Acute renal failure is a clinical syndrome characterized by an abrupt increase of serum creatinine and blood urea nitrogen
(BUN) concentrations to above normal (azotemia). An inability to regulate solute and water balance is often present and renal
synthetic and degratory functions are impaired to varying degrees. The term "acute renal failure" is commonly used to connote
acute intrinsic renal failure, but it is important to consider all possible causes, including pre-renal, intrinsic (primary)
renal, and post-renal. The finding of acute renal failure is not a specific diagnosis. Older definitions of AIRF required
that oliguria be documented during the clinical course-+, but this is no longer included. Oliguria, normal urine production,
or polyuria can all occur depending on the specific cause and severity of renal injury sustained during AIRF.
Differential diagnosis and frequency of AIRF
The frequency of underlying conditions associated with AIRF varies with the nature of the veterinary practice. Nephrotoxicity
is the leading cause for AIRF at The Ohio State University Veterinary Hospital, followed by nephritis and ischemia. The aggressive
use of potentially nephrotoxic antibiotics, particularly the aminoglycosides, can contributes to nephrotoxic AIRF. The exposure
to cholecalciferol rodenticides, indiscriminate use of non-steroidal anti-inflammatory drugs (NSAID), and exposure of veterinary
patients to extensive surgical procedures and aggressive post-traumatic resuscitative maneuvers as emergency patients can
result in AIRF. Ischemic and nephrotoxic AIRF occur more readily in patients that have underlying chronic renal disease or
renal failure. An increased frequency of AIRF has recently been noticed in cats given NSAID at the time of routine desexing.
Potential causes for AIRF due to renal ischemia (hypoperfusion)
Dehydration Shock
Trauma Hemorrhage
Anesthesia Surgery
Sepsis Burns
Hyperthermia Hypothermia
Hemolysis Myoglobinuria
ACE Inhibitors Non-Steroidal Anti-Inflammatory Drugs (NSAID)
Note that renal ischemia can occur in the absence of systemic arterial hypotension.
Potential nephrotoxins as a cause for AIRF
More common
- Glycols (Ethylene Glycol)
- Antimicrobials
o Aminoglycosides
o Amphotericin-B
o Sulfonamides - dehydration
o Tetracyclines - IV
o Easter Lilly – Cats
Less common
- Grapes/Raisin Toxicity – dogs
o Hypercalcemia/Hypercalciuria
o Cholecalciferol Rodenticide
o Cholecalciferol – Diet
o Calcipotriene
- Cancer Chemotherapeutics
- Radiocontrast Agents - IV
- Heavy Metals
- Hydrocarbons
- Fluorinated Inhalational Anesthesia
Miscellaneous causes of AIRF
o Acute glomerulonephritis
o Rapidly progressive glomerulonephritis (Borrelia associated)
o Cutaneous and renal glomerular vasculopathy (Greyhounds – "Alabama Rot")
o Hemolytic uremic syndrome (HUS)
o Systemic vasculitiis
o Renal thromboembolism – renal infarction
- Acute-on-chronic renal failure
- Renal amyloidosis with acute papillary necrosis
- Acute Hyperphosphatemia
o Tumor lysis syndrome
o Phosphate enema
o Phosphate acidifier
o Massive soft tissue trauma
- Sepsis/DIC
- Pancreatitis
- Food-associated renal failure
Pathophysiology of AIRF due to nephrosis
Exposure to nephrotoxins or ischemia causes tubular injury exhibited microscopically along a spectrum from degeneration to
necrosis, and is referred to as nephrosis or acute tubular necrosis (ATN). Some patients, however, exhibit minimal or no light
microscopic lesions yet exhibit severe renal excretory failure. Factors that can contribute to azotemia and or oliguria during
AIRF include tubular backleak, intraluminal and extraluminal tubular obstruction, and primary filtration failure (afferent
arteriolar vasoconstriction, efferent arteriolar vasodilatation, and or a decrease in glomerular permeability).
Diagnosis of AIRF
Rapid increases of BUN, serum creatinine, and serum phosphorus may be observed during AIRF. This is particularly helpful to
document AIRF in the absence of recent serum biochemistry values for comparison. For example, a patient's serum creatinine
of 4.3 mg/dl, 6.0 mg/dl, and 7.5 mg/dl sequentially over three consecutive days supports a diagnosis of AIRF. Serum creatinine
and BUN do not increase over this short a time period in hydrated patients with chronic renal failure. Hyperphosphatemia may
be out of proportion to the degree of increase in BUN or serum creatinine in those with acute renal failure compared to chronic
renal failure . The magnitude of elevation in BUN or serum creatinine concentrations is not generally helpful in the diagnosis
of AIRF vs CRF or in the differentiation of pre-renal, intrinsic renal, or post-renal azotemia. Urinalysis reveals a low specific
gravity (SG) during the maintenance phase of AIRF (SG less than 1.030, but most-often in the 1.007 to 1.015 range). Dipstrips
may show proteinuria, hematuria or glucosuria on occasion. Urinary sediment is typically "active" at early stages of the maintenance
phase exhibiting increased numbers of casts (particularly cellular casts) and small epithelial cells compatible with renal
tubular epithelium. Animals with AIRF should have smooth kidneys with normal or increased kidney size whereas those with chronic
renal failure may show small and or irregular kidneys both on palpation and abdominal radiographs. Renal ultrasonography can
provide additional anatomic information to confirm intrarenal lesions, but cannot be relied on to distinguish acute from chronic
renal failure or to suggest a specific microscopic lesion. Failure to document ultrasonographic renal changes does not exclude
a diagnosis of AIRF. Kidneys may enlarge during AIRF but this may not be detected if they are still within the normal range
for kidney size; kidneys tend to become "plump" before they measure elongated. Renal biopsy may be helpful to determine that
an azotemia is due to primary renal lesions and to characterize the changes as acute or chronic. Urine culture can be helpful
in selected cases to evaluate for upper or lower urinary tract infection.
