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Acute Kidney Failure

Acute Kidney Failure

Definition

Acute kidney failure (AKF) occurs when there is a sudden reduction in kidney function that results in nitrogenous wastes accumulating in the blood (azotemia).

Description

The kidneys are the body's natural filtration system. They perform the critical task of processing approximately 200 quarts of fluid in the bloodstream every 24 hours. Waste products like urea and toxins, along with excess fluids, are removed from the bloodstream in the form of urine. Kidney (or renal) failure occurs when kidney functioning becomes impaired somehow. Fluids and toxins begin to accumulate in the bloodstream. As fluids build up in the bloodstream, the patient with AKF may become puffy and swollen (edematous) in the face, hands, and feet. Their blood pressure typically begins to rise, and they may experience fatigue and nausea. Often urine output decreases drastically or is not produced at all.

Unlike chronic kidney failure, which is long term and irreversible, acute kidney failure is often a temporary condition. With proper and timely treatment, it can many times be reversed, leaving no permanent or serious damage to the kidneys.

Causes and symptoms

Acute kidney failure appears most frequently as a complication of serious illness, like heart and/or liver failure, serious infection, dehydration, severe burns, and excessive bleeding (hemorrhage). It may also be caused by an obstruction to the urinary tract or as a direct result of kidney disease, injury, or an adverse reaction to medicine. These conditions divide AKF into three main categories: prerenal, postrenal, and intrinsic (inside) conditions.

Prerenal AKF does not damage the kidney, but can cause diminished kidney function and significantly decreased renal (kidney) blood flow. It is the most common type of acute renal failure, and is often the result of:

  • dehydration
  • extracellular fluid (ECF) volume depletion (or other acute fluid loss from the gastrointestinal tract, kidneys, or skin)
  • drugs (NSAIDS, cyclosporine, radiopaque contrast materials, or any substance toxic to the kidneys)
  • hemorrhage
  • septicemia, or sepsis
  • congestive heart failure (CHF)
  • liver failure
  • burns
  • decreased intravascular volume (referred to as third spacing, also found in the presence of pancreatitis, post surgical patients, and patients with a nephrotic syndrome)

Postrenal AKF is the result of an obstruction of some kind somewhere in the urinary tract, often in the bladder or ureters (the tubes leading from the kidney to the bladder). The kidneys compensate to such a degree that one kidney can be completely obstructed and the other will maintain nearly normal kidney function for the body. The conditions that often cause postrenal AKF are:

  • inflammation of the prostate gland in men (prostatitis)
  • enlargement of the prostate gland (benign prostatic hypertrophy)
  • bladder or pelvic tumors
  • kidney stones (calculi)

Intrinsic AKF involves a type of kidney disease or direct injury to the kidneys. This type of AKF accounts for 20-30% of AKF reported among hospitalized patients. Intrinsic AKF can result from:

  • lack of blood supply to the kidneys (ischemia)
  • use of radiocontrast agents in patients with kidney problems
  • drug abuse or overdose
  • long-term use of nephrotoxic medications, like certain pain medicines
  • acute inflammation of the glomeruli, or filters, of the kidney (glomerulonephritis)
  • kidney infections (pyelitis or pyelonephritis)
  • infiltration by lymphoma, leukemia, or sarcoid carcinomas

Common symptoms of AKF include:

