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Acute Renal Failure
ARF is a clinical syndrome characterized by a rapid loss of renal fx. with progressive
azotemia (accumulation of nitrogenous waste products such as BUN and increasing
levels of serum creatinine)
Uremia: a condition in which renal fx. declines to the point that symptoms develop in
multiple body symptoms. ARF is often associated with oliguria to less than 400cc/day in
50% of cases.
ARF usually develops over hours or days with progressive elevation of BUN, creatinine,
and potassium with or without oliguria. ARF follows severe prolonged hypotension or
hypovolemia or exposure to nephrotoxic agents.
Classification of Acute Renal Failure:
1)Prerenal: (usually correctable) due to factors external to the kidneys that reduce renal
blood flow and lead to decreased glomerular perfusion and filtration. Hypovolemia,
decreased cardiac output, decreased peripheral vascular resistance and vascular
obstruction all can decrease the effective circulating volume of the blood
Causes of prerenal acute renal failure:
-hypovolemia- i.e. not enough blood to the kidney
-dehydration
-decreased cardiac output
2)Intrarenal acute renal failure: (tends to cause more problems than prerenal or
postrenal) damage to kidney itself. Intrarenal ARF is due to conditions that cause direct
damage to the renal tissue resulting in impaired renal function.
-intrarenal ARF is usually due to prolonged ischemia, nephrotoxins, hemoglobin released
from hemolyzed RBC, or myoglobin released from necrotic muscle cells. Nephrotoxins
can cause obstruction of intrarenal structures by crystallization or actual damage to the
epithelial cells of the tubules. Hemoglobin and myoglobin block the tubules and cause
renal vasoconstriction.
-primary renal disease (acute glomerulonephritis and system lupus erythematosus) may
cause ARF.
-acute tubular necrosis (ATN) is a type of intrarenal ARF caused by ischemia,
nehrotoxins or pigments. Ischemis and nephrotoxic ATN are responsible for 90%
of intrarenal ARF.
Examples of intrarenal acute renal failure
-proglonged prerenal ischemia i.e. shock state for 2 days with lack of blood to kidney
-nephrotoxic injury (drugs, hemolytic agents)
-acute glomerulonephritis
-systemic lupus erythematosus
-malignant hypertension
-infections
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3)Postrenal acute renal failure: (usually correctable) causes involve mechanical
obstruction of urinary outflow i.e. BPH, stones. As the flow of urine is obstructed, urine
refluxes into the renal pelvis impairing kidney fx.
-most common cause of postrenal ARF are BPH, prostate cancer, calculi, trauma.
Examples of postrenal acute renal failure
-BPH
-bladder cancer
-prostate cancer
-calculi
-strictures
-trauma
2 most common causes
-prolonged renal ischemia
-nephrotoxic injury
4 phases of clinical course for acute Renal Failure
** Initiating phase: phase begins at the time of insult and continues until the signs and
symptoms become apparent
**Oliguric Phase: the most common clinical manifestation of ARF is oliguria caused by
a reduction in the GRF. Oliguria, < 400cc/24 hrs., usually occurs within 1-7 days of
causative agent.
-duration 10-14 days, but can last months
-the longer the oliguric phase the poorer the prognosis for complete recovery.
-it is important to differentiate between prerenal oliguria and intrarenal oliguria.
In a prerenal oliguria there is no damage to the renal tissue. The oliguria is caused by a
decrease in circulatiog blood volume (result from dehydration or hypovolemia) and is
reversible. With a decrease in circulating blood volume, autoregulatory mechanisms that
increase angiotensin II, aldosterone, norephinephrine and antidurectic hormone attempt to
preserve blood flow to essential organs. Vasoconstriction occurs along with sodium and
water retention. Prerenal oliguria is characterized by urine with a high specific
gravity (>1.015) and a low sodium concentration (<10 to 20mEq/L). In contrast,
oliguria of intrarenal failure is characterized by urine with a normal specific
gravitiy (1.010) and a high sodium concentration (>40mEq/L) indicating that the
injured tubules cannot respond to autoregulatory mechanism. In addition, the
oliguria in the intrarenal failure caused by ATN from ischemia or toxins is characterized
by the presence of tubular, RBC and WCB casts in the urine. The casts are from
mucoprotein impressions of the necrotic renal tubular epithelial cells which detach or
slough into the tubules.
Oliguric phase: 3 major areas
-changes in urine output
-fluid & electrolyte imbalances
-uremia
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Urinary changes:
-urinary output decreases to less than 400cc/24hrs. for 50% of pts.
