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Acute-Renal-Failure Lecture Only
Acute-Renal-Failure Lecture Only
(ARF) refers to the abrupt loss of kidney function. Over a period of hours to a few days,
the Glomerular filtration Rate (GFR) falls, accompanied by concomitant rise in serum creatinine and urea
nitrogen.
A healthy adult eating a normal diet needs a minimum daily urine output of approximately 400 ml to excrete the
body’s waste products through the kidneys. An amount lower than this indicates a decreased GFR.
ARF affects approximately 1% of patients on admission to the hospital, 2% to 5% during the hospital stay, 4%
to 15% after cardiopulmonary bypass surgery and 10% of cases acute renal failure occurs in isolation (i.e.
single organ failure).
Acute renal failure (ARF) has four well-defined stages: onset, oliguric or anuric, diuretic, and convalescent.
Treatment depends on stage and severity of renal compromise. ARF can be divided into three major
classifications, depending on site:
Prerenal: Prerenal failure is caused by interference with renal perfusion (e.g., blood volume depletion, volume
shifts [“third-space” sequestration of fluid], or excessive/too-rapid volume expansion), manifested by decreased
glomerular filtration rate (GFR). Disorders that lead to prerenal failure include cardiogenic shock, heart
failure (HF), myocardial infarction (MI), burns, trauma, hemorrhage, septic or anaphylactic shock, and renal
artery obstruction.
Renal (or intrarenal): Intrarenal causes for renal failure are associated with parenchymal changes caused by
ischemia or nephrotoxic substances. Acute tubular necrosis (ATN) accounts for 90% of cases of acute oliguria.
Destruction of tubular epithelial cells results from (1) ischemia/hypoperfusion (similar to prerenal hypoperfusion
except that correction of the causative factor may be followed by continued oliguria for up to 30 days) and/or
(2) direct damage from nephrotoxins.
Postrenal: Postrenal failure occurs as the result of an obstruction in the urinary tract anywhere from the
tubules to the urethral meatus. Obstruction most commonly occurs with stones in the ureters, bladder, or
urethra; however, trauma, edema associated with infection, prostate enlargement, and strictures also cause
postrenal failure.
Statistics
In the United States, the annual incidence of acute renal failure is 100 cases for every million
people. It’s diagnosed in 1% of hospital admissions. Hospital-acquired acute renal failure occurs in
4% of all admitted patients and 20% of patients who are admitted to critical care units.
Each year an estimated 120 Filipinos per million population (PMP) develop kidney failure. This
means that about 10,000 Filipinos need to replace their kidney function each year.
The leading cause of kidney failure in the Philippines is diabetes (41%), according to the Philippine
Renal Disease Registry Annual Report in 2008, followed by an inflammation of the kidneys (24%)
and high blood pressure (22%). Patients were predominantly male (57%) with a mean age of 53
years.
Pathophysiology
Sudden decrease in kidney function, which may or may not be associated with a decrease in urine
output and results in a buildup of toxic wastes, such as urea and creatinine in the blood
Stages
Prerenal
Hypovolemia
Heart failure
Hemorrhage
Excessive diarrhea
Vomiting
Diuresis
Intrarenal
Acute tubular necrosis
Postrenal
Kidney stones
Tumor
Spinal cord injury
Benign Prostatic Hypertrophy
Manifestations
Critical illness and lethargy with persistent nausea, vomiting, and diarrhea.
Skin and mucous membranes are dry.
Central nervous system manifestations: drowsiness, headache, muscle twitching, seizures.
Urine output scanty to normal; urine may be bloody with low specific gravity.
Steady rise in blood urea nitrogen (BUN) may occur depending on degree of catabolism; serum
creatinine values increase with disease progression.
Hyperkalemia may lead to dysrhythmias and cardiac arrest.
Progressive acidosis, increase in serum phosphate concentrations, and low serum calcium levels
may be noted.
