course is designed to give an overview of the care and management of
the patient with acute renal failure. Focus will be placed on the
anatomy and physiology of the kidneys, pathophysiology, risk factors,
causes, signs/symptoms and diagnosis of acute renal failure. Medical
management (including types of dialysis) will also be explored. Nursing
assessment and interventions (including nursing responsibilities for
continuous renal replacement therapy) will also be presented. Nursing
diagnoses that will assist the nurse in guiding the plan of care will
be the final focus of this course. Course
completion of this course the student will be able to:
Describe the anatomy
and physiology of the kidneys.
pathophysiologic changes seen with acute renal failure.
List the causes and
risk factors associated with acute renal failure.
State the signs and
symptoms that present with acute renal failure.
Explain how acute renal
failure is diagnosed.
Describe the medical
management for the patient with acute renal failure.
Discuss the appropriate
nursing assessment and interventions when caring for the patient with
acute renal failure.
List 3 nursing
responsibilities when caring for the patient on continuous renal
Discuss 3 important
nursing diagnoses that will assist with planning patient care.
of the Renal System The
renal system is comprised of two kidneys, two ureters, the urinary
bladder and the urethra. Although the renal system is best known for
making and excreting urine, the system actually has many other vital
functions. For example; the renal system filters 1/5 of the cardiac
output at all times (which means that the kidneys filter approximately
1.2 liters of blood every minute). Additionally
the renal system plays a role in the following processes:
Excretion of urea (this
is a by product of protein metabolism).
The kidneys maintain
the pH balance (acid and base) throughout the body.
Regulation of the
amount of water that is retained and excreted by the body.
Assistance with fluid
and electrolyte balance throughout the body.
Production of EPO
hormone (which has a role in the production of red blood cells).
(such as assistance with increased/decreased blood pressure).
Anatomy and Function of the Kidneys:
The kidneys are bean
shaped and sit near the posterior wall of the abdomen (one on each side
of the vertebral column) and are located at the level of the 12th rib.
A normal kidney measures about 10cm (length) – 5cm (width)
– 2.5 cm (thick). The kidneys are protected from trauma and
infection by connective tissue, and fascia (which connect the kidneys
to the abdominal wall). The inner most layer of the kidney is comprised
of adipose tissue which forms a protective cushion for the kidneys.
The kidneys receive
oxygen rich blood from the renal arteries (which come off the abdominal
portion of the aorta); while the renal veins drain through the
abdominal portion of the inferior vena cava. The hilum is the entry and
exit port for the renal vessels and nerves.
The ureters measure
approximately 25-30 cm long and are lined with smooth muscle. The
ureters carry urine to the bladder and are situated in a downward
position to assure that urine can only move in a downward direction.
The outside region of
the kidney (reddish brown in color) is referred to as the renal cortex;
while the inner region (pinkish in color) is referred to as the renal
medulla. The renal cortex houses the nephrons which are considered to
be the “functional” parts of the kidneys.
The nephrons filter the
blood of small molecules and ions (forming urine) while retaining
useful minerals and sugars. In a 24 hour period it is estimated that
the nephrons reclaim 1,300 grams of sodium (NaCl), 400 grams of sodium
bicarbonate (NaHCO3), 180 grams of glucose and 180 liters of water.
The Glomerulus (the
main filter of the nephron system) is a semi-permeable membrane that is
located within Bowman’s capsule and allows water and solutes
(in the form of urine) to be excreted via afferent and efferent
The urinary bladder is
located midline in the abdominal pelvis. The urinary bladder is pyramid
shaped and very muscular. The main function of the urinary bladder is
to collect and store urine until it is excreted through the urethra.
The normal bladder can comfortably hold approximately 500 ml of urine
at any given time. The urethral sphincter which is located at the base
of the bladder consists of ring like muscles that open and close when
stretched bladder receptors signal the brain to do so.
