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Acute Renal Failure - 3 Nursing CEs
Acute Renal Failure - 3 Nursing CEs
Author: Kristi Hudson RN MSN CCRN

Course Description
This 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 Objectives
Upon completion of this course the student will be able to:
  • Describe the anatomy and physiology of the kidneys.
  • Discuss the 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 replacement therapy.
  • Discuss 3 important nursing diagnoses that will assist with planning patient care.  
Anatomy/Function 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).
  • Compensatory functions (such as assistance with increased/decreased blood pressure).
The 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 arterioles.
  • 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.
Pathophysiology 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 normal
  • 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.
In 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)
  • Increased BUN/Creatinine
  • Electrolyte abnormalities (hyperkalemia, hyperphosphatemia and hypocalcemia)
  • Metabolic acidosis
Diuretic Phase – 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 characterized by:
  • Increase in glomerular filtration rate (GFR)
  • Urine output as high as 2-4 L/day
  • Urine that flows through renal tubules
  • Renal cells that cannot concentrate urine
Increased 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)
  • Chronic renal insufficiency
  • Heart disease (heart failure)
  • Hypertension
  • Advanced age
  • Sepsis
Causes 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:
  • Nephrotoxic incident (chemicals can crystallize)
  • Ischemic incident (decreased renal blood flow)
  • Parenchymal damage
  • Obstruction (due to the release of hemolyzed hemoglobin/myoglobin)
Other Contributing Factors for Developing Acute Renal Failure
Prerenal Causes:
  • Hypotension
  • Hypovolemia (Shock)
  • Decreased cardiac output
  • Dehydration
  • Hepatorenal syndrome
  • Liver failure
  • Atheroembolic disease
  • Renal vein thrombosis
  • Nephrotic syndrome
  • Obstetrical Complications
  • Diabetes type I and type II
Intrarenal Causes:
  • Nephrotoxic episodes
  • Infection
  • Systemic inflammation
  • Injured red blood cells
  • Hemolytic blood transfusion reactions
  • Glomerular diseases (systemic lupus, glomerulonephritits)
  • Rhabdomylolysis
  • Pancreatitis
  • Hypercalcemia
Postrenal Causes:
  • Medication that interferes with normal bladder emptying.
  • Benign prostatic hypertrophy (BPH)
  • Prostate cancer
  • Ovarian cancer
  • Obstruction of a urinary catheter
  • Renal calculi
  • Bladder/pelvic neoplasms
  • Urethral strictures
  • Spinal disease
Medications that can Cause/Aggravate ARF
Cause ARF:
  • Contrast media
  • Diuretics (Furosemide)
  • Heavy metals (mercury, gold lead)
  • Ibuprofen
  • Organic chemicals or solvents
  • Nephrotoxic antibiotics (Gentamycin/Piperacillin)
  • ACE Inhibitors
Aggravate ARF:
  • Amiloride
  • Any medication containing magnesium tetracycline
  • Cisplatin
  • Aspirin
  • Lithium
  • Nonsteriodal anti-inflammatory agents
  • Spironolactone
Probable Cause of ARF Based on Physical Findings
Physical Finding Possible Cause
Elevated Temperature Infection
Hypertension Nephrotic syndrome/malignant hypertension
Hypotension Volume depletion/sepsis
Weight loss or gain Hypovolemia/hypervolemia
Dry mouth Hypovolemia
Jugular vein distention Hypervolemia
Heart (new murmurs) Endocarditis/heart failure
Bladder distention Urethral obstruction
Skin rash Interstitial nephritis/microvascular disease/splinter hemorrhages

Signs 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, vomiting)
  • Bitter or metallic taste in mouth
  • Dry itchy skin
  • Easy bruising
  • Fatigue
  • Seizures/LOC
  • Shortness of breath
  • Arrhythmias
  • Sudden weight gain
Diagnosing 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
Lab Test Prerenal Value Intrarenal Value
Urine Specific Gravity Greater than 1.020 1.010 to 1.020
BUN/Creatinine ratio Greater than 20:1 10-20:1
Urine Osmolality Greater than 500 mOsm/kg 300-500 mOsm/kg
Urine Sodium 10 mEq/L or less 20 mEq/L or more
Urine Sediment (urinalysis) Hyaline casts Granular casts
Fractional excretion of sodium percent (FENa) Less than 1% Greater than 1%

More about BUN and Creatinine
  • Although elevated 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 protein loading.
Imaging Studies/Procedures/Tests
Creatinine 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 limits.

Ultrasound – 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.

Doppler 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.

Nuclear Studies – 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 necrotizing vasculitis.

Renal 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 renal transplant.

The following table represents the selected diagnostic tests and the corresponding disease process that often correspond with a diagnosis of acute renal failure.
 
Diagnostic Testing/Corresponding Disease Process
Diagnostic Test Corresponding Disease Process
Elevated creatine kinase or elevated myoglobin level Rhabdomylolysis
Elevated uric acid level Gouty nephropathy, malignancy, tumor lysis syndrome
Elevated calcium level Malignancy
Monoclonal spike in serum protein Multiple myeloma
Positive HIV test HIV nephropathy
Evidence of hemolysis (on smear) Hemolytic uremic syndrome, thrombocytopenia, systemic lupus or autoimmune diseases.
Increased anion gap with increased osmolar gap Ethylene glycol or methanol poisoning
Eosinophiluria Allergic interstitial nephritis
Positive blood cultures (with murmur) Endocarditis

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 assessment and subsequent interventions should focus around the following physical findings (based on 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 (elevated T waves, depressed ST segment, prolonged PR interval, loss of P wave, wide QRS complex, arrhythmias)
  • S3 or S4 gallop
  • Pericardial friction rub
  • Pulsus paradoxus
  • 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
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).
References
Marini, J., J. MD. Wheeler, A., P. (2009). Critical care medicine: the essentials. (4th ed.). Lippincott, Williams & Wilkins. Philadelphia

Hargrove-Huttel, R., A. (2008). Lippincott’s review series: medical-surgical nursing. (2nd ed.). Lippincott, Williams & Wilkens. Philadelphia

Ackley, B., J & Ladwig, G., B. (2004). Nursing diagnosis handbook: A guide to planning care. (6th ed.). Mosby; St. Louis Missouri

Agraharkar, M., M.D. (2007). Acute renal failure. Retrieved on August 4, 2007 at:
emedicine.com/med/topic1595.htm

Drake-Melander, S. (2004). Case studies in critical care nursing: A guide for application and review (3rd ed.). Saunders, Philadelphia

Handbook of Critical Care. (1995). Acute renal failure. Springhouse Corporation, Philadelphia.

Needham, E., M.D. (2005). Management of acute renal failure. American Family Physician. Vol. 72/No. 9. Retrieved on August 4, 2007 at:
aafp.org/afp/20051101/1739.html

Sinert, R., D.O. (2006). Renal failure: Acute. Retrieved on July 29, 2007 at:
emedicine.com/emerg/topic500.htm

Virtual Renal Center. (2007). Anatomy and physiology of the kidney. Retrieved on July 22, 2007 at:
virtualrenalcentre.com/anatomy.asp?sid=14

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