Anemia from blood loss due to uremic GI lesions, reduced red blood cell lifespan, and reduced
erythropoietin production.
Complications
The following are the complications of acute renal failure
Volume overload. Due to non-functional excretion system.
Pulmonary edema. Due to fluid overload.
Electrolyte imbalance. Since excess electrolytes are not excreted.
Metabolic acidosis due to dramatic decrease of kidney’s excretory function.
Assessment Methods
Urine output measurements
fluid intake and output
Assessment
ACTIVITY/REST
May report: Fatigue, weakness, malaise
May exhibit: Muscle weakness, loss of tone
CIRCULATION
May exhibit: Hypotension or hypertension (including malignant hypertension, eclampsia/pregnancy-
induced hypertension)
Cardiac dysrhythmias
Weak/thready pulses, orthostatic hypotension (hypovolemia)
Jugular venous distension (JVD), full/bounding pulses (hypervolemia); flat neck veins (diuretic
phase)
Generalized tissue edema (including periorbital area, ankles, sacrum)
Pallor (anemia); bleeding tendencies
ELIMINATION
May report: Change in usual urination pattern: Increased frequency, polyuria (early failure and early
recovery), or decreased frequency/oliguria (later phase)
Dysuria, hesitancy, urgency, and retention (inflammation/obstruction/infection)
Abdominal bloating, diarrhea, or constipation
History of benign prostatic hyperplasia (BPH), or kidney/bladder stones/calculi
May exhibit: Change in urinary color, e.g., absence of color, deep yellow, red, brown, cloudy
Oliguria (may last 12–21 days and occurs in 70% of patients); polyuria (2–6 L/day of urine, lacking
concentration and regulation of waste products)
FOOD/FLUID
May report: Weight gain (edema), weight loss (dehydration)
Nausea, anorexia, heartburn, vomiting
Metallic taste
Use of diuretics
May exhibit: Changes in skin turgor/moisture
Edema (generalized, dependent)
NEUROSENSORY
May report: Headache, blurred vision
Muscle cramps/twitching; “restless leg” syndrome; numbness, tingling
May exhibit: Altered mental state, e.g., decreased attention span, inability to concentrate, loss of
memory, confusion, decreasing level of consciousness (LOC) (azotemia, electrolyte and acid-base
imbalance)
Twitching, muscle fasciculations, seizure activity
PAIN/DISCOMFORT
May report: Flank pain, headache
May exhibit: Guarding/distraction behaviors, restlessness
RESPIRATION
May report: Shortness of breath
May exhibit: Tachypnea, dyspnea, increased rate/depth (Kussmaul’s respiration); ammonia breath
Cough productive of pink-tinged sputum (pulmonary edema)
SAFETY
May report: Recent transfusion reaction
May exhibit: Fever (sepsis, dehydration)
Petechiae, ecchymotic areas on skin
Pruritus, dry skin
TEACHING/LEARNING
May report: Family history of polycystic disease, hereditary nephritis, urinary calculus, malignancy
History of exposure to toxins, e.g., drugs, environmental poisons; substance abuse
Current/recent use of nephrotoxic drugs, e.g., aminoglycoside antibiotics, amphotericin B;
anesthetics; vasodilators; nonsteroidal anti-inflammatory drugs (NSAIDs)
Recent diagnostic testing with radiographic contrast media
Concurrent conditions: Tumors in the urinary tract, Gram-negative sepsis; trauma/crush injuries,
hemorrhage, disseminated intravascular coagulation (DIC), burns, electrocution injury; autoimmune
disorders (e.g., scleroderma, vasculitis), vascular occlusion/surgery, diabetes mellitus (DM),
cardiac/liver failure
Diagnostic Procedures
Urine:
Volume: Usually less than 100 mL/24 hr (anuric phase) or 400 mL/24 hr (oliguric phase), which
occurs within 24–48 hr after renal insult. Nonoliguric (more than 400 mL/24 hr) renal failure also
occurs when renal damage is associated with nephrotoxic agents (e.g., contrast media or
antibiotics).
