Acute renal failure (ARF)
Acute renal failure (ARF) is an acute suppression of renal function. The insult causing
ARF equally and abruptly disrupts the function of all nephrons without time for
compensatory mechanisms which are involved in chronic renal failure to "kick
in". ARF is contrasted with chronic renal failure
(CRF)
in which there is a gradual death of nephrons with the remaining nephrons functioning in a
normal or supra normal capacity. ARF is potentially reversible whereas CRF is a
progressive and irreversible condition.
Most (~80 to 90%) of ARF patients are oliguric. Oliguria is defined as urine production
of less than 0.5 ml/lb/hr (1 ml/kg/hr). ARF patients which are polyuric (increased urine
output) have sustained a lesser degree of renal injury compared to oliguric patients and
therefore have a better prognosis. The damaged nephrons of ARF patients have reduced
abilty to form glomerular filtrate from blood, resulting in less filtration of urea
nitrogen, creatinine, phosphorus and potassium leading to an increase of these substances
in the blood.
It is important to differentiate ARF from prerenal
azotemia. Both prerenal azotemia and ARF can be caused by hypovolemia and uncorrected
prerenal azotemia can progress to ARF. The more severe and sustained the hypovolemia, the
greater the probabilty that ARF will occur. The kidneys are able to
"autoregulate" renal blood flow (RBF) and GFR to keep these parameters normal
when mean arterial blood pressure greater than 70 mm Hg. Mean blood pressures lower than
70 mm Hg are associated with reduction in renal blood flow and GFR. The prognosis for
prerenal azotemia is good if the underlying disease causing prerenal asotemia is
reversible. The prognosis for ARF is usually poor.
Urine specific gravity (USG) and urine sodium concentration are parameters which can be
used to differentiate prerenal azotemia from ARF.
The USG is concentrated and urine sodium is low in patients with prerenal azotemia. The
USG is isosthenuric (1.007 - 1.017) and urine sodium is high in patients with ARF.
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Possible causes of ARF include:
- ischemic injury
- chemical insults
- hypercalcemia (uncommon)
- infection (pyelonephritis)
- glomerular diseases
ARF is most often caused by chemical insults (drugs or toxins)
or by ischemic injury to the kidney. The kidneys are very active organs. In order to
function properly, the cells in the kidneys must be supplied with large amounts of oxygen
and nutrients via the blood. If blood flow to the kidneys is diminished by hypovolemia,
the kidney cells are "deprived" of oxygen and nutrients which results in
cellular death. The death of epithelial cells lining the renal tubules is called
"acute tubular necrosis" (ATN). The causes of hypovolemia include the same
causes as those resulting in prerenal azotemia
but the insults are more profound and sustained to result in ARF. An additional cause of
reduced renal blood flow which will result in ARF is thrombosis of the renal arteries.
Renal artery thrombosis may occur as part of a generalized hypercoagulable state (e.g.
disseminated
intravascular coagulation).
Hypercalcemia is an uncommon cause of
acute renal failure. Hypercalcemic patients often have polyuria, polydipsia and dilute
urine but infrequently develop irreversible renal failure.
Infection including leptospirosis or bacterial kidney infections (pyelonephritis) can
cause ARF. Leptospirosis is an uncommon disease. Untreated bacterial pyelonephritis is
more likely to compromise renal function over time resulting in CRF but can cause an
abrupt disruption of function (ARF).
Glomerulonephropathy, which is usually immune mediated, can cause
ARF but more often if glomerular disease results in azotemia, there is a gradual loss of
renal function (CRF) rather than an abrupt decline in function (ARF).
All the etiologies of ARF are additive. For example, if a patient with bacterial
pyelonephritis is treated with a nephrotoxic antibiotic and also becomes dehydrated, that
patient is at greater risk for developing ARF than if only one of the conditions were
present. (infection = pyelonephritis + chemical insult = nephrotoxic antibiotic +
ischemia = dehydration)
Very young and very old animals are at greater risk for development of ARF; the young
because the kidneys are immature and the old because pre-existent renal disease is likely
present.
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Pathophysiology
There is a large body of work which has been performed in an attempt to elucidate the
mechanisms responsible for the reduction of GFR and urine flow in ARF patients. Four major
mechanisms are believed to be involved in the initiation and maintenance of reduced GFR
and reduced urine output.
- reduced renal blood flow/renal artery vasoconstriction
- intratubular obstruction
- backleak
- decreased glomerular permeability
Renal artery vasoconstriction leads to a reduction of renal blood flow.
