Acute Renal Failure

• It is a rapid loss of renal function due to the damage of the kidneys.

• It is a syndrome of varying causation that results in sudden decline in renal function

Pathophysiology:

Prerenal, Intrarenal, Post renal causes

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Hypoperfusion of the kidneys
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Alteration in kidney function
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Decreased glomerular filtration rate
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Retention of fluids and urinary sediments
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Increase in serum concentration of renal substances
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Kidney damage

Categories:
A. Prerenal Azotemia
- The most common cause of acute renal failure; cause is due to renal hypoperfusion:
1. Decrease in intravascular volume
Cause of volume depletion includes:
a. Hemorrhage
b. Gastrointestinal losses
c. Dehydration
d. Excessive diuresis
e. Extravascular space sequestration
f. Pancreatitis
g. Burns
h. Trauma
i. Peritonitis

2. Changes in vascular resistance:

a. Sepsis
b. Anaphylaxis
c. Anesthesia
d. Afterload-reducing drugs
- ACE Inhibitors- prevent efferent renal arteriolar constriction out of proportion to the
afferent arteriole= GFR will decrease
- NSAIDS prevent afferent arteriolar vasodilation by inhibiting prostaglandin-mediated
signals
- Epinephrine, Norepinephrine, dopamine, anesthetic agents and cyclosporine= cause
renal vasoconstriction
e. Renal artery stenosis- causes increased resistance and decreased perfusion

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 3. Low cardiac output- state of low effective renal arterial blood flow
- It is the result of impaired blood flow that leads to hypoperfusion of the kidney and a decrease in
the GFR.
- Causes:
a. Cardiogenic shock
b. CHF
c. Pulmonary embolism
d. Pericardial tamponade

B. Intrarenal/ Intrinsic Renal failure

- It is the result of actual parenchymal damage to the glomeruli or kidney tubules
- Sites of injury are the tubules, interstitium, vasculature and glomeruli

C. Post renal Azotemia

- Least common cause
- It occurs when urinary flow from both kidneys or a single functioning kidney, is obstructed.
- Causes include:
a. Urethral obstruction
b. Bladder dysfunction or obstruction
c. Obstruction of both ureters and renal pelvises
d. Benign Prostatic Hyperplasia- most common in men
e. Anticholinergic drugs
f. Bladder, prostate or cervical cancer
g. Blood clots. Bilateral ureteral stones, urethral stones or stricture and bilateral papillary necrosis-
less common cause
h. Single functioning kidney, obstruction of solitary ureter

Phases of Acute Renal Failure

I. Onset/Initiation
- begins with the initial insult and ends when oliguria develops
II. Oliguric-Anuric phase
- accompanied by an increase in serum concentration of substances usually excreted by the kidneys (urea,
creatinine, uric acid, organic acids and intracellular cations- potassium and magnesium).
- Increased urea reabsoption as GFR falls acutely
- Kidneys will reabsorb salt and water avidly if there is no tubular dysfunction
- Oliguria =urinary output less than 400-500 ml/d
- Hyperkalemia usually develop

* The minimal amount of urine needed to rid the body of normal metabolic products is 400 ml.

*Non-oliguric form of renal failure= with decreased renal function, increasing nitrogen retention, normal
excretion of urine (2L/day or more)= common in patient who were exposed to nephrotoxins, burns,
traumatic injury and use of halogenated anesthetic agents.

III. Diuretic Phase

- Marked by a gradual increase in urine output= signals that the glomerular filtration has started to recover
- Laboratory values stabilize and eventually decrease
- Uremic symptoms may still be present because the renal function may still be abnormal

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 * Closely observe the patient for signs and symptoms of dehydration wherein uremic symptoms may likely
increase.
IV. Recovery phase
- Improvement of renal function; may take 3 to 12 months
- Laboratory values return to normal level but with 1%-3% reduction in the GFR=not clinically significant

Clinical Manifestations
1. Lethargy
2. Prerenal disease- hypovolemia
a. Dehydration- dry skin and mucous membranes
3. Intrinsic or post renal disease- Hypervolemia
a. Hyperkalemia- irritability, abdominal cramping, diarrhea, paresthesia, generalized muscle weakness
(slurred speech, difficulty breathing, paresthesia, paralysis)
b. Arrythmias- Tall, tented or peaked T waves
c. Rales
4. Azotemia
a. Nausea and vomiting
b. Body malaise
c. Altered sensorium
d. Pericardial effusion/ pericardial friction rub
5. CNS
a. Encephalopathic changes- asterixis and confusion
6. Drowsiness
7. Headache
8. Muscle twitching
9. Seizures
10. Non-specific diffuse abdominal pain and ileus
11. Platelet dysfunction- bleeding

Assessment and Diagnostic Findings

• Urine assessment
a. Scanty to normal volume
b. Hematuria may be present
c. Low specific gravity
d. Unconcentrated urine- earliest manifestation of tubular damage
e. Prerenal Azotemia- decreased sodium and normal urinary sediment and other cellular debris
f. Intrarenal Azotemia- increased sodium with urinary casts= may occur from prerenal
azotemia→sodium increases as the kidneys fail and unable to concentrate urine= isothenuria
(presence of urinary sediments)
• Renal UTZ/ CT or MRI- show evidence of anatomic changes
• BUN- increases steadily at a rate dependent on the degree of protein breakdown or catabolism, renal
perfusion and protein intake.
• Serum Creatinine levels- monitor kidney function and disease progression= usually increase with glomerular
damage.
• Electrolyte imbalance
 Hyperkalemia= results from protein catabolism wherein there is a release of cellular
potassium in the body fluids
 Increase phosphate levels

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  Hypocalcemia- due to decreased absorption of calcium from the intestine and as a
compensatory mechanism for the elevated blood phosphate levels
• Metabolic disturbance:
Metabolic acidosis-
- Patient cannot eliminate the daily metabolic load of acid-type substances produced by the
normal metabolic processes
- Renal buffer mechanisms fail.
*Co2 (potential acid combined with H2O) decreased= carbonic acid is decreased
renal compensation
*pH decreased= if bicarbonate and carbonic acid is altered pH will change
• CBC
Anemia – due to reduced erythropoietin production, uremic GI lesions, reduced RBC lifespan and
blood loss from GIT.