Color: Dirty, brown sediment indicates presence of RBCs, hemoglobin, myoglobin, porphyrins.
Specific gravity: Less than 1.020 reflects kidney disease, e.g., glomerulonephritis, pyelonephritis
with loss of ability to concentrate; fixed at 1.010 reflects severe renal damage.
pH: Greater than 7 found in urinary tract infections (UTIs), renal tubular necrosis, and chronic renal
failure (CRF).
Osmolality: Less than 350 mOsm/kg is indicative of tubular damage, and urine/serum ratio is often
1:1.
Creatinine (Cr) clearance: Renal function may be significantly decreased before blood urea nitrogen
(BUN) and serum Cr show significant elevation.
Sodium: Usually increased if ATN is cause for ARF, more than 40 mEq/L if kidney is not able to
resorb sodium, although it may be decreased in other causes of prerenal failure.
Fractional sodium (FeNa): Ratio of sodium excreted to total sodium filtered by the kidneys reveals
inability of tubules to reabsorb sodium. Readings of less than 1% indicate prerenal problems, higher
than 1% reflects intrarenal disorders.
Bicarbonate: Elevated if metabolic acidosis is present.
Red blood cells (RBCs): May be present because of infection, stones, trauma, tumor, or altered
glomerular filtration (GF).
Protein: High-grade proteinuria (3–4+) strongly indicates glomerular damage when RBCs and casts
are also present. Low-grade proteinuria (1–2+) and white blood cells (WBCs) may be indicative of
infection or interstitial nephritis. In ATN, proteinuria is usually minimal.
Casts: Usually signal renal disease or infection. Cellular casts with brownish pigments and
numerous renal tubular epithelial cells are diagnostic of ATN. Red casts suggest acute glomerular
nephritis.
Blood:
BUN/Cr: Elevated and usually rise in proportion with ratio of 10:1 or higher.
Complete blood count (CBC): Hemoglobin (Hb) decreased in presence of anemia. RBCs often
decreased because of increased fragility/decreased survival.
Arterial blood gases (ABGs): Metabolic acidosis (pH less than 7.2) may develop because of
decreased renal ability to excrete hydrogen and end products of metabolism. Bicarbonate
decreased.
Sodium: Usually increased, but may vary.
Potassium: Elevated related to retention and cellular shifts (acidosis) or tissue release (red cell
hemolysis).
Chloride, phosphorus, and magnesium: Usually elevated.
Calcium: Decreased.
Serum osmolality: More than 285 mOsm/kg; often equal to urine.
Protein: Decreased serum level may reflect protein loss via urine, fluid shifts, decreased intake, or
decreased synthesis because of lack of essential amino acids.
Radionuclide imaging: May reveal calicectasis, hydronephrosis, narrowing, and delayed filling or
emptying as a cause of ARF.
Kidney, ureter, bladder (KUB) x-ray: Demonstrates size of kidneys/ureters/bladder, presence of
cysts, tumors, ad kidney displacement or obstruction (stones).
Retrograde pyelogram: Outlines abnormalities of renal pelvis and ureters.
Renal arteriogram: Assesses renal circulation and identifies extravascularities, masses.
Voiding cystoureterogram: Shows bladder size, reflux into ureters, retention.
Renal ultrasound: Determines kidney size and presence of masses, cysts, obstruction in upper
urinary tract.
Nonnuclear computed tomography (CT) scan: Cross-sectional view of kidney and urinary tract
detects presence/extent of disease.
Magnetic resonance imaging (MRI): Provides information about soft tissue damage.
Excretory urography (intravenous urogram or pyelogram): Radiopaque contrast concentrates in
urine and facilitates visualization of KUB.
Endourology: Direct visualization may be done of urethra, bladder, ureters, and kidney to diagnose
problems, biopsy, and remove small lesions and/or calculi.
