Acute intrinsic renal failure (AIRF) - causes and prevention (Proceedings)
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)
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
Miscellaneous causes of AIRF
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.