  • Anemia. The kidneys are responsible for producing erythropoietin (EPO), a hormone that stimulates red blood cell production. If kidney disease causes shrinking of the kidney, red blood cell production is reduced, leading to anemia.
  • Bad breath or bad taste in mouth. Urea in the saliva may cause an ammonia-like taste in the mouth.
  • Bone and joint problems. The kidneys produce vitamin D, which helps the body absorb calcium and keeps bones strong. For patients with kidney failure, bones may become brittle. In children, normal growth may be stunted. Joint pain may also occur as a result of high phosphate levels in the blood. Retention of uric acid may cause gout.
  • Edema. Puffiness or swelling in the arms, hands, feet, and around the eyes.
  • Frequent urination.
  • Foamy or bloody urine. Protein in the urine may cause it to foam significantly. Blood in the urine may indicate bleeding from diseased or obstructed kidneys, bladder, or ureters.
  • Cola-colored urine followed by oliguria (decreased urine output) or anuria (no urine output)
  • Headaches. High blood pressure may trigger headaches.
  • Hypertension, or high blood pressure. The retention of fluids and wastes causes blood volume to increase. This makes blood pressure rise.
  • Increased fatigue. Toxic substances in the blood and the presence of anemia may cause the patient to feel exhausted.
  • Itching. Phosphorus, normally eliminated in the urine, accumulates in the blood of patients with kidney failure. An increased phosphorus level may cause the skin to itch.
  • Lower back pain. Patients suffering from certain kidney problems (like kidney stones and other obstructions) may have pain where the kidneys are located, in the small of the back below the ribs.
  • Nausea. Urea in the gastric juices may cause upset stomach.

Diagnosis

Kidney failure is diagnosed by a doctor, whether the patient is in the hospital or seen as an outpatient. He or she will take a complete medical history and make a thorough review of the patient's medical record, looking for exposure to nephrotoxic (medicines that can be hard on the kidneys) drugs or other clues to the patient's condition. The physician will then conduct a thorough physical examination, making a careful assessment of the patient's ECF volume and effective circulating blood volume (EBV). A nephrologist, a doctor that specializes in the kidney, may be consulted to confirm the diagnosis and recommend treatment options. He or she will look for a recent history of changes in body weight and try and determine whether the patient is taking in much more fluid than he or she is excreting. Capillary wedge pressure and cardiac output values are also effective tools in pinpointing the cause and extent of the AKF.

The patient that is suspected of having AKF will have blood and urine tests to determine the level of kidney function. A blood test will assess the levels of creatinine, blood urea nitrogen (BUN), uric acid, phosphate, sodium, and potassium. The kidney regulates these agents in the blood. Urine samples will also be collected, usually over a 24-hour period, to assess protein loss and/or creatinine clearance.

Determining the cause of kidney failure is critical to proper treatment. Prerenal or obstructive causes are often looked into first because they are the quickest types of AKF to treat. A full assessment of the kidneys is necessary to determine if the underlying disease is treatable and if the kidney failure is chronic or acute. X rays, magnetic resonance imaging (MRI), computed tomography scan (CT), ultrasound, renal biopsy, and/or arteriogram of the kidneys may be used to determine the cause of kidney failure and level of remaining kidney function. X rays and ultrasound of the bladder and/or ureters may also be needed.

Treatment

Treatment for AKF varies, since it is directed to the underlying, primary medical condition that triggered the kidney failure. Prerenal conditions may be treated with replacement fluids given through a vein, diuretics, blood transfusion, restricted salt intake, or medications. Postrenal conditions and intrarenal conditions may require surgery and/or medication.

Frequently, patients in AKF require hemodialysis, hemofiltration, or peritoneal dialysis to filter fluids and wastes from the bloodstream until the primary medical condition can be controlled.

Hemodialysis

Hemodialysis involves circulating the patient's blood outside of the body through an extracorporeal circuit (ECC), or dialysis circuit. The ECC is made up of plastic blood tubing, a filter known as a dialyzer (or artificial kidney), and a dialysis machine that monitors and maintains blood flow and administers dialysate. Dialysate is a sterile chemical solution that is used to draw waste products out of the blood. The patient's blood leaves the body through the vein and travels through the ECC and the dialyzer, where fluid removal takes place.

During dialysis, waste products in the blood-stream are carried out of the body. At the same time, electrolytes and other chemicals are added to the blood. The purified, chemically-balanced blood is then returned to the body.

A dialysis "run" typically lasts three to four hours, depending on the type of dialyzer used and the physical condition of the patient. Dialysis is used several times a week until AKF has resolved.

Blood pressure changes associated with hemodialysis may pose a risk for patients with heart problems. Peritoneal dialysis may be the preferred treatment option in these cases.

