallic taste in the mouth

Seizures and coma may occur in very severe acute kidney failure.

Fatigue Causes
What Are Some of the Common Causes of Fatigue?
There are numerous potential causes of fatigue as a major complaint. They range from those that cause poor blood supply to the body's tissues to
illnesses that affect metabolism, from infections and inflammatory diseases to those that cause sleep disturbances. Fatigue is a common side effect of
many medications.
Some common cause of fatigue include:

 metabolic or endocrine disorders (anemia, thyroid, diabetes, etc.);

 infectious diseases (mononucleosis, hepatitis, TB, HIV, flu, etc.);
 heart or lung conditions (heart failure, heart disease, asthma, etc.);
 medications (some antidepressants, some blood pressure medications);
 mental health conditions (depression, anxiety, grief, eating disorders, etc.);
 sleep problems (sleep apnea, insomnia, etc.); and
 a variety of other conditions

Exams and Tests

Many people with acute renal failure notice no symptoms. Even with symptoms, they are nonspecific, meaning they could be caused
by many different conditions. A physical examination typically reveals few, if any, abnormal findings.

Kidney failure is often detected from blood or urine tests. These tests might be ordered because the patient is in the hospital for
another reason, because they don't feel well and can't tell why, or as part of a routine health screening.

 Levels of urea (blood urea nitrogen [BUN]) and creatinine are high in kidney failure of prerenal origin. This is called
azotemia.

 Electrolyte levels in the blood may be abnormally high or low because of improper filtering.

 When the duration and severity of kidney failure is severe, the red blood cell count may be low. This is called anemia.

The amount of urine produced over a period of hours may also be measured for quantity and quality or the amount of wastes being
excreted. When kidney tissue is injured, protein and desirable substances may be inappropriately excreted in the urine. In some
 cases, the amount of urine remaining in the bladder after urination will be measured by inserting a catheter (a thin, rubber tube) that
drains the bladder.

 Urine retained in the bladder after urinating suggests postrenal failure, usually due to prostate enlargement in men.

 The urine may be dark, indicating that creatinine and other substances are concentrated.

 The urine will be examined under a microscope to detect signs of specific kidney problems. Some of these signs include
blood, pus, and solid materials called casts.

 Electrolyte levels in the urine may help pinpoint the exact cause of the kidney failure.

If the diagnosis is not certain after laboratory tests, an ultrasound of the kidneys and bladder may be done. These can help reveal
signs of specific causes of kidney failure.

In some cases, tissue samples of the kidneys are taken (biopsy) to find the cause of the renal failure.

Acute Kidney Failure Treatment

Treatment of acute renal failure depends partly on the cause and extent of the failure. The patient should
be referred to a kidney specialist (nephrologist) for care. The first goal is to pinpoint the exact cause of the
kidney failure, as that will partly dictate the treatment. Secondly, the degree to which accumulating wastes
and water are affecting the body will impact treatment decisions about medications and the need for
dialysis.

Self-Care at Home

Self-treatment of acute kidney failure is not recommended. Kidney failure can be a very serious condition that requires medical care.

 It may be possible to receive some or all treatment at home. Treatment in some cases can be administered by a home
health nurse under the supervision of a healthcare provider.

 In cases in which recovery of kidney function is incomplete, the artificial kidney may be needed to clear excess water and
accumulating wastes. This is done by dialysis, a process by which the blood is cleared of wastes and excess water. Dialysis,
when needed for acute renal failure, is performed at a hospital or dialysis center. Home dialysis may be appropriate in cases in
which kidney failure is permanent and dialysis is needed indefinitely.

Medical Treatment

Treatment is focused on removing the cause of the kidney failure.

Medications and other products the patient ingests will be reviewed. Any that might harm the kidneys will be eliminated or the dose
reduced.

Other treatments will be offered, with the following goals:

 Correct dehydration - Intravenous fluids, with electrolyte replacement if needed

 Fluid restriction - For those types of kidney failure in which excess fluid is not appropriately eliminated by the kidneys

 Increase blood flow to the kidney - Usually related to improving heart function or increasing blood pressure

 Correct chemical (electrolyte) abnormalities - Keeps other body systems working properly
 If the patient's kidneys do not respond to treatment, and adequate kidney function does not return, they will need to undergo
dialysis. Dialysis is done by accessing the blood vessels through the skin (hemodialysis) or by accessing the abdominal cavity
through the lining that encases the abdominal organs (peritoneal dialysis).

 With hemodialysis, the patient is connected to a machine by a tube running from a conduit created surgically between a
large artery and vein. Blood is circulated through the artificial kidney, which removes toxins and wastes. The blood is then
returned to the patient's body.