-urinalysis may show casts, RBC, WBC, specific gravity fixed (around 1.010; urine
osmolarity 300MOsm/kg- this is the same specific gravity and osmolarity as for
plasma, reflecting tubular damage with a loss of concentrating ability by the kidney.
-proteinuria may be present if the renal failure is related to glomelular membrane
dysfunction
-decrease urine output
-proteinuria
-casts
-decreased specific gravity
-decreased osmolarity
-increased Na
Fluid volume excess:
-urine output decreases leads to fluid retention
-the severity of the symptoms depends on the extend of the fluid overload
-edema
-fluid overload
-neck vein distention
-hypertension
-bounding pulse
-CHF, pulmonary edema
-weight gain
-pleural effusion
Metabolic Acidosis:
-in renal failure, the kidneys cannot synthesize ammonia, which is needed for hydrogen
ion excretion or excrete acid products of metabolism. The serum bicarbonate level
decreases b/c bicarbonate is used up in buffering ions. In addition, defective reabsorption
and regeneration of bicarbonate occurs. Symptoms include: kussmaul respiration (rapid,
deep breathing) to increase the excretion of carbon dioxide, lethargy and stupor.
-increased BUN
-increased creatinine
-decreased sodium
-increased potassium
-decreased pH
-decreased bicarbonate
-decreased calcium
-increased phosphate
Na Balance
-damaged tubules cannot conserve sodium. Urinary excretion of sodium may increase,
resulting in normal or below normal serum sodium
-excessive intake of sodium should be avoided b/c it can lead to volume overload,
hypertension and CHF
-uncontrolled hyponatremia or water excess can lead to cerebral edema
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Potassium Excess
-serum potassium level increase b/c the normal ability of the kidneys to excrete 80-90%
of the body’s potassium is impaired
-if ARF caused by trauma, damaged cells release additional potassium into extracellular
fluid
-bleeding and blood transfusion cause cellular destruction, releasing more potassium into
the extracellular fluid
-acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven
out of the cells into the extracellular fluid
-potassium > 6mEq/L or arrhythmia is identified, treat IMMEDIATELY
-Hyperkalemia: Tall peaked T waves; widening of QRS complex, depressed ST wave
Hematologic Disorder
-Anemia occurs b/c renal failure results in impaired erythropoietin production
(develops in 48 hrs.)
-decreased platelets
-WBC deficiency- increase susceptibility to infection (leads to bleeding from
multiple sources i.e. GI & brain, immunodeficiency; infection is a major cause of
death in ARF)
Calcium Deficit: Phosphate Excess
-low serum calcium level results in decreased GI absorption of calcium
-to absorb calcium, activated vitamin D must be present. Only functioning kidneys can
activate Vitamin D
-when hyocalcemia occurs, PTH (parathyroid gland) secretes PTH, parathyroid
hormone), which stimulates bone demineralization thereby releasing calcium from bones.
-hypocalcemia is rarely asymptomatic in renal failure. This is b/c in the acidosis state
associated with renal failure, more calcium is in the ionized form (free physiologically
active) rather than bound to protein.
-low ionized calcium level can lead to tetany
-INCREASED phosphate is released also, worsening hyperphosphatemia. Elevated
phosphate results from decrease excretion by kidneys.
Waste Product Accumulation
-increased BUN & Creatinine
-the kidneys are the primary excretory organ for urea, the end product of protein
metabolism
-BUN increase must be viewed with caution. Other factors besides renal failure can
cause an elevation in BUN i.e. dehydration, corticosteroids, catabolism, resulting from
infection, fever, severe injury or GI bleeding.
-the BEST indicator of renal failure is CREATININE b/c it is not significantly
altered by other factors
-measuring 24 hour Creatinine clearance is best measure of Creatinine and renal
fx., but most use serum creatinine for convenience.
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Neurological Disorders
-Neurological changes can occur as the nitrogenous waste products accumulate in the
brain and other nervous tissue. Symptoms may be as mild as fatigue and escalate to
seizures, stupor and coma.
-lethargy
-seizures
-asterixis (hand-flapping tremor)
-memory impairment
**Diuretic Phase: begins with a gradual increase in daily urine output to 1-3L per day,
but it may reach 3-5 L or more per day. Although urine output increases, the nephrons
are still not functioning. High urine output is caused by osmotic diuresis from the high
urea concentration in the glomelular filtrate and the inability of the tubules to concentrate
urine. In this phase, the kidneys have recovered their ability to excrete wastes, but not to
concentrate the urine.
-Hypovolemia and hypotension can occur from massive fluid losses. The most
critical this is to monitor fluid volume deficit **hydrate**
-Uremia (the condition in which the renal function declines to the point that symptoms
develop in multiple body systems) may still be severe as evident by low creatinine
clearances, elevated serum creatinine and BUN levels and persistent symptoms.
