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Acute Renal Failure

Chris is a diabetic patient but is not undergoing treatment. He does not buy his maintenance medications because he believes that those could just aggravate his condition. As months passed by, he began noticing changes in his urine output. He began having decreased urine output for a week then was surprised to have an output greater than normal in the following week. He is unusually lethargic and has dry skin. His laboratory results show an increase in creatinine and potassium. His doctor diagnosed him with acute renal failure secondary to diabetes mellitus.

Description


Renal failure results when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions.
  • Acute renal failure (ARF) is a rapid loss of renal function due to damage to the kidneys.
  • Acute renal failure is also known today as acute kidney injury (AKI).
  • It is a problem seen in hospitalized patients and those in outpatient settings.
  • 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.

Pathophysiology


Although the pathogenesis of ARF and oliguria is not always known, many times there is a specific underlying problem.
  • Underlying problems. There are underlying problems that cause the development of ARF such as hypovolemia, hypotension, reduced cardiac output and failure, and obstruction of the kidney.
  • Blood flow. As these underlying problems affect the body, the blood flow to the kidneys reduces.
  • Decreased kidney function. With inadequate blood flow to the kidney, there is impaired kidney function.
  • Failure. If the underlying conditions are not treated and corrected, they can lead to permanent damage of the kidneys.

Statistics and Incidences


Here’s the statistics and incidences for acute renal failure:
  • 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).
  • 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.

Categories


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.

Phases


There are four phases of ARF: initiation, oliguria, diuresis, and recovery.
  • Initiation. The initiation period begins with the initial insult, and ends when oliguria develops.
  • Oliguria. The oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by kidneys.
  • Diuresis. The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover.
  • Recovery. The recovery period signals the improvement of renal function and may take 3 to 12 months.

Causes


The causes of ARF depend on its categories: prerenal, intrarenal, and postrenal.
  • Prerenal. Examples of prerenal causes are volume depletion, impaired cardiac efficiency, and vasodilation.
  • Intrarenal. Examples of intrarenal causes are prolonged renal ischemia, nephrotoxic agents, and infectious processes.
  • Postrenal. An example of postrenal cause is urinary tract obstruction.

Clinical Manifestations


Almost every system of the body is affected with failure of the normal renal regulatory mechanisms.
  • Lethargy. Since waste products cannot be filtered, it slowly accumulates in the different parts of the body.
  • Dryness. The skin and mucous membrane are dry from dehydration.
  • Central nervous system symptoms. This include drowsiness, headache, muscle twitching, and seizures.
  • Increased creatinine. All phases of ARF exhibit an increase in creatinine.

Prevention


Preventing renal failure involves the following:
  • Hydration. Provide adequate hydration to patients at risk for dehydration.
  • Shock. Prevent and treat shock promptly with blood and fluid replacement.
  • Close monitoring. Monitor central venous and arterial pressures and hourly urine output of critically ill patients to detect the onset of renal failure as early as possible.
  • Blood administration. Take precautions to ensure that the appropriate blood is administered to the correct patient in order to avoid severe transfusion reactions.
  • Infections. Prevent and treat infections promptly because they can produce progressive renal damage.
  • Toxic drug effects. To prevent toxic drug effects, closely monitor dosage, duration of use, and blood levels of all medications metabolized or excreted by the kidneys.

Complications


Depending on the duration and severity of ARF, a wide range of potentially life-threatening complications can occur.
  • Metabolic acidosis. Waste products could not be eliminated by the kidneys and they can contribute to metabolic acidosis.
  • Fluid and electrolyte imbalances. Imbalances may occur due to hemorrhage, renal losses, and gastrointestinal losses.

Assessment and Diagnostic Findings


Assessment and diagnosis of a patient with ARF include evaluation for changes in the urine, diagnostic tests that evaluate the kidney contour, and a variety of normal laboratory values. 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.
    • Creatinine is a breakdown product of normal muscle breakdown.
    • Urea is the waste product of breakdown of protein.
    • 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.
    • High potassium (hyperkalemia) is a particular concern.
    • 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.
    • 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.

Medical Management

The objectives of treatment of ARF are to restore normal chemical balance and prevent complications until repair of renal tissue and restoration of renal function can occur.
  • Pharmacologic therapy. Cation-exchange resins or Kayexalate can reduce elevated potassium levels; IV dextrose 50%, insulin, and calcium replacement may be administered to shift potassium back into cells; diuretic agents are often administered to control fluid volume.
  • Nutritional therapy. Replacement of dietary proteins is individualized to provide the maximum benefit and minimize uremic symptoms; likewise, caloric requirements are met with high-carbohydrate meals, because carbohydrates have a protein-sparing effect; foods and fluids containing potassium or phosphorus are restricted; and after diuretic phase, the patient is placed on a high-protein, high-calorie diet.

Nursing Management


The nurse has an important role in caring for the patient with ARF.

Nursing Assessment

Assessment usually focuses on the characteristics of the urine.
  • Assess urine output. Urine output varies from scanty to a normal volume.
  • Assess blood in the urine. Hematuria may be present in patients with ARF.
  • Assess laboratory results. Laboratory results may increase, decrease, or stabilize and these may indicate each phase of ARF.