Electrocardiogram (ECG): May be abnormal, reflecting electrolyte and acid-base imbalances.
Urine tests
Urinalysis: Analysis of the urine affords enormous insight into the function of the kidneys.
Twenty–four–hour urine tests: This test requires you to collect all of your urine for 24 consecutive
hours. The urine may be analyzed for protein and waste products (urea nitrogen and creatinine).
The presence of protein in the urine indicates kidney damage. The amount of creatinine and urea
excreted in the urine can be used to calculate the level of kidney function and the glomerular
filtration rate (GFR).
Glomerular filtration rate (GFR): The GFR is a standard means of expressing overall kidney
function. As kidney disease progresses, GFR falls. The normal GFR is about 100–140 mL/min in
men and 85–115 mL/min in women. It decreases in most people with age. The GFR may be
calculated from the amount of waste products in the 24–hour urine or by using special markers
administered intravenously. Patients are divided into five stages of chronic kidney disease based on
their GFR.
Urine Specific Gravity – This is a measure of how concentrated a urine sample is. A concentrated
urine sample would have a specific gravity over 1.030 or 1.040
Blood tests
Creatinine and urea (BUN) in the blood: Blood urea nitrogen and serum creatinine are the most
commonly used blood tests to screen for, and monitor renal disease.
o Creatinine is a breakdown product of normal muscle breakdown.
o Urea is the waste product of breakdown of protein.
o The level of these substances rises in the blood as kidney function worsens.
Electrolyte levels and acid–base balance: Kidney dysfunction causes imbalances in electrolytes,
especially potassium, phosphorus, and calcium.
o High potassium (hyperkalemia) is a particular concern.
o The acid–base balance of the blood is usually disrupted as well.
Decreased production of the active form of vitamin D can cause low levels of calcium in the
blood. Inability to excrete phosphorus by failing kidneys causes its levels in the blood to rise.
Blood cell counts: Because kidney disease disrupts blood cell production and shortens the survival
of red cells, the red blood cell count and hemoglobin may be low (anemia). Some patients may also
have iron deficiency due to blood loss in their gastrointestinal system. Other nutritional deficiencies
may also impair the production of red cells.
Other tests
Ultrasound: Ultrasound is often used in the diagnosis of kidney disease. An ultrasound is a
noninvasive type of test.
o In general, kidneys are shrunken in size in chronic kidney disease, although they may
be normal or even large in size in cases caused by adult polycystic kidney disease,
diabetic nephropathy, and amyloidosis.
Biopsy: A sample of the kidney tissue (biopsy) is sometimes required in cases in which the cause
of the kidney disease is unclear. Usually, a biopsy can be collected with local anesthesia only by
introducing a needle through the skin into the kidney.
Gerontologic Considerations
Half of all patients who develop acute renal failure during hospitalization are older than 60 years.
The etiology of ARF in older clients include prerenal causes, such as dehydration, intrarenal causes
such as nephrotoxic agents, and complications of major surgery.
Thirst suppression, enforced bed rest, lack of access to water and confusion all contribute to elder
patient’s failure to consume adequate fluids.
All medications need to be monitored for potential side effects that could result in damage to the
kidney either through reduced circulation or nephrotoxicity.
Outpatient procedures that require fasting or a bowel preparation may cause dehydration and
therefore require careful monitoring.
Care Settings
Clients with acute renal failure are treated in inpatient medical or surgical care unit.
Nursing Priorities
1. Reestablish or maintain fluid and electrolyte balance.
2. Prevent complications.
3. Provide emotional support for client and significant other (SO).
4. Provide information about disease process, prognosis, and treatment needs.
Nursing Diagnosis
Excess fluid Volume related to compromised regulatory mechanism.
Risk for Decreased Cardiac Output (RF may include: fluid overload, fluid shifts, fluid deficit).