-Profound fluid volume loss places pt. at high risk for fluid and electrolyte imbalances.
Monitor for:
-hyponatremia
-hypokalemia
-dehydration
-Diuretic phase lasts 1-3 weeks. At the end of the diurectic phase, pt.’s acid-base,
electrolyte and waste products (BUN/creatinine) begin to normalize.
**Recovery Phase: begins when the GFR increases, allowing the BUN/Creatinine levels
to plateau and then decrease. Although major improvements occur in the first 1-2 weeks
of this phase, renal fx. may take up to 12 months to stabilize
Labs/Diagnostics
ARF Stage
-Urine osmolarity
Oliguric
Fixed
300 mOsm/kg
Diuretic
Increased
Recovery
Decreased
-Urine Sodium
Increased
Increased
Decreased
-Urine SP, Gravity
Fixed
Increased
Decreased
-Serum Creatinine
Increased
Increased
Decreased
-Serum BUN
Increased
Increased
Decreased
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Management
Because ARF is potentially reversible, the primary goal of tx. is to eliminate the cause,
manage signs and symptoms and prevent complication
-tx. precipitating cause
-fluid restriction (600 cc + previous 24 fluid loss)***
-nutritional therapy: adequate protein intake (0.6-2g/kg/day), potassium restriction,
phosphate restriction, sodium restriction
-measures to lower potassium
-calcium supplements or phosphate-binding agents
-TPN if indicated
-enteral feeding if needed
-dialysis if necessary
PRIORITY: determine if adequate intravascular volume and cardiac output to
ensure profusion of kidneys
-diuretic therapy and volume expanders
-duiretic therapy usually indicates loop diuretics, lasix, bumex or osmotic diurectic
(mannitol)
-if ARF is already established, forcing fluids and diuretics will not be effective and may
in fact be harmful. Conservative therapy may be all that is necessary until renal fx.
improves.
-fluid intake must be monitored closely during oliguric phase
**General rule for calculating fluid- add all losses from previous 24 hours (urine,
diarrhea, emesis, blood) PLUS 600cc for insensible loss
i.e. if pt. total output for Wednesday = 300cc then total intake for Thursday is 900 cc.
Treatment of hyperkalemia:
-Regular insulin Administration IV
Potassium moves into the cell when insulin is given. Glucose is given concurrently to
prevent hypoglycemia. When effects of insulin diminish, potassium shifts back out of the
cell. * this is only for acute tx.
-Sodium bicarbonate. Therapy can correct acidosis and cause shift of potassium into
the cell. Both insulin and NaHCO3 temporarily shift potassium into the cell, but will
eventually shift back out.
-Calcium Gluconate IV. Therapy is given IV and generally used in advanced cardiac
toxicity. Calcium raises the threshold for excitation, resulting in decreasing likelihood of
dysrhythmia.
-Dialysis- Hemodialysis brings potassium levels to normal within 30 minutes to 2 hours
-Kayexalate- cation-exchange resin is administered by mouth or retention enema. When
resin is in the bowel, potassium is exchanged for sodium Therapy removes 1mEq of
potassium per gram of drug. It is mixed in water with sorbitol to produce osmotic
diuresis, allowing evacuation of potassium rich stool from the body.
** only dialysis and kayexalate actually move potassium
-Dietary restriction- daily potassium intake is limited to 40mEq
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Clinical indicator for Dialysis
-volume overload (compromised cardiac/pulmonary compromise)
-elevated K+ > 6mEq with EKG changes
-metabolic acidosis
-BUN >120mg/d/
-mental change status
-pericarditis, cardiac tamponade
Nutritional Management: provide adequate calories regardless of restrictions required
to prevent electrolyte & fluid disorders and azotemia. If pt. does not receive adequate
nutrition catabolism of body proteins will occur
-calorie intake = 30-35kcal/kg of body weight
-protein decreased = 1.2-1.3g/kg (may be up to 2.0g/kg if catabolic)
-potassium & sodium regulated based on serum lab values
-Sodium restriction to prevent edema
-fats increased (pt. receives 30-40% of total calories from fat)**
-fat emulsion IV infusion can be given as a nutritional supplement and provide good
source of non-protein calories
Inerventions
-Prevention of ARF to high risk groups (massive bleeding, post code, burns, etc.).
-Caution w/ pts. taking potential nephrotoxic agents
-Caution pts. about NSAID- these drugs worsen renal fx. in borderline renal
insufficiency pts. by decreasing glomerular pressure.
-ACE inhibitors can decrease perfusion pressure and cause hyperkalemia** ACE
inhibitors are contraindicated with renal insufficiency
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