Nursing Diagnosis

Based on the assessment data, appropriate nursing diagnoses for a patient with ARF include:
  • Electrolyte imbalance related to increased potassium levels.
  • Risk for deficient volume related to increased in urine output.

Nursing Care Planning & Goals

Main Article: 6 Acute Renal Failure Nursing Care Plans

The goals for a patient with ARF are:
  • Improve nutritional intake.
  • Restore fluid balance.
  • Reduce metabolic rate.
  • Promote pulmonary function.
  • Prevent infection.

Nursing Interventions

Nursing interventions are aimed at restoring renal function and reducing potential causes of increased renal injury.
  • Monitor fluid and electrolyte balance. The nurse monitors the patient’s fluid and electrolyte levels and physical indicators of potential complications during all phases pf the disorder.
  • Reducing metabolic rate. Bed rest is encouraged and fever and infection are prevented or treated promptly.
  • Promoting pulmonary function. The patient is assisted to turn, cough, and take deep breaths frequently to prevent atelectasis and respiratory tract infection.
  • Preventing infection. Asepsis is essential with invasive lines and catheters to minimize the risk of infection and increased metabolism.
  • Providing skin care. Bathing the patient with cool water, frequent turning, and keeping the skin clean and well moisturized and keeping the fingernails trimmed to avoid excoriation are often comforting and prevent skin breakdown.
  • Provide safety measures. Patient with CNS involvement may be dizzy or confused.

Evaluation

A successful nursing care plan has achieved the following:
  • Improved nutritional intake.
  • Restored fluid balance.
  • Reduced metabolic rate.
  • Promoted pulmonary function.
  • Prevented infection.

Discharge and Home Care Guidelines

The nurse plays an important role in teaching the patient and family with ARF.
  • Nutrition. A referral to the nutritionist is made because of the dietary changes required.
  • Problems to report. The patient and family must know what problems to report to the healthcare provider.
  • Follow-up examinations. The importance of follow-up examinations and treatment is stressed to the patient and family because of changing physical status and renal functions.

Documentation Guidelines

The focus of documentation in a patient with ARF include:
  • Vital signs.
  • Muscle strength and reflexes.
  • Results of laboratory tests and diagnostic studies.
  • Degree of deficit and current sources of fluid intake.
  • I&O and fluid balance.
  • Plan of care.
  • Teaching plan.
  • Client’s responses to treatment, teaching, and actions performed.
  • Attainment or progress towards the desired outcomes.
  • Modifications to plan of care.
  • Long term needs.

Practice Quiz: Acute Renal Failure


Here’s a 5-item quiz about the study guide. For more questions, visit: Renal Disorders Nursing Management NCLEX Practice Quiz 1 (50 Items)

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1. Acute renal failure caused by parenchymal damage to the glomeruli or kidney tubules results in all of the following except: A. Decreased GFR. B. Increased urine specific gravity. C. Impaired electrolyte balance. D.Impaired electrolyte balance. 2. Oliguria is a clinical sign of ARF that refers daily to a urine output of: A. 1.5L B. 1.0L C. Less than 400ml D. Less than 50ml 3. A fall in CO2-combining power and blood pH indicates what state accompanying renal function? A. Metabolic acidosis. B. Metabolic alkalosis. C. Respiratory acidosis. D. Respiratory alkalosis. 4. Hyperkalemia is a serious electrolyte imbalance that occurs in ARF and results from: A. Protein catabolism. B. Electrolyte shifts in response to metabolic acidosis. C. Tissue breakdown. D. All of the above. 5. Potassium intake can be restricted by eliminating high-potassium foods such as: A. Butter. B. Citrus fruits. C. Cooked white rice D. Salad oil. Answers and Rationale
1. Answer: B. Increased urine specific gravity.
  • B: The urine has a low specific gravity as a result of tubular damage.
  • A: Decreased GFR is a result of ARF.
  • C: Impaired electrolyte balance is a result of ARF.
  • D: Progressive azotemia is a result of ARF.
2. Answer: C. Less than 400ml.
  • C: Oliguria refers to a daily urine output of less than 500ml.
  • A: A daily urine output of less than 1.5L is normal.
  • B: A daily urine output of less than 1.0L is normal.
  • D: A daily urine output of less than 50ml is called anuria.
3. Answer: C. Respiratory acidosis.
  • C: Respiratory acidosis is a fall in CO2-combining power and blood pH.
  • A: Metabolic acidosis is a fall in bicarbonate levels and a decrease in the blood pH.
  • B: Metabolic alkalosis is a fall in bicarbonate levels and an increase in blood pH.
  • D: Respiratory alkalosis is a fall in CO2-combining power and increase in blood pH.
4. Answer: B. Electrolyte shifts in response to metabolic acidosis.
  • B: Hyperkalemia is caused by electrolyte shifts in response to metabolic acidosis.
  • A: Hyperkalemia is not caused by protein catabolism.
  • C: Hyperkalemia is not caused by tissue breakdown.
  • D: Not all of the options cause hyperkalemia.
5. Answer: B. Citrus fruits.
  • B: Citrus fruits have a high potassium content.
  • A: Butter is rich in cholesterol.
  • C: Cooked white rice is rich in carbohydrates.
  • D: Salad oil is rich in sodium.

See Also


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