Vasoconstriction can be catecholamine induced, caused by alteration of renal prostaglandin
activity (reduced vasodilatory prostaglandins or increased vasoconstrictor
prostaglandins), or the renal arteries may be occluded by thrombi.
Renal tubules can be obstructed from cell debris as tubular epithelial cells die from
what ever insult is responsible for causing ARF. Drugs such as sulfonamides can
precipitate in the lumen of the tubules causing obstruction. In experimental models of
ARF, tubular obstruction appears to play a minor role in the genesis of ARF as the debris
deposited in the tubular lumen can be "flushed" from the tubule with low
pressures. Therefore tubular debris is probably a consequence of low fluid flow through
the tubule rather than a cause of it.
The backleak theory is described as reabsorption of filtrate into blood after leakage
through damaged tubular epithelium.
Decreased glomerular permeability caused by swelling of endothelial or epithelial cells
which comprise the glomerulus may impair formation of glomerular filtrate.
All 4 of these mechanisms may contribute to the development of oliguria and
accumulation of wastes in ARF patients.
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Clinical course
The clinical course of ARF proceeds through a sequence of overlapping phases:
- initiation phase
- oliguric phase
- polyuric phase
- phase of functional recovery
The initiation phase is defined as the time from renal insult to recognition of
decreased GFR, decreased urine output and increased BUN and creatinine. This phase lasts
1-2 days. As an example, suppose a cat is under anesthesia for an exploratory surgery and
becomes hypotensive during the procedure due to blood loss, the hypotensive effects of
anesthesia and inadequate fluid administration. If hypotension is severe and not
corrected, the kidneys are deprived of blood with resultant death of tubular epithelial
cells. The BUN will not increase immediately and unless urine volume is being measured, it
will not be immediately detected that urine production is decreasing. Within 1 to 2 days
it will become apparent that the cat is in acute renal failure with decreased USG, reduced
urine output and increased BUN.
The oliguric phase which is also called the maintenance phase, is the period of time
during which oliguria persists. Some ARF patients are never oliguric. Whether an ARF
patient is oliguric or polyuric probably reflects the severity of insult which caused the
ARF. This has been demonstrated in rodents with chemical or ischemic induced ARF. The more
severe the insult, the lower the urine output. As the majority (80 to 90%) of ARF dogs and
cats become oliguric, it indicates that the situations which cause ARF in these species
are severe and correlates with the poor prognosis for ARF patients.
In those patients which can repair the renal damage, the oliguric phase lasts 1-2
weeks. Many animals die or are euthanized during the oliguric phase because of the poor
prognosis. The most life-threatening consequences of the oliguric phase include
hyperkalemia and overzealous fluid therapy resulting in overhydration.
The polyuric phase = high output phase = diuretic phase is characterized by a
progressive increase in urine volume in patients which were initially oliguric. The
patients have an increased BUN and creatinine and isosthenuric USG. The polyuric phase may
indicate the beginning of renal repair and return of function or may be indicative of a
less severe insult to the kidneys. Glomerular filtrate is entering tubules that are not
fully functional and are acting as simple conduits for fluid without performing any work
on the fluid. There are several causes for polyuria in these patients:
- impaired tubular sodium reabsorption causing loss of sodium in the urine
- excretion of solutes retained in the oliguric phase (small molecules like urea are
osmotically active)
- impaired response of tubular cells to ADH (nephrogenic diabetes insipidus)
- medullary washout of solute (It requires tubular work to maintain a hypertonic gradient
in the renal interstitium)
- iatrogenic over hydration during the oliguric phase
During the polyuric phase, renal loss of sodium and water can be substantial. If the
patient can not drink enough to keep up with the renal loss of water, they will dehydrate
resulting in a prerenal insult superimposed upon the already existent renal disease. Fluid
therapy must be diligently managed to prevent dehydration. This phase lasts a few days to
several weeks or longer.
The phase of functional recovery has neither a clearly defined beginning or end. In
patients capable of repairing the renal injury, BUN, creatinine, and urine volume
gradually return to normal. Concentrating ability is the slowest to return. Permanent
defects in concentration, acidification, or permanent decreases in GFR may persist. Some
ARF patients progress to CRF.
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Diagnosis
The patient history, physical examination and laboratory data may all support a
diagnosis of ARF.
