Acute Renal Failure Is a Serious Medical

Acute renal failure is a serious medical condition. The gravity of the condition is manifested itself in the fact that the survival rate for renal failure has not improved for more than forty years. It occurs in 5% of all hospitalized patients and dialysis treatment is required in approximately .5 of cases. Dialysis is required to sustain "fluid and electrolyte balances, minimize nitrogenous waste production and sustain nutrition Infection accounts for 75% of deaths in patients with acute renal failure, and cardiorespiratory complications are the second most common cause of death" (Agrawal & Swartz 2000). Pathophysiology can vary depending upon the type: "patients who develop AKI can be oliguric or nonoliguric, have a rapid or slow rise in creatinine levels, and may have qualitative differences in urine solute concentrations and cellular content.... Oliguria is defined as a daily urine volume of less than 400 mL/d and has a worse prognosis, except in prerenal failure. Anuria is defined as a urine output of less than 100 mL/d and, if abrupt in onset, suggests bilateral obstruction or catastrophic injury to both kidneys" (Workeneh, 2011).

The three types of acute renal failure are categorized as prerenal, intrinsic and postrenal failure. Prerenal acute renal failure or acute tubular necrosis "a type of intrinsic acute renal failure that is usually caused by ischemia or toxins" is the most common form of the illness (Agrawal & Swartz 2000). In acute renal failure the excretion of nitrogenous waste is reduced, and the patient's fluid and electrolyte balances are disturbed. "The glomerular filtration rate decreases over days to weeks" (Agrawal & Swartz 2000). Often, the patient is asymptomatic. However, symptoms, when presents may include a lack of urine output despite drinking adequate fluids, edema in the extremities, anorexia, nausea, vomiting, disorientation, or fatigue. There may also be pain in the kidney area or back pain (Epstein 1997; Agrawal & Swartz 2000).

"Diagnoses are usually given based upon elevations of blood urea nitrogen (BUN) and serum creatinine levels. Most authorities define the condition as an acute increase of the serum creatinine level from baseline (i.e., an increase of at least 0.5 mg per dL [44.2 µmol per L]). Complete renal shutdown is present when the serum creatinine level rises by at least 0.5 mg per dL per day and the urine output is less than 400 mL per day (oliguria)" (Agrawal & Swartz 2000).

However, not all BUN and serum creatinine elevations are caused from acute renal failure. The side effects of corticosteroids, gastrointestinal tract bleeding and other intestinal diseases can produce abnormal results. However, a negative reaction to corticosteroids is also a common cause of the most prevalent form of the disease, prerenal acute failure. For this reason, a thorough battery of tests must be ordered. Blood and urine tests as well as BUN and serum electrolyte, creatinine, calcium, phosphorus and albumin levels, and a complete blood count with differential are recommended when all forms of acute renal failure are suspected (Agrawal & Swartz 2000).

The patient's lifestyle should also be evaluated as a factor when screening for the likelihood of acute renal failure. Alcoholism, for example, can put the patient at increased risk. The side effects of excessive alcohol consumption can disrupt a cell's retention of sodium, potassium, calcium, and phosphate, and this intensifies over time (Epstein 1997). Alcohol directly affects the kidneys by altering the form and structure of the organs. Significant kidney enlargement is commonly noted in chronic alcoholic-afflicted cirrhosis of the liver (Epstein 1997). Other demographics more likely to experience kidney failure include older adults, patients with kidney or liver disease; diabetics; patients with high blood pressure, heart failure, or obese patients. Patients who have experienced trauma to the kidneys, patients in the ICU, patients that have had heart or intestinal surgery or a bone marrow transplant are also statistically more likely to have kidney failure (Epstein 1997).

As well as determining whether acute renal failure has occurred, a through diagnosis also demands determining the type of renal failure that the patient is suffering. "Prerenal acute renal failure is characterized by diminished renal blood flow (60 to 70% of cases). In intrinsic acute renal failure, there is damage to the renal parenchyma (25 to 40% of cases). Postrenal acute renal failure occurs because of urinary tract obstruction (5 to 10% of cases)" (Agrawal & Swartz 2000).

In prerenal acute renal failure, impaired renal blood flow "as a result of true intravascular depletion" causes "decreased effective circulating volume to the kidneys or agents that impair renal blood flow" (Agrawal & Swartz 2000). Intrinsic acute renal failure can take the form of tubular disease, glomerular disease, vascular disease and interstitial disease. "In intrinsic acute renal failure, the renal parenchyma itself is injured, producing the pathology" (Agrawal & Swartz 2000). "Postrenal acute renal failure can only occur if both urinary outflow tracts are obstructed or the outflow tract of a solitary kidney is obstructed. The condition is most often due to obstruction of the lower urinary tract" (Agrawal & Swartz 2000).

Initially, pharmaceutical treatment and dietary reform is prescribed. "Therapy for acute renal failure is directed at treating the underlying cause, correcting fluid, electrolyte and uremic abnormalities, and preventing complications, including nutritional deficiencies" (Agrawal & Swartz 2000). For example, a dehydrated or volume-depleted patient may be administered saline. However, in the more typical instance, "volume overload is present, especially if patients are oliguric or anuric" (Agrawal & Swartz 2000). Determining what is the case with this particular patient is essential, to insure that the electrolyte correction is not generated in the wrong direction. The diuretic Lasik is usually given in the case of volume overload. Intravenous calcium is used to reverse the effects of hyperkalemia. Potassium deficiencies are addressed with insulin beta agonists or sodium bicarbonate. Acidosis "is treated with intravenously or orally administered sodium bicarbonate" (Agrawal & Swartz 2000).