Risk for Imbalanced Nutrition: Less than Body Requirements
Risk for Infection
Deficient Knowledge
Medical Management
I. Promote fluid and Electrolyte and Acid Base Balance
A. Fluid Balance
Monitor fluid volume status
Weight – most accurate indicator (daily)
Input and Output monitoring
Assessment of skin turgor and mucous membrane
fluid restrictions. Amount of fluids to be taken per day (400 ml (insensible fluid loss) + previous days
urine output.
Moisten the lips, give ice chips
Diuretic therapy. Furosemide and Mannitol are often use
B. Electrolyte Balance
1. Hyperkalemia – impaired potassium excretion; indication for dialysis; result from metabolic acidosis
If there is Emergency Hyperkalemia – give 50% dextrose and regular insulin
Can give sodium bicarbonate – for acidosis
Client can be given with Sodium Polystyrene Sulfonate (Kayexalate) – can be given with Sorbitol to
promote evacuation; can be given orally or rectally
Avoid salt substitutes
2. Hyponatremia – restriction of fluids
fluid restrictions
3. Hypocalcemia – decreased activation of Vit. D; hyperphosphatemia
Calcium Carbonate, Calcium Lactate and Vitamin D
Emergency Hypocalcemia – give Calcium Gluconate IV
4. Hyperphosphatemia – impaired excretion of Phosphate by the kidneys in the urine
Phosphate binders – they bind phosphate in the GI tract for excretion
o Aluminum hydroxide –cause constipation so stool softener maybe given
o Aluminum Carbonate –if use for a long period, this can caused dementia
Calcium base phosphate binders – excrete phosphorus but increased Ca.
Calcium Carbonate
Calcium Acetate
5. Hypermagnesemia – impaired excretion of Magnesium by the kidneys
Magnesium – mainly excreted in the urine; seen in antacids or enemas
Diuretic therapy
Avoid magnesium containing antacids or enemas
Emergence Hypermagnesemia – Give Calcium Gluconate
C. Acid Base Balance
Metabolic Acidosis
Impaired hydrogen ion excretion
Increased excretion of bicarbonate
Accumulation of urea, creatinine and uric acid
Hyperkalemia
o Give Sodium Bicarbonate – alkalinic meds
o Give Sodium Lactate – alkalinic meds
o Give Shohl’s solution – treatment of metabolic acidosis; caused stomatitis
II. Reserve Renal Function
Dopamine Hydrochloride – to dilate renal arteries promoting renal perfusion
Control of hypertension with the use of ACE inhibitors, diet and weight control
III. Optimal Nutrition
High CHO diet – to spare CHON metabolism
Low CHON diet but with essential amino acids (50 proteins); 50 mg/day
Serve foods in small amount – because of nausea, anorexia and stomatitis
IV. Improve Body Chemistry
Dialysis
o Hemodialysis
o Peritoneal dialysis
Kidney Transplantation
Nursing Management
Monitor for potential complications.
Assist in emergency treatment of fluid and electrolyte imbalances.
Assess progress and response to treatment; provide physical and emotional support.
Keep family informed about condition and provide support.
Monitoring fluid and Electrolyte Balance
Screen parenteral fluids, all oral intake, and all medications for hidden sources of potassium.
Monitor cardiac function and musculoskeletal status for signs of hyperkalemia.
Pay careful attention to fluid intake (IV 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 dif- ficulty in breathing.
Maintain daily weight and intake and output records.
Report indicators of deteriorating fluid and electrolyte status immediately. Prepare for emergency
treatment of hyperkalemia. Prepare patient for dialysis as indicated to correct fluid and electrolyte
imbalances.
Reducing Metabolic Rate
Reduce exertion and metabolic rate with bed rest.
Prevent or treat fever and infection promptly.
Promoting Pulmonary Function
Assist patient to turn, cough and take deep breaths frequently.
Encourage and assist patient to move and turn.
Preventing Infection
Practice asepsis when working with invasive lines and catheters.
