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• Acute renal failure is defined as sudden, rapid, potentially reversible deterioration of renal function.

It can be classified according to underlying cause as:

• Prerenal azotemia – stemming from decreased blood flow to kidneys

• Intrarenal acute renal failure – involving intrinsic damage to renal structures

• Postrenal obstruction – involving obstruction of urine outflow

II. Risk Factors

Prerenal azotemia – is caused by factors that interfere with renal perfusion.

• Hypovolemia (e.g. hemorrhage, shock, burns)

• Increased intravascular capacity (e.g. from sepsis, neurogenic bladder)

• Cardiac disorders (e.g. myocardial infarction, arrhythmias_

• Renal artery obstruction

• Hepatorenal syndrome

Intrarenal acute renal failure

• Acute tubular necrosis – which accounts for about 75% of all cases of acute renal failure

• Acute glomerulonephritis

• Acute pyelonephritis

Postrenal obstruction

• Ureteral obstruction due to calculi, strictures, trauma, or pregnancy

• Bladder obstruction (e.g. cancer, prostatic hypertrophy)

III. Pathophysiology

• The exact pathogenesis of acute renal failure is not always known, but it is associated with a severe
reduction in the glomerular filtration rate. This may be caused by decreased renal blood flow that leads
to increased renal-vascular resistance, increased hydrostatic pressure in Bowman’s capsule, or a
disruption of tubular epithelium.


• The onset phase – extends from the time of the precipitating event to the beginning of the oliguric-
anuric phase.

• The oliguric-anuric phase – is marked by urine output of less than 400 ml/day, volume overload,
elevated blood urea nitrogen (BUN) and creatinine levels, electrolyte abnormalities, metabolic acidosis,
and uremia.

• The diuretic phase – extends from the time that output becomes more than 400ml/day to the time the
BUN stops rising and stabilizes in normal range. During this phase, electrolyte and acid-base problems
begin to normalize.

• The convalescent phase – extends from the time the BUN stabilizes until the client returns to normal
activity. The client may take up to 2 years to regain 70%to 80% of normal function.

Systemic effects of acute renal failure are widespread and may include:

• Fluid and electrolyte imbalances

• Acidosis

• Increased susceptibility to infection

• Anemia

• Platelet dysfunction

• GI disturbances (e.g. anorexia, nausea, vomiting, diarrhea, or constipation, stomatitis)

• Pericarditis

• Uremic encephalopathy

IV. Assessment/Clinical Manifestations/Signs and Symptoms

• Altered urine output, may be oliguria, anuria, or rarely polyuria

• Hypertension or hypotension

• Tachypnea

• Signs of fluid overload or extracellular fluid depletion

Laboratory and diagnostic study findings


Urine osmolality

• In prerenal – values are higher than 900 mOsm/kg

• In intrarenal parenchymal failure – values are less than 250 mOsm/kg

• In postrenal obstruction – values may be normal

Blood analysis

• BUN, serum creatinine, and potassium levels are elevated

• Blood pH, bicarbonate, hemoglobin, and hematocrit values are decreased

V. Medical Management
• Treatment objectives are to restore normal chemical balance and prevent complications until renal
tissues are repaired and renal function is restored. Possible causes of damage are identified and treated.

• Fluid balance is managed based on daily weight, serial measurements of central venous pressure,
serum and urine concentrations, fluid losses, blood pressure, and clinical status. Fluid excesses are
treated with mannitol, furosemide to initiate dieresis and prevent or minimize subsequent renal failure.

• Blood flow is restored to the kidneys with the use of intravenous fluids, albumin or blood product

• Dialysis (hemodialysis, hemofiltration, or peritoneal dialysis) is started to prevent complications of

uremia, including hyperkalemia, pericarditis and seizures.

• Ion exchange resins (orally or by retention enema)

• Intravenous glucose and insulin or calcium glutamate as an emergency and temporary measure to
treat hyperkalemia.

• Sodium bicarbonate to elevate plasma pH.

• Parenteral erythropoietin (Epogen) to treat reduced erythropoietin production and prevent anemia

• Shock and infection are treated if present

• Arterial blood gases are monitored when severe acidosis is present.

• If respiratory problems develops, ventilator measures are started.

• Phosphate-binding agents such as aluminum hydroxide to control elevate serum phosphate


• Dietary protein is limited to about 1g/kg during oliguric phase to minimize protein breakdown and to
prevent accumulation of toxic end products.

• Caloric requirements are met with high-carbohydrate feedings; parenteral nutrition

• Foods and fluids containing potassium and phosphorus are restricted; potassium intake is limited to 40
to 60 mEq/d. Sodium intake is restricted to 2 g/d.

• Blood chemistries are evaluated to determine amount of replacement sodium, potassium, and water
during oliguric phase.

• After the diuretic phase, high-protein, high-calorie diet is given with gradual resumption of activities.

VI. Nursing Diagnosis

• Fluid volume excess related to decreased urine output
• Activity intolerance related to fatigue, toxins and fluid build up
• Risk for impaired skin integrity related to edema, toxins, or impaired tissue perfusion
• Risk for infection related to intravenous lines or catheters or uremic toxins
• Deficient knowledge regarding condition and its treatment

VII. Nursing Management

Promote measures to ensure normal potassium levels.

• Monitor potassium level and assess for effects of hyperkalemia.
• Restrict dietary potassium as necessary.
• Monitor cardiac telemetry for electrocardiographic changes.
• Prepare to administer insulin and glucose, which drives potassium back into the cell.

Promote measures to maintain acid-base balance.

• Monitor for acidosis
• Administer an alkalinizing agent
• Monitor arterial blood gas values for signs of metabolic acidosis or alkalosis.
• Be prepared to institute ventilator measures if respiratory problems develop.

Promote measures to assess and prevent infection.

• Assess for infection, especially of the respiratory and urinary tracts.
• Do not leave the urinary catheter in place.
• Administer prophylactic antibiotics as prescribed.
• Monitor for hyperphosphatemia.
• Administer phosphate-binding agents.
• Monitor serum phosphorus level.

Promote measures to ensure normal calcium levels.

• Monitor for hypocalcemia
• Administer calcium supplements
• Assess for hypercalcemia by checking for Chvostek’s and Trousseau’s signs.

Prevent GI bleeding by administering histamine receptor antagonists and proton pump inhibitors.

Promote comfort and encourage bed rest to reduce exertion and metabolic rate. As prescribed,
administer short-acting barbiturates to control pain, and assess for central nervous system
complications such as drowsiness, confusion, delirium, coma, and convulsions.

Provide a high-calorie and low-protein diet, with hyperalimentation if the client cannot eat.

If indicated, prepare the client for dialysis to correct hyperkalemia, fluid overload, acidosis, or
severe uremia.
Administer prescribed medication, which may include alkalinizing agents, antibiotics,
phosphate-binding agents, ion exchange resins, calcium supplements, histamine receptor
antagonists, and proton-pump inhibitors.

Promote measures to maintain fluid balance. Assess fluid balance, and restrict intake to 24-hour
urine output plus 500 ml/day.

Promote measures to ensure normal sodium and phosphate levels. Instruct the client to restrict
sodium intake, drink plenty of fluids, and follow a low-phosphate diet.

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