 Most people require hemodialysis three times per week.

With peritoneal dialysis, wastes and excess water from the bloodstream cross into the abdominal cavity (peritoneal space) and are
eliminated from the body by coursing through a catheter that is surgically implanted (through the skin) into the peritoneal cavity.

Most people with acute kidney failure improve when the cause of the kidney failure is removed or treated and don't require dialysis.
Normal kidney function is usually restored, though in some cases, residual damage only allows partial restoration of the kidney
function. Such patients may not require dialysis but may need medicines to supplement lost kidney function.

Next Steps

Follow-up

The patient's healthcare provider will arrange follow-up visits as needed for the underlying cause of their kidney failure and the
severity of the disease. He or she will monitor the patient's underlying condition and do appropriate lab tests to be sure that the
kidney failure has resolved. Preventive measures may be needed in some situations to prevent the problem from occurring again.

Prevention

Yearly physical exams by a healthcare provider include blood tests and urinalysis to monitor kidney and urinary tract health.

Drink enough fluids to keep the kidneys functioning properly.

Avoid taking substances or medications that can poison or damage kidney tissues. Ask a healthcare provider about substances to
avoid.

Persons at risk for chronic kidney disease may need more frequent testing for kidney function and other problems that occur with
declining kidney function. Difficulties urinating or blood in the urine should prompt a visit to your physician as soon as possible.

Outlook

Recovery from acute kidney failure depends on what caused the disease. If the cause does not stem from damage to kidney tissue
itself, the patient will probably make a full recovery. Partial recovery of function may occur in situations in which the injury does not
completely resolve.

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Pathophysiology of Acute Renal Failure

The interaction of tubular and vascular events result in ARF. The primary cause of ATN is
ischemia. Ischemia for more than two hours results in severe and irreversible damage to the
kidney tubules. Significant reduction in glomular filtration rate (GFR) is a result of (1) ischemia,
(2) activation of the renin-angiotensin system , and (3) tubular obstruction by cellular debris. As
nephrotoxins damage the tubular cells and these cells are lost through necrosis, the tubules
become more permeable. This results in filtrate absorption and a reduction in the nephrons
ability to eliminate waste.
The clinical course of ARF is characterized by the following three phases:

Phase 1. Onset

ARF begins with the underlying clinical condition leading to tubular necrosis, for example
hemorrhage, which reduces blood volume and renal perfusion. If adequate treatment is provided
in this phase then the individual's prognosis is good.

Phase 2. Maintenance

A persistent decrease in GFR and tubular necrosis characterizes this phase. Endothelial cell
necrosis and sloughing lead to tubular obstruction and increased tubular permeability. Because of
this, oliguria is often present during the beginning of this phase. Efficient elimination of
metabolic waste, water, electrolytes, and acids from the body cannot be performed by the kidney
during this phase. Therefore, azotemia, fluid retention, electrolyte imbalance and metabolic
acidosis occurs. The patient is at risk for heart failure and pulmonary edema during this phase
because of the salt and water retention. Immune function is impaired and the patient may be
anemic because of the suppressed erythropoietin secretion by the kidney and toxin-related
shorter RBC life.

Phase 3. Recovery

Renal function of the kidney improves quickly the first five to twenty-five days of this phase. It
begins with the recovery of the GFR and tubular function to such an extent that BUN and serum
creatinine stabilize. Improvement in renal function may continue for up to a year as more and
more nephrons regain function.

Introduction
Acute renal failure (ARF) is an occasional but alarming complication of nephrotic syndrome (NS).
Causes include rapid progression of the original glomerular disease, renal vein thrombosis and
allergic interstitial nephritis (antibiotics, diuretics, NSAIDs). Sometimes, NS and ARF arise
simultaneously following treatment with drugs such as with NSAIDs or, as described in recent years,
foscarnet or interferon‐alpha. In other circumstances, ARF complicates pre‐existing idiopathic NS in
the absence of any of the above conditions, and haemodynamic derangements are suspected. In this
report I will discuss the latter.

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Clinical features
An excellent overview by Smith and Hayslett [1], covering the literature until 1992, describes the
following features in 75 patients with NS and ARF: (i) most patients are elderly (∼60 years of age)
and hypertensive; (ii) postural hypotension is not recorded; (iii) proteinuria is severe and plasma
albumin approximately half the normal level; (iv) two‐thirds are male; (v) most patients exhibit severe
oedema; (vi) the average length of time between the onset of the NS and ARF is 4 weeks; and (vii)
most patients show complete recovery of renal function over an average period of 7 weeks. Earlier,
we reviewed the literature and described roughly similar characteristics [2].