Avoid indwelling catheters if possible.
Providing Skin Care
Perform meticulous skin care
Bath the patient with cool water, turn patient frequently, keep the skin clean and well moisturized
and fingernails trimmed for patient comfort and to prevent skin breakdown.
Discharge Goals
1. Homeostasis achieved.
2. Complications prevented or minimized.
3. Dealing realistically with current situation.
4. Disease process, prognosis, and therapeutic regimen understood.
5. Plan in place to meet needs after discharge.
3. Risk for Imbalanced Nutrition
Nursing Diagnosis
Nutrition: imbalanced, risk for less than body requirements
Risk factors may include
Protein catabolism; dietary restrictions to reduce nitrogenous waste products
Increased metabolic needs
Anorexia, nausea/vomiting; ulcerations of oral mucosa
Possibly evidenced by
Not applicable. A risk diagnosis is not evidenced by signs and symptoms, as the problem has not
occurred and nursing interventions are directed at prevention.
Desired Outcomes
Maintain/regain weight as indicated by individual situation, free of edema.
Consult with dietitian support team. Determines individual calorie and nutrient needs within
the restrictions, and identifies most effective route and
product (oral supplements, enteral or parenteral
Nursing Interventions Rationale
nutrition).
Maintain proper electrolyte balance by strictly Medications and decrease in GFR can cause electrolyte
monitoring levels. imbalances and may further cause renal injury.
Antiemetics: prochlorperazine (Compazine),
Given to relieve N/V and may enhance oral intake.
trimethobenzamide (Tigan).
4. Risk for Infection
Not applicable. A risk diagnosis is not evidenced by signs and symptoms, as the problem has not
occurred and nursing interventions are directed at prevention.
Desired Outcomes
Encourage deep breathing, coughing, frequent Prevents atelectasis and mobilizes secretions to
position changes. reduce risk of pulmonary infections.
Monitor vital signs. Fever (higher than 100.4°F) with increased pulse and
respirations is typical of increased metabolic rate
resulting from inflammatory process, although sepsis
Nursing Interventions Rationale
Excessive loss of fluid (diuretic phase of ARF, with rising urinary volume and delayed return of
tubular reabsorption capabilities)
Possibly evidenced by
Not applicable. A risk diagnosis is not evidenced by signs and symptoms, as the problem has not
occurred and nursing interventions are directed at prevention.
Desired Outcomes
Display I&O near balance; good skin turgor, moist mucous membranes, palpable peripheral pulses,
stable weight and vital signs, electrolytes within normal range.
Measure I&O accurately. Weigh daily. Assessment can help estimate fluid replacement needs.
Calculate insensible fluid losses. Fluid intake should approximate losses through urine,
Nursing Interventions Rationale
Control environmental temperature; limit bed May reduce diaphoresis, which contributes to overall
linens as indicated. fluid losses.
6. Knowledge Deficit
May be related to
Lack of exposure/recall
Information misinterpretation
Unfamiliarity with information resources
Possibly evidenced by
Review disease process, prognosis, and Provides knowledge base from which patient can make
precipitating factors if known. informed choices.
Explain level of renal function after acute Patient may experience residual defects in kidney
episode is over. function, which may or may not be permanent.
Encourage patient to observe characteristics Changes may reflect alterations in renal function and
of urine and amount, frequency of output. need for dialysis.
Establish regular schedule for weighing. Useful tool for monitoring fluid and dietary needs.
Provide emotional support to the patient and To reassure them of the all the procedures that patient
family. may undergo.
Discuss activity restriction and gradual Patient with severe ARF may need to restrict activity
resumption of desired activity. Encourage use and/or may feel weak for an extended period during
of energy-saving, relaxation, and diversional lengthy recovery phase, requiring measures to conserve
Nursing Interventions Rationale
Recommend scheduling activities with Prevents excessive fatigue and conserves energy for
adequate rest periods. healing, tissue regeneration.