Acute Renal Failure-3 Nursing CEs

Author: Kristi Hudson RN MSN CCRN

Written: July 22, 2007

Updated: September 11, 2009

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 12^th 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

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

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.

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