The history may provide a clue as to the cause of ARF. For example the animal may have
had recent anesthesia/surgery causing hypotension, may have been receiving a drug which
has the possibilty of being nephrotoxic or may be a free-roaming animal which has the
potential for exposure to toxins such as antifreeze. Patients with chronic renal failure
may have a history of polyuria and polydipsia and may abruptly decompensate, presenting in
a crisis like an ARF patient. CRF patients can sustain acute insults (ARF super imposed
upon CRF).
 Physical examination often reveals a depressed, hypotensive,
hypovolemic and sometimes hypothermic patient. Hypovolemia is due to fluid loss in vomitus
and diarrhea and lack of intake and in some patients, hypovolemia is the cause of ARF.
Given the acute nature of their disease, the patient is often in good body condition
compared to the chronic renal failure patient which may be in poor body condition.
Fever may be present if ARF is from an infectious cause such as acute pyelonephritis or
leptospirosis. Tachypnea may be observed and is present to eliminate CO2 to
compensate for metabolic acidosis.
Bradycardia may exist due to hyperkalemia but hyperkalemic patients may have a normal
heart rate. As the patients are usually hypovolemic and the cardiac response to
hypovolemia is to increase the heart rate, the two opposing influences on heart rate may
result in a normal heart rate.
The kidneys may palpate normal to large. Enlarged kidneys may be painful when palpated
as pain receptors in the capsule of the kidney are stretched as the kidney enlarges.
The most common change in mentation is depression but seizures may occur in terminal
uremia or due to toxins such as ethylene glycol.
Hematology
The CBC often discloses increased total protein and PCV due to hemoconcentration,
unless blood loss caused hypovolemia and subsequent renal failure in which case total
protein and PCV are decreased. Platelet number is normal but function is abnormal
(thrombocytopathia). Thrombocytopathia is due to the retention of a waste product which
makes the platelets less aggregable (less sticky). WBC is either normal or shows a stress
response. Uremia interferes with the function of WBC which may predispose ARF patients to
infection.
Chemistry
Biochemical analysis will show increased BUN and creatinine.
Sodium may be increased, decreased, or normal and depends upon the type of dehydration
that is present and upon any previous fluid therapy. Dehydration in the ARF patient is
primarily due to losses in vomiting and diarrhea and to lack of intake. Gastrointestinal
losses of fluid contain electrolytes in addition to water in proportions comparable to
blood resulting in
isotonic
dehydration. Therefore the proportion of electrolytes to water in the blood remains
close to normal even though the actual amount of water and electrolytes is decreased
compared to health. Sodium will be increased if the patient has greater than normal
insensible losses (respiratory) as insensible losses contain primarily water and little
electrolyte.
 |
Elevated potassium (hyperkalemia)
is often associated with oliguria. There may be cardiac disturbances when K > 6.0
mEq/L. Normal intracellular K is 160 mEq/L. The normal ICF to ECF ratio for K is 40:1.
When ECF K increases, this ratio is reduced. This elevates the normal resting membrane
potential (RMP) to a less negative state, creating partial depolarization of myocardial
cells. The action potential produced is weaker and the spread of depolarization across the
myocardium is slowed. |
Inorganic phosphorus is increased. Calcium is usually normal early in ARF but may
decrease within several days of onset. Calcium may deposit in damaged muscle with
extensive rhabdomyolysis (muscle breakdown) (example "heat stroke" or crush
injury) causing a rapid decline in serum calcium. This is followed by hypercalcemia during
recovery as the calcium is mobilized from muscle. Calcium may be decreased in ethylene
glycol poisoning due to the formation of calcium oxalate. Rapid correction of acidosis
results in a decrease in ionized calcium and may precipitate hypocalcemic tetany. If hypercalcemia exists, the patient should be
evaluated for the source of the increased calcium which could be the cause of ARF (primary
or pseudohyperparathyroidism).
 |
The urinalysis may show signs of tubular dysfunction
which include isosthenuric specific gravity (1.007-1.017), proteinuria, glucosuria,
increased urine sodium, or casts. Crystals may disclose the cause of ARF (e.g., calcium
oxalate crystals of antifreeze poisoning). |
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Radiology can be used to determine kidney size if size cannot be
determined from palpation. Kidneys are normal to large in patients with ARF as compared to
small kidneys in CRF. Ultrasound can also be used to assess renal size. Contrast studies of the kidneys (IVP) should not be performed
simply to determine renal size. The quality of the contrast study is influenced by renal
function as normal kidneys will concentate the injected dye which delineates their
structure. Inabilty to concentrate the dye results in a poor quality contrast study in
patients with renal disease. Additionally, the contrast agent can be nephrotoxic.