The kidneys (as well as
the lungs) play a vital role in the ph balance by holding on to or
excreting hydrogen ions and Co2.
of Acute Renal Failure Changes
in the renal hemodynamics, nephron structure/function and cellular
metabolism are the pathophysiologic changes that are seen with acute
renal failure. When tubular hydrostatic pressure equals that of
glomerular filtration pressure; a decrease in the production of urine
occurs and kidney filtration ceases. The most common cause of decreased
glomerular filtration is a decline in renal blood flow (RBF). This
decrease in RBF causes tissue ischemia and eventually cell necrosis or
cell death, which produces oxygen free radicals and other enzymes which
exacerbate the problem. The cell damage caused by oxygen free radicals
causes sloughing of cells which in turn block renal tubules and cause a
back leak of glomerular filtrate. The
Four Phases of Acute Renal Failure Onset Phase
– this period represents the time from the onset of injury
through the cell death period. This phase can last from hours to days
and is characterized by:
Renal flow at 25% of
Oxygenation to the
tissue at 25% of normal
Urine output at 30 ml
(or less) per hour
Urine sodium excretion
greater than 40 mEq/L.
this phase only 50% of the patients are noted to be oliguric. With
prompt treatment, irreversible damage can be achieved during this pre
renal failure onset phase. Oliguric/Anuric
Phase – this phase
usually lasts between 8-14 days and is characterized by further damage
to the renal tubular wall and membranes. Other characteristics in the
oliguric-anuric phase include:
Great reduction in the
glomerular filtration rate (GFR)
abnormalities (hyperkalemia, hyperphosphatemia and hypocalcemia)
– this phase occurs when the source of obstruction has been
removed but the residual scarring and edema of the renal tubules
remains. This phase usually lasts and additional 7-14 days and is
Increase in glomerular
filtration rate (GFR)
Urine output as high as
Urine that flows
through renal tubules
Renal cells that cannot
GFR in this phase contributes to the passive loss of electrolytes which
requires the administration of IV crystalloids to maintain hydration. Recovery Period
Phase – The
recovery phase can last from several months to over a year. During this
phase, edema decreases, the renal tubules begin to function adequately
and fluid and electrolyte balance are restored (if damage was
significant, BUN and Creatinine may never return to normal levels). At
this point the GFR has usually returned to 70% to 80% of normal. Risk
Factors for Acute Renal Failure
Diabetes (Type I or II)
Heart disease (heart
of Acute Renal Failure When
reductions in renal blood flow interrupt glomerular pressure; the
result is the development of acute renal failure. The following
categories better explain how acute renal failure develops. Prerenal ARF
– this results from any type of condition
“outside” the kidney that impedes blood flow to the
renal vasculature (and subsequently causes a decrease in perfusion
pressure to the glomerulus and oliguria). Although there is decreased
perfusion to the glomerulus and other nephrons; they continue to
function normally. With prompt correction of the underlying problem;
the kidneys can return to full normal function at this stage. Postrenal ARF
– this is caused by a mechanical back up of urine into the
renal pelvis. As with prerenal failure, prompt removal of the
obstruction will allow the kidneys to return to normal function. Intrarenal ARF
– this results from anything that causes a direct insult to
the kidneys (such as infection, glomerulonephritis, hypertension,
diabetes). Acute tubular necrosis (ATN) is the most common intrarenal
condition and accounts for approximately 75% to 90% of all intrarenal
ARF. With ATN the epithelial layers of the nephrons (at the tubular
portion of the kidneys) become damaged leading to changes in urine
concentration, waste filtration, electrolytes and acid base balance.
ATN most commonly occurs due to one of the following mechanisms:
(chemicals can crystallize)
(decreased renal blood flow)
Obstruction (due to the
release of hemolyzed hemoglobin/myoglobin)
Contributing Factors for Developing Acute Renal Failure Prerenal
and Symptoms of Acute Renal Failure The
signs and symptom that may be experienced with acute renal failure
depend on the phase, the degree of azotemia (abnormal levels of urea
and creatinine) and the degree of metabolic acidosis. The following
signs and symptoms are consistent with acute renal failure:
Decreased urine output
(urine may be pink or reddish in color)
Edema (face, arms,
legs, feet eyes)
Flank pain/Pelvic pain
Poor appetite (nausea,
Bitter or metallic
taste in mouth
Dry itchy skin
Shortness of breath
Sudden weight gain
Acute Renal Failure There
are several lab tests to assist the diagnosis of acute renal failure.
The following table breaks down these lab values as they would be seen
in both prerenal and intrarenal failure. Confirmatory Lab Values
for Acute Renal Failure
than 500 mOsm/kg
mEq/L or less
mEq/L or more
excretion of sodium percent (FENa)
about BUN and Creatinine
levels BUN/Creatinine are considered to be the
“hallmarks” of acute renal failure, the rate of
rise is actually dependant on the degree of renal ischemia and injury
and in regards to BUN; the rate of protein uptake.
