Acute renal failure may be defined as an abrupt reduction in renal function resulting in accumulation of nitrogenous waste
products and dysregulation of water, electrolyte, and acid base balance. Differentiating acute from chronic kidney disease
is important for both therapeutic and prognostic reasons. Inherent in the diagnosis of acute kidney injury is the potential
for complete functional recovery. In contrast, patients with end-stage CKD lack substantial recovery potential. Careful examination
of medical history, physical exam, past and current laboratory data and imaging studies will usually enable differentiation.
Acute uremia may be classified as pre-renal, intrinsic renal, and/or post-renal in origin. A thorough clinical exam of patients presenting with signs of an acute uremic crisis usually provides adequate information
to identify pre-renal, renal and post-renal components of uremia. Although these categories help establish cause and predict
prognosis, they share many features and may overlap. Pre-renal azotemia develops as an adaptive response to any cause of reduced
renal perfusion (e.g., hypovolemia, inadequate cardiac output, marked vasodilatation). Initially, nephrons remain intact allowing
a rapid return to function once perfusion has been restored. If correcting renal perfusion does not ameliorate the azotemia,
the patient should be carefully evaluated for intrinsic renal and/or post-renal causes of azotemia. Acute intrinsic renal
failure occurs when damage occurs to the nephron itself. Acute intrinsic renal failure is commonly caused by nephrotoxins
or an ischemic event; other etiologies include infection, prolonged urine outflow obstruction, and severe non-renal systemic
disease (e.g., pancreatitis, neoplasia).
There are generally 4 stages of acute intrinsic renal failure; 1) initiation, 2) extension, 3) maintenance, and 4) recovery.
Clinically, transition from one stage to the next may not be clearly evident and not all stages need be present in an individual
patient. Initiation is the period during which the kidneys are exposed to the damaging agent or event. Initiation may last
hours to days and is often clinically silent; however, therapeutic intervention at this phase may reduce severity of renal
damage and enhance the likelihood of recovery. During the extension phase, damage occurs to the tubular epithelium leading
to a decline in glomerular filtration rate (GFR), the loss of urine concentrating ability and potentially oliguria.
During the maintenance phase, polysystemic signs of kidney damage may become apparent and the animal may be presented for
veterinary care. Unfortunately, significant renal damage may have already occurred thus limiting management to supportive
and symptomatic therapies. The forth stage, recovery, represents tubular epithelial regeneration, and, if it occurs, may last
for days to months. Recovery is characterized by increasing GFR, improved urine quality, and amelioration of the polysystemic
consequences of renal dysfunction.
Post-renal azotemia results from obstruction of urine flow after it has left the nephron, or leakage of urine from the urinary
tract within the body. Fairly classic clinical signs and physical exam findings of urethral obstruction facilitate rapid diagnosis
and relief of the obstruction. Likewise, urinary tract leakage from the urinary tract is usually readily identified from physical
exam and imaging.