ACUTE RENAL FAILURE

Acute kidney injury (AKI), previously called acute renal failure (ARF),[1] is a rapid loss of
kidney function. Its causes are numerous and include low blood volume, exposure to toxins, and
prostate enlargement. AKI is diagnosed on the basis of clinical history, such as decreased urine
production, and characteristic laboratory findings, such as elevated blood urea nitrogen and
creatinine. Depending on its severity, AKI may lead to a number of complications, including
metabolic acidosis, high potassium levels, changes in body fluid balance, and effects to other
organ systems. Management includes supportive care, such as renal replacement therapy, as well
as treatment of the underlying disorder.

Etiology of Acute Renal Failure

Prerenal Causes

Any condition that significantly reduces renal perfusion pressure and causes a decreased
glomerular filtration rate and azotemia may cause prerenal kidney failure. Clinical conditions
that may result in prerenal kidney failure include but are not limited to: extracellular fluid losses
secondary to burns, prolonged vasoconstriction (hypertension), and reduced cardiac output as
seen in patients with shock syndrome or congestive heart failure. If prerenal failure is identified
early and treated correctly, the kidney dysfunction may be reversible. If the underlying cause
continues to affect renal perfusion, it may lead to ischemic damage to the nephron and acute
tubular necrosis (ATN).

Renal Causes

Actual damage to the nephrons and renal parenchyma characterize intrarenal failure. Clinical
conditions that result in intrarenal damage can be categorized under kidney disease or acute
tubular necrosis. ATN is a common type of acute renal failure in the critically ill patient. The use
of nephrotoxic drugs (streptomycin, penicillin, and amphotericin) in older patients or in
individuals with underlying renal insufficiency place patients at a higher risk of developing
ATN. The risk for ATN is also higher in patients with prolonged prerenal factors. ATN is a
potentially reversible type of renal failure but it may take weeks or months before adequate renal
function returns.

Post-renal Causes

Post-renal failure is caused by clinical conditions that cause obstruction to urine flow. Any
problem that stops the excretion of urine may cause this type of ARF. Common conditions
associated with post-renal failure are tumors, benign prostatic hypertrophy, kidney stones and
bladder neck obstruction. If post-renal failure is untreated it may result in actual nephron damage
and intrarenal failure.
PATHOPHYSIOLOGY
 SYMPTOMS

 Swelling, especially of the legs and feet.

 Little or no urine output.
 Thirst and a dry mouth.
 Rapid heart rate.
 Feeling dizzy when you stand up.
 Loss of appetite, nausea, and vomiting.
 Feeling confused, anxious and restless, or sleepy.
 Pain on one side of the back, just below the rib cage and above the waist (flank pain).
The symptoms can help your doctor find out what type of kidney failure is present.

 Severe dehydration, a common cause of prerenal acute renal failure, may cause extreme
thirst, lightheadedness or faintness, and a weak, rapid pulse.
 A blockage in the urinary tract, which causes postrenal acute renal failure, may cause
pain in the side or lower back, blood in the urine (hematuria), or reduced urine output (oliguria).

Signs and symptoms of acute kidney failure may include:

 Decreased urine output, although occasionally urine output remains normal

 Fluid retention, causing swelling in your legs, ankles or feet
 Drowsiness
 Shortness of breath
 Fatigue
 Confusion
 Nausea
 Seizures or coma in severe cases
 Chest pain or pressure
The phase of renal failure

Onset Phase:
 Mild reduction in normal daily urine output
 Mild lethargy
 Mild malaise

Oliguric/Anuric Phase:
 24 hour urine total 400 ml or less
 Listlessness/fatigue
 Confusion or altered LOC (from electrolyte imbalances)
 ECG changes
 Pericardial friction rub
 Fever
 Chest pain
 Crackles upon lung auscultation (due to fluid overload)
 Shortness of breath (due to fluid overload)
 Jugular vein distention (due to fluid overload)
 Periorbital, peripheral or sacral edema (due to fluid overload)
 Ascites (due to fluid overload)
 Capillary fragility as evidenced by easy bruising
 Metabolic acidosis
 Anorexia, nausea, vomiting, diarrhea, constipation
 Uremic frost (pale, yellow, dry or itchy skin)

Diuretic Phase:
 Urine output of 3 to 5 liters in a 24 hour period
 Lethargy or muscle weakness (due to hypokalemia)
 Decreased blood pressure (due to fluid depletion)
 Dry mucous membranes (due to fluid depletion)
 Poor skin turgor and delayed capillary refill (due to fluid depletion)

