The partial or complete impairment of kidney function. Results in an inability to excrete metabolic waste products and water, as well as contributing to disturbances of all body systems. Can be classfied as acute (Acute kidney injury aka AKI) or chronic (chronic kidney disease aka CKD)
Acute kidney injury (acute kidney failure)
The term used to encompass the entire range of the syndrome including a very slight deterioration in kidney function to severe impairment. Characterized by a rapid loss of kidney function demonstrated by a rise in serum creatinine and/or a reduction in urine output. Usually develops over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium with or without a reduction in urine output.
An accumulation of nitrogenous waste products (urea, nitrogen, creatinine) in the blood that is severe enough to warrant renal replacement therapy. Develops from acute kidney disease.
Prerenal causes of AKD
Factors external to the kidneys that reduce systemic circulation causing a reduction in renal blood flow and lead to decreased glomerular perfusion and filtration of the kidneys. No damage to the kidney tissue. Oliguria is caused by a decrease in circulating blood volume (ex. severe dehydration, decreased cardiac output, burns) and is usually reversible. Body attempts to preserve blood flow to essential organs. Results in the reduction of sodium (less that 20 meq/L), increased salt and water retention, and decreased urine output. Can lead to intrarenal disease if not treated because the kidneys lose their ability to compensate.
Immune complexes are deposited in the glomerular basement membrane, causing decreased plasma filtration and thus water and sodium retention
A disorder characterized by increased glomerular permeability to plasma protein, which results in massive urinary protein loss
proteinuria, edema, low blood protein
cause: damage to glomerulus
Febrile urinary tract infection coexisiting with systemic signs of bacterial illness
Renal Lithiasis, Nephrolithiasis
Also called urinary calculi, these stones cause symptoms when they obstruct urinary flow
Acute Tubular Necrosis (ATN)
May be caused by ischemia, nephrotoxins, hemolyzed RBCs or myoglobin released from necrotic muscle cells
The backup of urine above an obstruction causing dilation of the renal pelvis from distention; eventually causes pressure destruction to renal parenchyma
Inflammation of the upper urinary tract and kidneys
Manifestations include changes in specific gravity and osmolality of the urine
Fluid Volume Excess
Edema, hypertension, CHF, and pulmonary edema are symptoms
Hydrogen ions build up, serum bicarb is used up and lethargy and stupor result
This vital electrolyte may not be conserved by the kidney
The kidneys normally excrete 80-90% of this electrolyte. Thus this level rises, putting the heart at risk.
Anemia results from decreased erythropoietin, while altered WBCs lead to infection
Calcium deficit and phosphate excess
The failing kidney does not activate Vitamin D, and thus Ca++ is not absorbed and PO4 levels rise
Waste produce accumulation
Serum creatinine or creatine clearance measures this best, but BUN (interpreted cautiously) is helpful
Mild symptoms are fatigue and difficulty concentrating, seizures, stupor, and coma occur as condition worsens
The condition in which azotemia progresses to a symptomatic state
Symptoms include: N/V, lethargy, fatigue, impaired thought processes, headache
Used as an indication of glomerular filtration rate. Compares the amount of creatinine in the urine with the amount in the blood.
Glomerular filtration rate GFR
The amount of blood filtered by the glomeruli in a given time
Normal = 125 mL/hour which produces about 1mL/minute of urine
Due to factors external to the kidneys that reduce renal blood flow and lead to decreased glomerular perfusion and filtration.
Hypovolemia: dehydration, hemorrhage, GI losses, excessive diuresis
Decreased Cardiac Output: cardiac dysrhythmias, cardiogenic shock, heart failure, myocardial infarcation
Decreased Peripheral Vascular Resistance: anaphylaxis, septic shock
Decreased Renovascular Blood Flow: thrombosis, embolism, hepatorenal syndrome
Acute tubular necrosis (ATN)- responisble for 50% of intrarenal ARF: Ischemia, nephrotoxcitity
Include conditions that cause direct damage to renal tissue (parenchyma) resulting in impaired nephron function
Drugs, radiocontrast (IV dye), hemolytic blood tx, severe crush injury, chemical exposure, interstitial nephritis, acute glomerulonephritis
Involves mechanical obstruction of urine outflow
Benign prostate hypertrophy, bladder cancer, calculi (stone) formation
Usually occurs within 1 (more common) to 7 days of the causitive event. Can be prerenal, intrarenal or postrenal in origin. Clinical manifestations include:
Fluid volume excess
Calcium deficit and phosphate excess
Waste product accumulation
Gradual increase in daily urinary output, up to 5L/day. Signals beginning recovery, as kidneys have regained the ability to excrete wastes, but not to concentrate urine (reabsorb water). This phase may last 1-3 weeks. Assess for Fluid Volume Deficit as evidenced by hypovolemia and hypotension.
May last up to 12 weeks. GFR increases, so BUN and creatinine gradually decrease
If a patient is thought to have a prerenal cause of decreased urinary output of elevated BUN, a "bolus" or rapid infusion (usually over 30-60 minutes) of IV fluid (200-500 mL for adults) may be ordered to "challenge" the kidneys. If the kidneys can function normally, they will respond with an increased urine output. This procedure may be repeated more than once and be followed by the administration of furosemide (Lasix) or other diuertic. Nursing implications are to assess for signs of fluid volume excess and pulmonary edema by monitoring:
Vital signs: increased BP, increased pulse, increased respirations
Lung sounds: Rales, dyspnea
Jugular Veins: distended