 Renal biopsy is not necessary to make a diagnosis of ARF but may
yield prognostic information. The cause of ARF may be determined from renal biopsy, for
example oxalate crystals are observed in the biopsy of patients with antifreeze poisoning.
If a patient is not responding to therapy after 7 to 10 days, a biopsy may give clues as
to the potential for reversibilty based on the severity of renal damage and evidence for
repair.
Renal biopsy can be performed "blindly", using ultrasound guidance, via a
laparotomy or via laproscopy. Risks associated with biopsy include bleeding as uremic
patients have abnormal platelet function, and hypovolemia if the animal is sedated or
anesthetized for biopsy. The risks versus benefits of biopsy must be weighed carefully. A
tru cut needle is pictured.
A fine needle aspirate performed in an awake animal can sometimes yield information
such as the presence of oxalate crystals, without the need to perform a biopsy.
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Conservative therapy of the ARF
patient: Depending upon the degree of renal damage, the kidneys may repair themselves. The
goal of treatment is to sustain life while the pathologic process in the kidneys heals
itself. Management of the ARF patient is divided into 2 phases; immediate care when you
first see the patient and maintenance encompassing both the oliguric and polyuric phases.
Immediate care includes:
- identify if possible, and eliminate the inciting cause
- correct fluid deficits (dehydration) in an attempt to reestablish adequate renal
perfusion
| Mini quiz: |
A 25 kg dog is 10% dehydrated based on physical parameters. What volume of fluid is
required to rehydrate this patient? |
ANSWER
 Initially the
patient must be rehydrated and the amount of urine produced evaluated in response to fluid
administration.
KEEP WRITTEN RECORDS OF ALL FLUID INPUT AND OUTPUT.
 Isotonic saline or a polyionic solution such as LRS should be used for
rehydration and the fluid deficit replaced over 2-6 hours at a rate of 10-20 ml/kg/hr or
faster if the animal is hypovolemic. Avoid K+ containing fluids (such as LRS) if urine
output is diminished, unknown or if K+ is increased.
A fluid pump is useful to deliver large volumes of fluid rapidly.
Failure to induce urine production of at least 1/2 ml/lb/hour (1 ml/kg/hr) indicates
either that fluid replacement is inadequate or the presence of intrinsic renal failure.
The patient must be closely monitored for signs of fluid overload.
Monitoring may include:
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Diuretics may be administered if after fluid
replacement urine production is inadequate. The value of diuretics in intrinsic renal
failure is questionable but as a single dose of a diuretic carries minimal risk, diuretics
are frequently tried in oliguric patients. Diuretics which may be used include:
- furosemide (lasix) (2 mg/kg IV, if no response in 1-2 hours increase dose to 4 mg/kg IV)
- mannitol (0.25-0.5 g/kg IV over 5 minutes)
- hypertonic dextrose (10 - 20%) (0.5 g/kg IV over 20 minutes)
Dextrose and mannitol are osmotic diuretics, drawing water from cells into extracelluar
spaces. Both can cause vascular overload if diuresis does not occur. Do not administer
osmotic diuretics if the patient already shows signs of fluid overload. Do not repeat
osmotic diuretics if diuresis fails to occur. If diuresis occurs, mannitol can be repeated
every 4-6 hours for 24 hours. If urine output increases in response to hypertonic
dextrose, it can be continued for 1-2 days at 50 ml/kg/24hrs. Divide this dose into
several portions and alternate with 2-3 cycles of 3-5% body weight LRS or normal saline to
maintain urine output. Furosemide (lasix) is the diuretic of choice if the patient is
already showing signs of fluid overload.
Dopamine causes selective renal arterial vasodilation when administered at 2-5
ug/kg/min. Dopamine has a duration of action of a few minutes so it is delivered as a
constant drip in 5% dextrose. Dopamine potentiates the effects of furosemide.
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Hyperkalemia is life threatening due to
negative effects on myocardial cells. About 90% of body potassium is located within cells.
As cells die in response to normal catabolic processes, intracellular potassium is
released into extracellular fluid. Uremia is a state of accelerated catabolism resulting
in a greater rate of celluar breakdown and release of intracellular potassium into blood.