BUN may also be
elevated in other conditions not directly related to acute renal
failure such as; GI or mucosal bleeding, steroid treatment therapy or
Clearance Test –
this is believed to be the most accurate test to determine glomerular
filtration rates. This test requires urine collection for a 24 hour
period with normal clearance levels being 95 ml/min to 125 ml/min.
Levels less than 50 ml/min are consistent with intrarenal disease.
Prerenal disease levels vary depending on how long low renal flow has
existed, with postrenal failure levels usually falling within normal
– renal ultrasound
can be effective in determining existing renal failure and/or
obstruction of the urinary collecting system. Kidney detection and
possible obstruction can be difficult to evaluate in obese patients. An
ultrasound that shows “small kidneys” can be a sign
of chronic renal failure.
Studies – doppler
scans can be effective in determining the presence and nature of renal
blood flow. Doppler scans are also useful in detecting thromboembolic
disease, renal vascular disease or hepatorenal syndrome.
radionuclear imaging can be effective in determining renal blood flow
and tubular function. The use of aortorenal angiography can be helpful
in determining renal vascular disease, renal artery stenosis,
atheroembolic disease, atherosclerosis with aortorenal occlusion and/or
Biopsy – renal
biopsy can be effective in diagnosing intrarenal failure, but should
only be done if the result will alter the treatment plan. Renal biopsy
is usually only indicated if there is a prolonged period of renal
failure (without response to treatment) and it will assist with the
development of a long term treatment plan. Renal biopsy is most
commonly used to diagnose acute cellular or humoral rejection post
The following table represents the selected diagnostic tests and the
corresponding disease process that often correspond with a diagnosis of
acute renal failure.
Testing/Corresponding Disease Process
creatine kinase or elevated myoglobin level
uremic syndrome, thrombocytopenia, systemic lupus or autoimmune
anion gap with increased osmolar gap
glycol or methanol poisoning
blood cultures (with murmur)
Management of Acute Renal Failure Medical
management of acute renal failure must focus on first identifying and
treating the cause. Maintaining volume homeostasis and correcting
biochemical abnormalities remain the primary goals of treatment.
Gathering a detailed
patient history (pre-hospital and current)
nephrotoxic medications (NSAIDS, Gentamycin)
Eliminating exposure to
any other nephrotoxins
(sodium bicarbonate for severe acidosis)
abnormalities (blood transfusion may be required)
electrolyte abnormalities (Hyperkalemia is very common)
Strict monitoring on
intake and output/daily weight (Hydration for prerenal failure)
Serial monitoring of
labs (BUN/Creatinine/Osmolality [urine/blood], etc)
Diet and fluid
restrictions/replacement (in a state of oliguria or polyuria)
short term intervention when fluids and electrolytes cannot be managed
by other means).
This may involve the use of any of the following three methods: Peritoneal
peritoneal dialysis is not commonly used as a treatment with acute
renal failure. Although efficient, it is slow process that involves the
transfer of fluid and solutes between the peritoneal cavity and the
peritoneal capillaries. The clearance that occurs with peritoneal
dialysis is thought to be less effective than other types of dialysis. Hemodialysis
– hemodialysis remains the primary method of renal
replacement therapy in patients with acute renal failure. It provides
ultrafiltration for rapid water removal and diffusion for solute
removal. It is indicated for uremia, electrolyte imbalances, fluid
overload and severe metabolic acidosis. Hemodialysis is recommended
when there is a need for quick removal of water and toxins. One concern
with using hemodialysis for critically ill patients with acute renal
failure is that the process requires moving large amounts of fluid out
of the intravascular system which can lead to acute and severe
hypotension (secondary to hypovolemia). Continuous Renal
Replacement Therapy (CRRT)
– CRRT therapy works similarly to hemodialysis except it is a
continuous ongoing process that is less likely to cause acute
hypotension. Other benefits to using CRRT as a method of dialysis
Correction of metabolic
Quicker kidney recovery
Interventions Furosemide (Lasix)
– a loop diuretic that can be used to increase urinary flow
with the intent of flushing out cellular debris that may be causing an
– an osmotic diuretic that can be used to dilate renal
arteries by increasing the synthesis of prostaglandins (resulting in
restored renal flow). Dopamine –
at low doses (1-5 mcg/kg/min), dopamine dilates renal arterioles and
increases renal blood flow and glomerular filtration. Because dopamine
(even at low doses) can cause tachycardia, myocardial ischemia and
arrhythmias it use should be considered carefully. N-acetylcysteine
(Mucomyst) – this
medication can help reverse acute renal failure when the cause is