However, this is not the only presentation of ARF with NS. In fact, the presentation can be very
different, as it can also occur early on in the disease, with a very fast occurrence and resolution. This
feature is found more commonly in children and occasionally in (young) adults (see below). This
form of ARF may be reported less often because it is milder in both severity and duration. Protracted
ARF necessitating dialysis and followed by delayed recovery occurs rarely in children [1,2]. However,
one series reported that of 27 children referred for acute dialysis treatment, six (27%) had nephrosis
[3]. Recently, four more such children were reported; in three of these, the dialysis period was only a
few days [4].

Early reports of ARF in adults with NS mentioned hypotension and sometimes overt hypovolemic
shock preceding ARF. It was considered that NS patients were more liable to develop hypotension
and subsequently ARF upon circulatory challenges such as fluid withdrawal, surgery or septicaemia.
However, a thorough review of reported cases could not identify such factors in many cases [1,2].
Indeed, blood pressure was mostly normal or somewhat elevated. Two clinical presentations are
observed in children who develop ARF in the initial phase of NS. In one group blood pressure is low
and classical hypovolemia symptoms (pallor, cold skin, tachycardia, abdominal cramps) are present.
Laboratory examination may show severe haemoconcentration [5]. These symptoms, as well as
oliguria, respond favourably to albumin expansion. In the other group, blood pressure is normal or
high [4], and albumin infusion can be dangerous. Both types are characterized by marked
proteinuria, but their plasma albumin is not necessarily low yet.

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Pathology
Most patients (85%) with ARF and NS have minimal lesions [1]. In 60%, tubulointerstitial changes
compatible with acute tubular necrosis (ATN) are present: rarefaction of proximal tubule cells,
tubular cell necrosis, granular casts, interstitial oedema and slight peritubular infiltration with
mononuclear cells. In 40% no tubular damage is found, although there is considerable interstitial
oedema [1,6]. Jennette and Falk [7] compared 21 patients with minimal lesion NS and ARF (plasma
creatinine >177 μmol/l; average 486 μmol/l) with 50 patients with minimal lesion NS and normal
kidney function. Histological signs of tubular necrosis were present in 71% of the ARF group, but
never in the non‐ARF group. The ARF group also showed more severe signs of arteriolosclerosis
(intimal hyperplasia and hyalinosis), which was considered important for the pathogenesis of the ARF
[1,7]. Biopsies taken from children in whom ARF necessitated dialysis showed similar changes,
compatible with ATN [4]. Renal histology during early, quick resolving ARF is not available.

Previous SectionNext Section

Pathophysiology
In view of the different clinical presentations, ARF in the NS is not a single, uniform
pathophysiological entity. Factors that can be singled out to contribute to the decrease in glomerular
filtration rate (GFR) are a low renal perfusion pressure, a decreased filtration coefficient, high
intratubular pressure, ATN, interstitial nephritis and interstitial oedema.

In the case of overt hypotension, a pre‐renal cause can be suspected. This is encountered particularly
in children with persistent proteinuria that is so severe that blood volume cannot be maintained,
such as in congenital NS. In children with relapsing minimal lesion NS, hypovolemic ARF may be
encountered early during a relapse. The acute start of heavy proteinuria probably causes a
disequilibrium between plasma and interstitial albumin concentrations. However, when plasma
protein drops, proteinuria diminishes, and is often insufficient to remain a threat for hypovolemia as
in congenital NS. We have tried to amend this in children presenting with early relapse of minimal
lesion NS [8]. Half of them had ‘hypovolemic symptoms’. Compared with non‐symptomatic children,
they had stimulated neurohumoral factors and strong tubular sodium reabsorption, and a
suppressed urinary dilution capacity, compatible with the presence of a pre‐renal factor. However,
even in these children renal plasma flow was high, and the decreased GFR thus reflected a decreased
filtration fraction.

In adults, proteinuria is generally not marked enough to endanger the circulation [9]. Relapses of
minimal lesion NS develop more slowly, but may occasionally be acute, as occurs in children. It
cannot be excluded, however, that adults with established NS are more liable to develop ARF if they
suffer from some other complications such as septicaemia or blood loss. Indeed, blood volume that
is normal while recumbent may drop below normal when standing. On the other hand, mobilization
of excess tissue fluid in hypoproteinemic conditions is highly efficient [9]. Excess fluid can mostly be
removed without inducing hypotension or renal failure. However, complete removal of excess fluid
may create an unsteady condition were changes in blood volume cannot be compensated.

