Acute kidney injury (AKI) often results from ischemic or toxic insults and usually affects the most metabolically active tubular portions of the nephron. If the ischemic or toxic insult is severe enough, acute renal failure (ARF) may result. In many cases, AKI and ARF inadvertently develop in the hospital setting in conjunction with diagnostic or therapeutic procedures. For example, renal damage may result from decreased renal perfusion associated with anesthesia and surgery or with the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Similarly, renal damage may occur in patients treated with potential nephrotoxicants like gentamicin, amphotericin, and cisplatin. The nephron damage that occurs with ischemic or toxic insults is not always reversible; animals that do recover adequate renal function usually require prolonged and expensive intensive care. Several retrospective studies have documented the poor prognosis associated with ARF in dogs and cats. In a study of hospital-acquired ARF, the survival rate was only 40%. In another retrospective study of 99 dogs with all types ARF, 22% died, 34% were euthanized, 24% survived but progressed to chronic kidney disease (CKD), and only 19% regained normal or adequate renal function. Similarly, in a retrospective study of 32 cats with all types of ARF, 16% died, 31% were euthanized, 28% survived but progressed to CKD, and only 25% regained normal or adequate renal function. These studies underscore the importance of early detection of AKI and prevention of ARF. Several risk factors have been identified that predispose dogs to gentamicin-induced ARF, however it is likely that many of these risk factors also predispose dogs and cats to other types of toxicant-induced ARF as well as ARF induced by ischemia. A combination of decreased renal perfusion and/or use of nephrotoxic therapeutic agents superimposed on more chronic, pre-existing risk factors is usually responsible for AKI/ARF in the clinical setting. Early detection of AKI facilitates appropriate intervention that can arrest or at least attenuate tubular cell damage and the development of established ARF.

Pathophysiology

Acute renal failure has three phases, which are categorized: 1) initiation, 2) maintenance, and 3) recovery. The initial insult occurs resulting in sub-lethal cellular injury in the initiation phase. Therapeutic measures started during this initiation phase may reduce the renal insult and prevent development of established ARF. The maintenance phase is characterized by tubular cell death and established nephron dysfunction. Therapeutic intervention during the maintenance phase, although often life saving, usually does little to diminish existing renal lesions or improve renal function. The recovery phase is the period when renal lesions resolve and renal function improves. Tubular damage may be reversible if the tubular basement membrane is intact and viable epithelial cells are present. Although additional nephrons cannot be produced and irreversibly damaged nephrons can not be repaired, functional hypertrophy of surviving nephrons can often adequately compensate for the decrease in nephron numbers. Even if renal functional recovery is incomplete, adequate function may be reestablished in some cases.