With impaired renal function potasium cannot be excreted and serum levels rise rapidly.
The immediate management of hyperkalemia is based on antagonizing its cardiotoxic effects
or by driving potassium back into cells in order to "buy" time until potassium
elimination through urine or feces can be increased.
There are 3 intravenous treatments which can have immediate impact on the negative
cardiac effects of potassium:
- sodium bicarbonate ( 0.5 - 1.0 mEq/kg)
- glucose (0.5 g/kg) with or without regular insulin ( 0.25 u/Kg)
- calcium gluconate (10% solution, 0.5 - 1.0 ml/kg)
Sodium bicarbonate combines with hydrogen ions in ECF. This creates a gradient for
additional hydrogen ions to move out of cells, into ECF. As hydrogen ions move out of
cells, potassium ions move into the cells.
 |
As glucose moves into cells under the influence of insulin,
potassium "tags" along into the cells. Glucose can be administered without
insulin, depending upon endogenous insulin release from the pancreas or regular insulin
can be administered with glucose. Regular insulin (crystalline) is very soluble and
readily available. Do not administer insulin without administrating glucose or
hypoglycemia will result. |
 |
Calcium counteracts the effects of hyperkalemia on the
cardiac conduction system by re establishing the normal resting membrane potential
of -90 MV. Calcium should be administered slowly over 5-10 minutes with
electrocardiographic monitoring as calcium itself can be cardiotoxic. Calcium chloride can
be used instead of calcium gluconate but use ~1/10 the dose. |
All 3 treatments have rapid effect but are of short duration lasting about 30-60
minutes. They can be repeated.
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 Infections are common complications of ARF. Infection
aggravates the catabolic state of the uremic patient resulting in a faster rate of protein
breakdown and generation of nitrogen containing wastes and potassium. Indwelling
intravenous and urinary catheters used in the management of ARF patients are convenient
avenues for infection. Strict attention to aseptic technique in catheter placement and
management is essential. The benefits of catheters must be weighed against risks.
If an infection develops care must be taken in selecting antibiotics that are not
nephrotoxic. If an antibiotic is eliminated from the body by the kidneys the dose may need
to be altered to prevent accumulation of the antibiotic. The package insert for the drug
is a good source of information regarding the need to alter the dose in patients with
impaired reanl function.
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Once the immediately life threatening consequences of ARF are addressed, it becomes a
"waiting game" to maintain the animal until it can be determined whether renal
function can be re established.
Maintenance includes:
- maintaining normal hydration
- maintaining normal potassium concentration
- acid- base balance
- providing nutrition
- controlling vomiting and hemorrhagic gastritis
Maintaining normal hydration: During the oliguric phase of ARF one of
the most serious potential complications is iatrogenic fluid overload. After the initial
correction of dehydration, fluid therapy consists of replacing ongoing losses including:
- insensible loss from skin and respiratory tract (approximately 10-12 ml/lb/day
(hypotonic))
- urinary loss (estimated or measured -
isotonic)
- losses from vomiting and diarrhea (estimated or measured -
isotonic)
Careful records need to be kept of fluid intake, administration and losses.
The patient should be monitored frequently for signs of overhydration or
dehydration by looking at:
- packed cell volume and total protein
- central venous pressure (CVP)
- blood pressure
- skin turgor
- body weight. An anoretic patient should lose 0.5 - 1% of body weight per day. Once this
loss is considered any gain or loss of 1 kg body weight should be regarded as an excess or
deficit of 1 liter of fluid.
Daily fluid administration should be divided rather than all at once to allow for
easier correction of over or under assessment of fluid balance. As the patient enters the
polyuric phase of ARF, exogenous fluid administration must be increased to prevent
hypovolemia.
Sodium and potassium losses during the polyuric phase of ARF may be substantial and
must be replaced. If it is necessary to administer potassium it should be done slowly, no
faster than 0.5 mEq/kg/hr.
During the oliguric phase, hyperkalemia must be prevented. Sodium polystyrene
sulphonate (kayexylate) is an ion exchange resin which exchanges sodium for potassium in
the intestinal tract resulting in removal of potassium from the body. The exchange resin
is administered orally at 2 g/kg in 3 divided doses. It can also be given as a high enema
if the animal is vomiting and cannot take oral medications. If the exchange resin is
unsuccessful in controlling hyperkalemia, dialysis is necessary.