Recovery Phase:
 Urine output of 1500 to 1800 ml in a 24 hour period
 Stabilization of serum potassium, bicarbonate, BUN and creatinine
 Stabilization of cardiac rhythm and rate
 Reduction in lethargy and shortness of breath
 Reduction in adventitious breath sounds
Medical 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)

 Maintaining adequate intravascular volume
 Maintaining mean arterial pressure
 Discontinuing all nephrotoxic medications (NSAIDS, Gentamycin)
 Eliminating exposure to any other nephrotoxins
 Correcting acidosis (sodium bicarbonate for severe acidosis)
 Correcting hemolytic abnormalities (blood transfusion may be required)
 Correcting all 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)

Dialysis: (a 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 Dialysis – 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 include:

 Hemodynamic stability
  Correction of metabolic acidosis
 Quicker kidney recovery time
 Correction of malnutrition
 Solute removal

Pharmaceutical 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 obstruction.
 
Mannitol – 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)
 Recent infections (especially those that may have been streptococcal in nature)
 Recent episodes of hypotension (from surgery or bleeding)
 Exposure to nephrotoxins or chemical agents
 Recent blood transfusions
 Recent urinary tract disorders
 Toxemia from pregnancy or abortion
 Recent severe muscle damage
 Recent burn trauma
Nursing Responsibilities for CRRT
 Patient family teaching regarding the procedure and equipment
 Monitoring of hemodynamic stability
 Frequent observation of the patients response to fluid removal
 Continuous assessment of vital signs/CVP/PAWP/PAP/Cardiac Output
 Monitoring changes in mental status
 Assessing breath sounds
 Assessing skin turgor/edema
 Monitoring for signs of bleeding/infection
 Monitor specifically 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 replacement fluid).
 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.
Appropriate 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 refill).
 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).
  Decreased cardiac 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).
 Ineffective 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).
 Altered thought processes - (the goal of the patient is to demonstrate improved
cognitive function and be able to participate in activities of daily living).
 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).

MANAGEMENT

1. Volume Status
1. Normal Volume Status
1. Limit Fluid Intake to Urine Output + 300-500 ml/day
2. Limit Sodium Intake to 2 grams per day
2. Volume Overloaded
1. Limit Fluid intake to less than Urine Output
2. Limit Sodium Intake to less than 2 grams per day
3. Consider Loop Diuretic
4. Consider Dialysis
3. Volume Depleted
1. First: Restore Volume with Isotonic saline
2. Next: Limit Intake to Urine Output + 300-500 ml/day
3. Limit sodium intake to 2 grams per day
2. Management: Potassium
1. Hyperkalemia
1. Look for potassium source
2. Eliminate parenteral potassium
3. Reduce Dietary Potassium intake <50 meq per day
4. Consider potassium binding resin (Kayexalate)
5. Aggressive management if Serum Potassium >6 mEq/L
 1. See Hyperkalemia
2. Consider dialysis
2. Normokalemia
1. Limit Potassium intake to 50 meq per day
3. Management: Acid-Base Status
1. Acidemia
1. Look for cause of acidosis (See Arterial Blood Gas)
2. Reduce protein intake to 0.6 g/kg/day
3. Aggressive management if pH <7.2 or bicarbonate <15
1. Consider oral bicarbonate or
2. Consider isotonic IV bicarbonate
3. Consider dialysis
2. Normal pH
1. Limit protein intake to 0.8 g/kg/day
4. Nutritional Intake
1. Maintain 30-50 KCal/Kg/day
5. Management: Uremia
1. Absent
1. Limit protein intake to 0.9 g/kg/day
2. Present
1. Reduce protein to 0.6 g/kg/day
2. Check for Gastrointestinal Bleeding
3. See Dialysis indications below
6. Management: Dialysis Indications
1. Blood Urea Nitrogen >100 mg/dl
2. Serum Creatinine >10
3. Uremic Signs (e.g. Pericarditis, Encephalopathy)
4. Significant bleeding
5. Refractory severe Metabolic Acidosis (pH <7.20)
6. Refractory severe Hyperkalemia (potassium >6.0)
7. Volume Overload
7. Management: Medications
1. Assess medications for toxicity
1. Check drug levels
2. Adjust dosages for Renal Function
2. Stop Nephrotoxic Drugs
1. NSAIDs
2. ACE Inhibitors
3. Aminoglycosides
4. Avoid repeating Radiocontrast Material
5. Avoid high dose Diuretics in critically ill patients
1. Avoid Diuretics in relatively resistant patients
2. Associated with higher mortality
3. Discourages prior strategy to overcome oliguria
4. Mehta (2002) JAMA 288:2547
6. Dopamine does not drop ARF risk in critically ill
1. Kellum (2001) Crit Care Med 29:1526