Hemofiltration

Hemofiltration, also called continuous renal replacement therapy (CRRT), is a slow, continuous blood filtration therapy used to control acute kidney failure in critically ill patients. These patients are typically very sick and may have heart problems or circulatory problems. They cannot endure the rapid filtration rates of hemodialysis. They also frequently need antibiotics, nutrition, vasopressors, and other fluids given through a vein to treat their primary condition. Because hemofiltration is continuous, prescription fluids can be given to patients in kidney failure without the risk of fluid overload.

Like hemodialysis, hemofiltration uses an ECC. A hollow fiber hemofilter is used instead of a dialyzer to remove fluids and toxins. Instead of a dialysis machine, a blood pump makes the blood flow through the ECC. The volume of blood circulating through the ECC in hemofiltration is less than that in hemodialysis. Filtration rates are slower and gentler on the circulatory system. Hemofiltration treatment will generally be used until kidney failure is reversed.

Peritoneal dialysis

Peritoneal dialysis may be used if the patient in AKF is stable and not in immediate crisis. In peritoneal dialysis (PD), the lining of the patient's abdomen, the peritoneum, acts as a blood filter. A flexible tubelike instrument (catheter) is surgically inserted into the patient's abdomen. During treatment, the catheter is used to fill the abdominal cavity with dialysate. Waste products and excess fluids move from the patient's bloodstream into the dialysate solution. After a certain time period, the waste-filled dialysate is drained from the abdomen, and replaced with clean dialysate. There are three types of peritoneal dialysis, which vary according to treatment time and administration method.

Peritoneal dialysis is often the best treatment option for infants and children. Their small size can make vein access difficult to maintain. It is not recommended for patients with abdominal adhesions or other abdominal defects (like a hernia) that might reduce the efficiency of the treatment. It is also not recommended for patients who suffer frequent bouts of an inflammation of the small pouches in the intestinal tract (diverticulitis).

Prognosis

Because many of the illnesses and underlying conditions that often trigger AKF are critical, the prognosis for these patients many times is not good. Studies have estimated overall death rates for AKF at 42-88%. Many people, however, die because of the primary disease that has caused the kidney failure. These figures may also be misleading because patients who experience kidney failure as a result of less serious illnesses (like kidney stones or dehydration) have an excellent chance of complete recovery. Early recognition and prompt, appropriate treatment are key to patient recovery.

Survival statistics also depend on the type of AKF the patient has, age at time of onset, and general health. If the patient has prerenal AKF, there is a good recovery prognosis, but the mortality rate is higher among those who fail to respond to diuretics and vasodilator therapy. Since 1980, age has become a risk factor that increased mortality in patients with acute tubular necrosis (ATN), an intrinsic form of AKF.

Up to 10% of patients who experience AKF will suffer irreversible kidney damage. They will eventually go on to develop chronic kidney failure or end-stage renal disease. These patients will require long-term dialysis or kidney transplantation to replace their lost renal functioning.

Health care team roles

The patient who suffers from AKF will come in contact with a number of different health care professionals during both the diagnosis and treatment phase of the illness. Patients will require (according to the type and severity of their condition) laboratory work, diagnostic radiology services, pharmaceutical and nutritional interventions, dialysis (in some cases), nursing care, and disease management by a nephrologist.

The medical history, taken by a physician in the emergency room, the patient's family doctor, a fellow nurse practitioner, physician's assistant (PA), or a nephrologist is the most essential tool in determining the cause and type of AKF. The admitting physician or nephrologist will conduct a thorough physical, looking at the following areas for specific clues.

Skin. Checking the patient for areas of small, purple or red spots (petechiae), hemorrhage beneath the skin (purpura), and bluish discoloration of a fairly large area of the skin (ecchymosis) can lead to a diagnosis of an inflammatory or vascular cause for the AKF.

Eyes. Certain conditions in the eyes can point to a diagnosis of interstitial nephritis (inflammation between the cells and tissues of the kidney) or necrotizing vasculitis (inflammed blood vessels ).