thought to be from a nephrotoxic source. Nursing
Care and Management Because
acute renal failure often progresses through four phases, it is
important for the nurse to detect which phase of failure the patient is
experiencing in order to develop an appropriate plan of care. A
detailed history should be obtained to help direct nursing care; this
history should include the following information:
History of chronic
illness (hypertension, diabetes)
(especially those that may have been streptococcal in nature)
Recent episodes of
hypotension (from surgery or bleeding)
nephrotoxins or chemical agents
Recent urinary tract
Toxemia from pregnancy
Recent severe muscle
Recent burn trauma
assessment and subsequent interventions should focus around the
following physical findings (based on the phase of renal failure): Onset
Mild reduction in
normal daily urine output
24 hour urine total 400
ml or less
Confusion or altered
LOC (from electrolyte imbalances)
ECG changes (elevated T
waves, depressed ST segment, prolonged PR interval, loss of P wave,
wide QRS complex, arrhythmias)
S3 or S4 gallop
Pericardial friction rub
Crackles upon lung
auscultation (due to fluid overload)
Shortness of breath
(due to fluid overload)
Jugular vein distention
(due to fluid overload)
or sacral edema (due to fluid overload)
Poor skin turgor and
delayed capillary refill (due to fluid depletion)
Urine output of 1500 to
1800 ml in a 24 hour period
Stabilization of serum
potassium, bicarbonate, BUN and creatinine
cardiac rhythm and rate
Reduction in lethargy
and shortness of breath
adventitious breath sounds
Responsibilities for CRRT
Patient family teaching
regarding the procedure and equipment
Frequent observation of
the patients response to fluid removal
of vital signs/CVP/PAWP/PAP/Cardiac Output
Monitoring changes in
Assessing breath sounds
Monitoring for signs of
for hypotension in response to hypovolemia (aggressive fluid
replacement with a crystalloid and/or alteration of the ultrafiltration
rate may be necessary).
Monitoring for fluid
volume overload (requiring a decrease or temporary discontinuation of
Monitor that all
equipment connections are secure (due to the risk for vast hemorrhage
if a break in the system occurs).
Close monitoring of
electrolyte and acid-base imbalances (prompt replacement is required).
Adjusting care based on
the mobility restrictions that occur with CRRT equipment.
Close monitoring of
extremity distal to catheter placement (pulses/perfusion).
Assessment of catheter
insertion site/dressing changes as per policy.
Nursing Diagnosis for Consideration
Alteration in urinary
elimination - (the goal is that the patient is euvolemic and has no
symptoms suggestive of fluid deficit or overload).
Fluid volume deficit -
(the goal is that the patient is euvolemic; with urine output that is
approximately 30 ml/hr and has no symptoms suggestive of fluid deficit
i.e. dry mouth, hypotension, poor skin turgor, delayed capillary
Fluid volume overload -
(the goal is that the patient is euvolemic and has no symptoms
suggestive of fluid overload such i.e. edema, wt. gain, JVD).
Altered nutrition (less
than bodily requirement) - (the goal is that the patient will have
balanced nutrition and fluid balance with weight within normal limits).
Potential for impaired
skin integrity - (the goal is that the patient remains free from
pressure ulcers and dry itchy skin).
Knowledge deficit -
(the goal is that the patient/family has a better understanding of the
disease process and understand the need for follow up care).
output - (the goal for the patient is to have improved clinical
findings based on adequate cardiac output i.e. normal vital signs,
adequate capillary refill, absence of hypotension)
Fear (anxiety) - (the
goal for the patient will have a low level of anxiety and be able to
effectively express concerns and questions regarding care. The patient
will also be able to verbalize symptoms of anxiety and mechanisms for
dealing with these symptoms).
Activity intolerance -
(the goal for the patient is to participate in activities of daily
living without become exhausted).
individual/family coping - (the goal of the patient/family is to be
able to participate in care without becoming overwhelmed. The goal is
also to be able to verbalize where counseling/support can be found i.e.
American Association of Kidney Patients or the National Kidney
Foundation for example).
Body image disturbance
- (the goal of the patient who may require a shunt for hemodialysis is
to state or demonstrate acceptance of this change).
processes - (the goal of the patient is to demonstrate improved
cognitive function and be able to participate in activities of daily
Potential for injury -
(the goal for the patient is to remain injury free and be able to
verbalize and explain methods to prevent injuries and/or falls).
Risk of infection -
(the goal for the patient is to remain free from symptoms of infection
(WBC’s within normal limits) and to be able to state what
symptoms of infection are).
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