Approximately 30% of children [10] and adults [11] with idiopatic NS have a significant decrease in
GFR. This is due to an intrinsic filtration impairment, since filtration fraction is low. Conceivably, ARF
may reflect worsening of this intrinsic problem. However, glomerular changes, i.e. obliteration of
epithelial slit pores as visible with electron microscopy, are not correlated with the reduction in GFR
in humans. Filtration can also be impaired by a high intratubular pressure caused by protein casts
[1,2], but this possibility has received little attention. The following case history illustrates the
possible importance of this factor.
  Is a sudden decline in
renal function, usually marked by increased concentrations of blood urea nitrogen (BUN;
azotemia) and creatinine; oliguria (less than 500 ml of urine in 24 hours); hyperkalemia;
and sodium retention.
 Acute renal failure are classified into following:

1. Prerenal failure – results from conditions that interrupt the renal blood supply;
thereby reducing renal perfusion (hypovolemia, shock, hemorrhage, burns
impaired cardiac output, diuretic therapy).
2. Postrenal failure – results from obstruction of urine flow.
3. Intrarenal failure – results from injury to the kidneys themselves (ischemia,
toxins, immunologic processes, systemic and vascular disorders).

 The disease progresses through three clinically distinct phase which is oliguric-anuric,
diuretic, and recovery, distinguished primarily by changes in urine volume and BUN and
creatinine levels.
 Complication of ARF include dysrhythmias, increased susceptibility to infection,
electrolyte abnormalities, GI bleeding due to stress ulcers, and multiple organ failure.
Untreated ARF can also progress to chronic renal failure, end-stage renal disease, and
death from uremia or related causes.

Assessment:

1. Oliguric-anuric phase: urine volume less than 400 ml per 24 hours; increased in serum
creatinine, urea, uric acid, organic acids, potassium, and magnesium; lasts 3 to 5 days in
infants and children, 10 to 14 days in adolescents and adults.
2. Diuretic phase: begins when urine output exceeds 500 ml per 24 hours, end when BUN
and creatinine levels stop rising; length is availabe.
3. Recovery phase: asymptomatic; last several months to 1 year; some scar tissue may
remain.
 4. In prerenal disease: decreased tissue turgor, dryness of mucous membranes, weight loss,
flat neck veins, hypotension, tachycardia.
5. In postrenal disease: difficulty in voiding, changes in urine flow.
6. In Intrarenal disease: presentation varies; usually have edema, may have fever, skin
rash.
7. Nausea, vomiting, diarrhea, and lethargy may also occur.

Diagnostic Evaluation:

1. Urinalysis shows proteinuria, hematuria, casts. Urine chemistry distinguishes various

forms of ARF(prerenal, postrenal, intrarenal).
2. Serum creatinine and BUN levels are elevated; arterial blood gas (ABG) levels, serum
electrolytes may be abnormal.
3. Renal untrasonography estimates renal size and rules out treatable obstructive uropathy.

Therapeutic and Pharmacologic Interventions:

1. Surgical relief of obstruction may be necessary.

2. Correction of underlying fluid excesses or deficits.
3. Correction and control of biochemical imbalances.
4. Restoration and maintenance of blood pressure through I.V. fluids and vasopressors.
5. Maintenance of adequate nutrition: Low protein diet with supplemental amino acids and
vitamins.
6. Initiation of hemodialysis, peritoneal dialysis, or continuous renal replacement therapy
for patients with progressive azotemia and other life-threatening complications.

Nursing Interventions:

1. Monitor 24-hour urine volume to follow clinical course of the disease.

2. Monitor BUN, creatinine, and electrolyte.
3. Monitor ABG levels as necessary to evaluate acid-base balance.
4. Weigh the patient to provide an index of fluid balance.
5. Measure blood pressure at various times during the day with patients in supine, sitting,
and standing positions.
6. Adjust fluid intake to avoid volume overload and dehydration.
7. Watch for cardiac dysrhythmias and heart failure from hyperkalemia, electrolyte
imbalance, or fluid overload. Have resuscitation equipment available in case of cardiac
arrest.
8. Watch for urinary tract infection, and remove bladder catheter as soon as possible.
9. Employ intensive pulmonary hygiene because incidence of pulmonary edema and
infection is high.
10. Provide meticulous wound care.
11. Offer high-carbohydrate feedings because carbohydrates have a greater protein-sparing
power and provide additional calories.
12. Institute seizure precautions. Provide padded side rails and have airway and suction
equipment at the bedside.
 13. Encourage and assist the patient to turn and move because drowsiness and lethargy may
reduce activity.
14. Explain that the patient may experience residual defects in kidney function for a long
time after acute illness.
15. Encourage the patient to report routine urinalysis and follow-up examinations.
16. Recommend resuming activity gradually because muscle weakness will be present from
excessive catabolism.

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