Cardiovascular and volume status. Evaluating the condition of the heart and the rest of the circulatory system plus volume status (fluid balance ) is the most important part of diagnosing and managing AKF. Nurses and nurses' aides will measure and chart daily intake and output (measuring how much fluid the patient takes in and how much he or she excretes in a 24-hour period of time). This is one of the best ways to get a good estimate of volume status. The pulse rate and blood pressure will be taken by the physician, nurses, and nurses' aides often in both the upright (standing or sitting on the side of the bed with legs dangling down) and supine (lying down) positions. The physician will also check the pulse in the neck, examine the heart and lungs, and check for edema (fluid buildup) in the arms and legs. Different combinations of the results of these assessments point to different causes for and types of AKF.

Abdomen. The physician will feel for signs of urinary tract obstruction by palpating (pressing) on the bladder and the upper corners of the abdomen that may reveal an obstruction in the ureter (tube between the kidney and the bladder) somewhere. If the entire abdomen is unusually swollen and filled with fluid (ascites), the AKF may be the result of liver failure.

Arms and legs (extremities). The physican and nursing staff will check the patients arms and legs for edema at the time of diagnosis and throughout treatment. Edema in the arms and legs is a sign of a decrease in oxygenated blood (ischemia), muscle tenderness from rhabdomyolysis (disease of the skeletal muscle), or arthritis. The presence and degree of edema is helpful in pinpointing the cause of AKF and in measuring the patient's progress with treatment.

Nervous system. The physician will assess the patient's degree of mental clarity and nerve responses, as abnormalities in these areas of the nervous system are often common symptoms of AKF. The nursing staff also monitors the patient's mental status during the course of treatment.

Laboratory personnel will draw blood and collect urine samples to help diagnose AKF and later, to evaluate treatment. Increases in BUN (blood urea nitrogen) and creatinine (substance formed from the metabolism of creatine) are indicators of AKF.

The urinalysis is the most important test run in the early stage of AKF evaluation. Significant color changes point to an intrinsic cause for AKF. Urine dipstick tests that prove positive for proteinuria (too much protein) and blood are helpful in diagnosing many causes of AKF. The different types of sediment readings from spun urine samples can further help to distinguish the cause and type of AKF. Urine electrolytes indicate how well the tubules (part of the kidney's nephron) are working.

Nurses and nurses' aides will keep track of fluids the patient takes in (intake) and eliminates (output) to help determine the type of AKF the patient is in and to help the physician manage the patient's course of treatment. Fluid management is critical in the patient with AKF, regardless of the cause.

Patients in AKF may undergo further evaluation in the Radiology Department to determine the cause of their disease and to plan an appropriate plan of treatment. They may undergo an ultrasound examination, doppler scan, nuclear scan, MRI, renal angiography, or a renal biopsy. The ultrasound, doppler scan, and MRI are the least invasive of the procedures. Contrast material is injected for the angiogram and the renal biopsy requires taking tissue samples from the kidney itself. These procedures are performed by trained and licensed radiologic technologists and radiologists.

Nutrition is crucial to the effective management of the patient in AKF. The dietician will work closely with the patient, physician, nursing staff, and pharmacist to ensure proper electrolyte balance, whether the patient eats regular foods or is nourished by total parenteral nutrition (TPN, nutrients mixed and fed through a tube).

Some patients will require kidney dialysis that will be performed by nurses and technicians from the renal or urology department.

Since many different medications are eliminated through the kidneys, the physician works closely with the pharmacist to modify dosing and minimize the use of medications that are toxic to the kidneys.

Prevention

Since AKF can be caused by many things, prevention is difficult. Medications that may impair kidney function should be given cautiously. Patients with pre-existing kidney conditions who are hospitalized for other illnesses or injuries should be carefully monitored for kidney failure complications. Treatments and procedures that may put them at risk for kidney failure (like diagnostic tests requiring radiocontrast agents or dyes) should be used with extreme caution.

KEY TERMS

Anuria— When the body ceases to make urine entirely or falls below 100 mL.

Azotemia— Too many nitrogenous compounds in the blood caused by the kidneys' failure to remove urea from the blood.

Blood urea nitrogen (BUN)— A waste product that is formed in the liver and collects in the blood-stream; patients with kidney failure have high BUN levels.

Capillary wedge pressure— The blood pressure inside of a capillary.

Cardiac output— The volume of blood pushed out by the ventricles.

Creatinine— A protein produced by muscle that healthy kidneys filter out.