Acid Base status: Most ARF patients are acidotic. Bicarbonate is
indicated to reestablish acid-base balance if blood pH < 7.2. The following formula can
be used to determine the amount of bicarbonate to administer.
Body weight (kg) x 0.3 x base deficit = bicarbonate dose in mEq
A similar formula using (0.6 x base deficit) assumes that the bicarbonate will be
immediately distributed through
total body water
which actually requires about 24 hours. Using a more conservative estimate to calculate
bicarbonate dose (0.3 x base deficit) is often sufficient to improve the patient's acid
base status to a point where the body's own buffer systems will re establish a closer to
normal, acid -base status.
Example: (10 kg canine)
pH = 7.20
pO2 = 88 mmHg
pCO2 = 31 mmHg
HCO3 = 11 mEq/L
Base excess (deficit) = -15
10 kg x 0.3 x -15 = 45 mEq of bicarbonate
To be even more conservative, administer 1/2 the calculated dose immediately and the
other 1/2 over 12- 24 hours. The goal is to "add to" the body's own buffering
systems, not to rapidly change acid-base status. Rapid correction of acidosis can
result in a decrease in ionized calcium by increasing the amount of calcium bound to
proteins and may precipitate hypocalcemic tetany. Rapid correction of acidosis can also
cause neurologic dysfunction through the development of
paradoxical CSF
acidosis.
If it is not possible to measure blood gas values, the degree of acidosis can be
estimated based on the degree of uremia:
| Uremic state |
Estimated base deficit |
| mild |
-5 |
| moderate |
-10 |
| severe |
-15 |
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Nutrition: To decrease the level of azotemia, the rate of protein
catabolism should be decreased. Glucose has a sparing effect on protein catabolism in the
fasting individual. If the patient can take food orally, diets should be comprised of high
caloric density fats, carbohydrates and small amounts of high biologic value protein. The
fluid content of the diet needs to be considered when calculating fluid intake. Anorexia
and vomiting frequently preclude oral alimentation. Total parenteral nutrition (TPN)
solutions may be administered IV. TPN solutions contain an energy source, usually
30-50% glucose, and protein hydrolysate to provide essential amino acids. TPN solutions
which contain hypertonic dexrose are irritating and must be administered in a large vein
such as the jugular vein.
Hemorrhagic gastritis
Gastrin levels in the blood are elevated in ARF due to reduced clearance. Gastrin
directly stimulates H2 receptors on parietal cells or stimulates mast cells to
release histamine which stimulates parietal cell H2 receptors with the result
being HCL liberation by the parietal cell. Parietal cells also have acetylcholine
receptors on their surface. Increased gastric acidity plus abnormal platelet function
causes mucosal irritation and hemorrhage.
The administration of an H2 blocker (cimetidine = tagamet, ranitadine =
zantac, famotadine = pepsid) reduces the severity of hemorrhagic gastritis in uremic
patients.
Central acting anti emetics may also be used to control vomiting.
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Drug elimination: The kidneys
provide the major route of elimination for many pharmacologic agents so avoid the use of
any unnecessary drugs. If drugs are used which are renally excreted, after the
initial loading dose is administered either the drug dose or dose interval must be altered
to prevent accumulation of the drug and subsequent intoxication. The drug package insert
is a good source of information regarding the use of the drug in patients with impaired
renal function.
One method to alter the dose interval is based on the calculated
endogenous creatinine clearance.
Iu = (In) CCn/CCu
Iu = dosage interval in uremic patient
In = normal dosage interval
CCn = normal creatinine clearance
CCu = creatinine clearance of uremic patient
A less accurate method using only serum creatinine level:
Iu = In Cu/Cn
Iu = dosage interval in uremic patient
In = dosage interval of normal patient
Cu = creatinine of uremic patient
Cn = creatinine of normal patient
For other methods consult a pharmacology textbook.
Prognosis: The prognosis for most ARF patients
is poor. These patients are usually very ill, unstable and difficult to manage. ARF
patients that are polyuric are much easier to manage and therefore have a better prognosis
than the oliguric patient. The presence of oliguria indicates a more severe renal insult.
If conservative measures are not successful in the treatment of an ARF patient dialysis should be considered.
Department of Veterinary Clinical Sciences
College of Veterinary Medicine
Washington State University
Pullman, WA 99164-7060
Telephone 509-335-0711
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College of Veterinary Medicine,
Washington State University, Pullman, WA,
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Copyright 1995-2001 Washington State University
Revised February 19, 2004
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