Acute Kidney Injury (AKI), formerly known as acute renal failure, is characterized by deterioration of renal function over hours to days, resulting in failure of the kidneys to excrete nitrogenous waste products and to maintain homeostasis. AKI affects 5%–7% of all hospitalized patients. The overall mortality rates for AKI is greater than 20% and, once dialysis is required, mortality rates rise to greater than 50%. Only 15% of patients developing AKI fully recover renal function. Survivors are left with either stable or progressive renal insufficiency, with many being at risk for developing a chronic kidney failure later in life.
Consensus criteria for classification of AKI by the Acute Kidney Injury Network (AKIN) require a rapid time course (less than 48 hours) and either an absolute increase in serum creatinine concentration of more than 0.3 mg/dL compared to baseline, a percentage increase in serum creatinine of 50% or a reduction in urine output to less than 0.5 mL/kg/min for more than 6 hours. The RIFLE criteria assess degree of elevation of serum creatinine or change in GFR, severity and duration of oliguria, and the requirement for renal replacement therapy (RRT). The acronym RIFLE stratifies findings by severity ranging from risk of injury (R) to end-stage renal disease (E) (Table 87-1).
++ Table Graphic Jump Location TABLE 87-1Risk, Injury, Failure, Loss and End-Stage Kidney (RIFLE) Classification ||Download (.pdf) TABLE 87-1 Risk, Injury, Failure, Loss and End-Stage Kidney (RIFLE) Classification
|Class ||Serum creatinine increase ||GFR decrease ||Oliguria (urine output < 0.5mL/kg/h) |
|Risk ||×1.5 ||>25% ||>6 h |
|Injury ||×2 ||>50% ||>12 h |
|Failure ||×3 (or>4 mg/dL, with an acute increase >0.5 mg/dL) ||>75% ||>24 h |
|Loss ||ARF > 4 weeks || || |
|ESRD ||ARF > 3 months || || |
AKI may be oliguric (urinary output less than 400 mL/d) or nonoliguric (urinary output > 400 mL/d). Azotemia, a hallmark of AKI, is a condition marked by abnormally high concentrations of nitrogen-containing compounds such as BUN and creatinine. The causes of AKI are divided into prerenal, intrinsic renal, and postrenal etiologies (Table 87-2).
++ Table Graphic Jump Location TABLE 87-2Causes of Acute Kidney Injury ||Download (.pdf) TABLE 87-2 Causes of Acute Kidney Injury
|Prerenal Azotemia ||Renal Azotemia ||Postrenal Azotemia |
|Hemorrhage ||Acute glomerulonephritis ||Nephrolithiasis |
|Gastrointestinal fluid loss ||Vasculitis ||Benign prostatic hyperplasia |
|Trauma ||Interstitial nephritis (drug allergy, infiltrative disease) ||Clot retention |
|Surgery ||Acute tubular necrosis ||Bladder carcinoma |
|Burns ||Ischemia || |
|Cardiogenic shock ||Nephrotoxic drugs (aminoglycosides, NSAIDs) || |
|Sepsis ||Solvents (carbon tetrachloride, ethylene glycol) || |
|Hepatic failure ||Heavy metals (mercury, cisplatin) || |
|Aortic clamping ||Radiographic contrast dyes || |
|Renal artery camping ||Myoglobinuria || |
|Thromboembolism || || |
Prerenal azotemia accounts for nearly half of all hospital-acquired cases of AKI and is rapidly reversible if the underlying cause is corrected. If sustained, prerenal azotemia is ...