Edema— The abnormal accumulation of fluid in the interstitial spaces of tissue.

Electrolytes— An element or a compound that can break into ions and conduct electrical current when melted or dissolved in water.

Erythropoietin (EPO)— A glycoprotein hormone made in the kidneys.

Extracellular fluid (ECF)— That part of body fluid made of interstitial fluid and blood plasma.

Extracorporeal— Outside of, or unrelated to, the body.

Glomeruli— The tiny structures that perform the actual mechanical filtering in the kidney.

Gout— A condition caused by error in uric acid metabolism.

Interstitial— The space between cells.

Intravascular volume— The volume of fluid inside a blood vessel.

Intrinsic— Starting from or situated inside an organ or tissue.

Ischemia— A lack of blood supply to an organ or tissue.

Lymphoma— Cancer of the lymph tissue.

Nephritis— Inflammation and abnormal functioning of the kidney.

Nephrologist— A physician who specializes in treating diseases of the kidney.

Nephrotoxic— Toxic, or damaging, to the kidney.

NSAIDS— Non-steroidal, antiinflammatory drugs.

Oliguria— Abnormally low urine production.

Radiocontrast agents— Dyes administered to a patient for the purposes of a radiologic study.

Sepsis— A bacterial infection of the bloodstream.

Urea— A systemic diuretic.

Vasopressors— Medications that constrict the blood vessels.

Resources

BOOKS

Anderson, Kenneth N., Anderson, Lois, E., and Glanze, Walter D., eds. Mosby's Medical, Nursing, & Allied Health Dictionary, 5th edition. New York: Mosby, 1998.

Beers, Mark H., M.D., and Berkow, Robert M.D., eds. The Merck Manual, New Jersey: Merck Research Laboratories, 2004.

Faubert, Pierre F., and Porush, Jerome G. Renal Disease in the Elderly. New York: Marcel Dekker, Inc., 1999.

Gennari, F. John, ed. Medical Management of Kidney and Electrolyte Disorders. New York: Marcel Dekker, Inc., 2001.

Greenberg, Arthur, Cheung, Alfred K., Coffmann, Thomas M., Falk, Ronald J., and J. Charles, Jeanette, eds. Primer on Kidney Diseases, Second Edition—National Kidney Foundation. New York: Academic Press, 1999.

PERIODICALS

Andreucci, M., Federico, S., and Andreucci, V.E. "Edema and Acute Renal Failure." Seminars in Nephrology 21, 3(May 2001): 251-6.

Forbes, J.M., Hewitson, T.D., Becker, G.J., and Jones, C.L. "Simultaneous Blockade of Endothelin A and B Receptors in Ischemic Acute Renal Failure is Detrimental to Long-term Kidney Function." Kidney International 59, 4(April 2001): 1333-41.

Gruberg, L., Mehran, R., Dangas, G., Mintz, G.S., Waksman, R., Kent, K.M., Pichard, A.D., Satler, L.F., Wu, H., and Leon, M.B. "Acute Renal Failure Requiring Dialysis After Percutaneous Coronary Interventions." Catheter Cardiovascular Interventions 59, 4(April 2001): 409-16.

Knoll, T., Schult, S., Birck, R., Braun, C., Michel, M.S., Bross, S., Juenemann, K.P., Kirchengast, M., and Rohmeiss, P. "Therapeutic Administration of an Endothelin-A Receptor Antagonist After Acute Ischemic Renal Failure Dose-Dependently Improves Recovery of Renal Function." Journal of Cardiovascular Pharmacology 37, 4(April 2001): 483-8.

Rana, A., Sathyanarayana, P., and Lieberthal, W. "Role of Apoptosis of Renal Tubular Cells in Acute Renal Failure: Therapeutic Implications." Apoptosis 6,1-2(February-April 2001): 83-102.

ORGANIZATIONS

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Natcher Building, 6AS-13K, 45 Center Dr., Bethesda, MD 20892-6600. 〈http://www.niddk.nih.gov〉.

National Kidney Foundation (NKF). 30 East 33rd St., New York, NY 10016. (800) 622-9020. 〈http://www.kidney.org〉.

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