Prevention:
1. Obtain a careful history to identify exposure to nephrotoxic agents or environmental toxins.
2. Patients should be monitored closely for changes in the renal function.
Examples of nephrotoxic drugs:
1. Aminoglycosides
2. Gentamysin
3. tobramycin
4. Colistimethate
5. Polymyxin B
6. Amphotericin B
7. Vancomycin
8. Amikacin
9. Cyclosporine
10. NSAIDS
* BUN and serum creatinine levels should be obtained at baseline within 24 hours after initiation of these
medications and at least twice a week while the patient is receiving them.
3. Provide adequate managements depending on its cause to prevent further occurrence of complications

Medical Management:
Objectives of treatment:
1. Restore normal chemical balance
2. Prevent complications until repair of renal tissue and restoration of renal function can occur.
1. Eliminate underlying cause
Prerenal azotemia- Optimize renal perfusion
Postrenal azotemia- Relieve the obstruction
Intrarenal azotemia- Supportive therapy with removal of causative agents, aggressive management of
prerenal and post renal failure and avoidance of associated risk factors.
2. Maintenance of fluid balance based on daily body weight, serial measurements of CVP, serum and urine
concentrations, fluid losses, BP and clinical status of the patient.
a. Fluid replacement- based on actual and insensible fluid losses
b. Assess for fluid excess-
 dyspnea
 tachycardia
 distended neck veins
 crackles- pulmonary edema

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  generalized edema- presacral and pretibial areas
c. Administer medications that will initiate diuresis as ordered:
 mannitol (Osmitrol)
 furosemide (Lasix)
 ethacrynic acid (Edecrin)
d. IV fluids or transfusions of blood products- with prerenal causes
e. Dialysis may be initiated to prevent complications (Hyperkalemia, metabolic acidosis, pericarditis,
pulmonary edema)
Variations:
a. Hemodialysis
- circulates the patient’s blood through a dialyzer to remove waste products and excess
fluid.
b. Peritoneal dialysis
- uses the peritoneal membrane as a semi-permeable membrane to exchange fluids and
solutes.
c. Continuous Renal replacement Therapies (CRRTs)
- Methods used to replace normal kidney function by circulating the patient’s blood
through a hemofilter.

Advantages of Dialysis:
1. To correct biochemical abnormalities
2. Allows liberalization of fluid, protein and sodium intake
3. Diminish bleeding tendencies
4. Promotes wound healing

Pharmacologic Therapy
1. Manage Hyperkalemia promptly
o Kayexalate- orally or retention enema (should be retained for 30-45 minutes to promote potassium
removal then a cleansing enema will be performed to remove remaining medication and prevent
fecal impaction)
o Sorbitol in combination with Kayexalate- to stimulate a diarrhea-type effect to induce water loss in
the GIT
o IV dextrose 50%, insulin and calcium replacement to shift potassium back into the cells
o Albuterol sulfate (ventolin HFA) by nebulizer can lower the plasma concentration.
* Shift of potassium back to the intracellular space is only temporary=dialysis should be done on
emergent basis.
2. Treat severe acidosis and increase in phosphate levels
* The arterial blood gases and serum bicarbonate levels (CO2 combining power) must be monitored to
identify if Sodium bicarbonate therapy or dialysis should be performed.
Phosphate-binding agents (Calcium or lanthanum carbonate)- to decrease absorption of phosphate from the
intestinal tract.

Nutritional therapy
* Weight loss of 0.2 to 0.5 kg (0.5-1 lb) daily= nitrogen balance is negative
* Fluid retention should be suspected if the patient gains or does not lose weight or develops hypertension.
* Nutritional support is based on underlying cause, catabolic response, type and frequency of renal replacement
therapy, comorbidities and nutritional status.

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1. High-protein diet- provide maximum benefit and minimize uremic symptoms.
2. High-carbohydrate meal- to increase caloric requirements; carbohydrates have a protein-sparing effect for growth
and tissue healing
3. Restrict foods and fluids that are high in potassium and phosphorus- bananas, citrus fruits and juices, coffee.

Nursing Management:
1. Monitoring Fluid and Electrolyte Imbalance
- Monitor serum electrolyte levels and physical indicators of complications during all phases of the disorder.
- Parenteral fluids, all oral intake and all medications are screened carefully to ensure that hidden sources of
potassium are not inadvertently administered or consumed.
- Monitor patient’s cardiac function and musculoskeletal status to signs of hyperkalemia.
- MIO and weigh daily accurately

2. Reducing Metabolic Rate

- Bed rest to reduce exertion and metabolic rate during the most acute stage.
- Prevent infection and fever.

3. Promoting Pulmonary Function

- Assist patient to turn, cough and take deep breaths frequently to prevent atelectasis and respiratory tract infection.

4. Prevent Infection
- Asepsis should be thoroughly practiced with handling of invasive lines and catheters to minimize the risk of
infection and increase in metabolism.

5. Providing Skin care

- Meticulous skin care should be performed to prevent breakdown as a result of edema.
- Bath the patient with cool water.
- Frequently turn the patient and keep the skin clean and well-moisturized.

6. Providing Psychosocial Support

- The patient and the family should be given assistance, thorough explanation and support during the lengthy
treatment.