Recognition and Prevention of Hospital-Acquired Acute Kidney Injury

There has been a shift in terminology in the human medical field within the last 10 years to establish a more concise and clinically relevant definition of acute renal failure (ARF). By the traditional definition, ARF is a rapid fall in glomerular filtration, which manifests clinically as an abrupt and sustained increase in the serum levels of urea and creatinine with an associated disruption of salt and water homeostasis. Since this definition cannot be quantified for clinical use, comparing incidence and outcome across clinical studies is challenging. To formulate guidelines to provide a more concise definition for ARF, physicians have proposed a definition of acute kidney injury (AKI) that includes reduction in kidney function within 48 hours defined by the occurrence of at least one of the following: (1) an absolute increase in serum creatinine concentration of at least 0.3 mg/dl (26.4 mmol/L), (2) an increase in serum creatinine concentration of more than 50% of baseline, or (3) oliguria of less than 0.5 ml/kg/hr for more than 6 hours. Through the use of two similar classification schemes to stratify human patients with regard to severity of AKI—the Risk-Injury-Failure-Loss-End-stage disease (RIFLE) criteria and the Acute Kidney Injury Network (AKIN) criteria (Table 186-1)—multiple retrospective and prospective studies have proven a significant association between increasing severity of AKI and mortality, even with minimal increases in creatinine concentration that previously were not considered important.

TABLE 186-1

Comparison of Acute Kidney Injury Network (AKIN) and Risk-Injury-Failure-Loss-End stage disease (RIFLE) Criteria for Evaluating Hospital-Acquired Acute Kidney Injury

GFR, Glomerular filtration rate.

In human medicine, AKI is recognized primarily as hospital acquired rather than community acquired. The term hospital-acquired acute kidney injury (HA-AKI) is used to identify this event. Veterinary patients have potential exposure to a wide variety of factors causing AKI, but people are less likely to be exposed to these factors in a community setting. In contrast, hospitalized people are more likely to be exposed to medications or diagnostic agents (e.g., radiocontrast agents) that predispose to AKI. Sepsis and the systemic inflammatory response also result in multiorgan dysfunction in the severely ill. Aged adults often have reduced renal function compared with younger individuals.

Epidemiology and Etiology of Hospital-Acquired Acute Kidney Injury

Both AKI and HA-AKI have been investigated in the veterinary literature. In a retrospective review by Thoen and Kerl (2011) of data for 164 dogs admitted to the intensive care unit (ICU), 14.6% were noted to have developed AKI, as defined by an increase in creatinine concentration of at least 150% of baseline or an absolute increase of 0.3 mg/dl or more during the hospital stay. In another retrospective review (Harison et al, 2012), 15.2% to 19.3% of dogs for which at least two creatinine measurements were taken within a 2-, 3-, or 7-day period (n = 401, 477, and 646, respectively) developed AKI, as defined by an increase in serum creatinine concentration of 0.3 mg/dl or more. In both studies, only cases with serum creatinine levels of less than 1.6 mg/dl on the initial sample were included. There are no published prospective studies of the incidence of HA-AKI in dogs admitted to the ICU, but preliminary data suggest an incidence of around 10% to 17%. In cats, 20% to 21.3% of the at-risk population for which at least two creatinine measurements were taken within 2, 3, or 7 days (n = 128, 165, and 221, respectively) developed AKI, as defined by an increase in serum creatinine concentration of 0.3 mg/dl or more (Harison et al, 2012).

Commonly recognized risk factors for HA-AKI include preexisting renal disease, dehydration and volume depletion, decreased cardiac output, advanced age, fever, hypotension, hypertension, hypoalbuminemia, sepsis, electrolyte imbalances, acidosis, hyperviscosity syndromes, liver disease, administration of nephrotoxic drugs, administration of radiocontrast media, pancreatitis, diabetes mellitus, anesthesia, and surgery. Of 29 dogs that developed HA-AKI, most had been exposed to a nephrotoxicant (72%); were older than 7 years of age (69%); had chronic heart disease (41%), preexisting renal disease (35%), a neoplastic condition (31%), or fever (28%); or had undergone anesthesia (14%) (Behrend et al, 1996). The nephrotoxicant drugs included aminoglycosides alone or in combination, cardiac drug combinations, cisplatin, and nonsteroidal antiinflammatory drugs. In contrast, almost 40% of 332 people who developed HA-AKI had experienced decreased renal perfusion (Nash et al, 2002). The causes of decreased renal perfusion included volume contraction, congestive heart failure, hypotension, cardiac arrest, inadequate blood pressure control, third-space losses, and arrhythmia. Other causes of HA-AKI were nephrotoxic medications, radiographic contrast media, postoperative status, and sepsis.