Kidneys are unable to remove accumulated metabolites from the blood which leads to altered fluid, electrolyte, and acid-base balance
The cause may be a primary kidney disorder or secondary to a systemic disease
May be acute or chronic
Acute
Abrupt onset and with prompt intervention is often reversible
Chronic
Develops slowly, is the end stage, and is not reversible
Azotemia
Nitrogen (protein) waste in the blood
Acute Renal Failure
A rapid decline in renal function with azotemia and fluid and electrolyte imbalances
The most common cause is ischemia and nephrotoxins
Risk factors
Major trauma or surgery
Infection
Hemorrhage
Heart failure
Liver disease
Urinary tract obstruction
Drugs and radiologic contrast that are toxic to the kidney
Pathophysiology
Prerenal
Hypoperfusion (decreased blood volume and cardiac output, vascular resistance) and ischemia lead to ARF
Intrarenal
Direct damage to functional kidney tissue
Ex. Glomerulonephritis, vasculitis, hypertension
Postrenal
Urinary tract obstruction with resulting kidney damage is the cause
Acute tubular failure
Destruction of tubular epithelial cells causes decreased renal function
Ischemia and nephrotoxins are the cause of acute tubular failure
Risk factors
Major surgery
Severe hypovolemia
Sepsis
Trauma
Burns
Ischemia lasting more than 2 hours causes severe and irreversible damage to kidney tubules
Common nephrotoxins associated with ATN include aminoglycoside ABX and contrast media
Signs and symptoms
Initiation phase
May last hours to days
Begins with initiating event and ends when tubular injury occurs
If event is treated during this stage, prognosis is good
This phase has few s/s
Maintenance phase
Significant fall in GFR and tubular necrosis
Oliguria may develop
Azotemia, fluid retention, electrolyte imbalances, and metabolic acidosis develops
Salt and water retention cause edema, increasing the risk for heart failure and pulmonary edema