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Acute kidney injury (AKI; previously called acute renal failure) is the sudden loss of renal function necessary to maintain normal fluid and electrolyte balance and clear metabolic waste.1,2 AKI is typically manifested by an increase in serum creatinine, although the increase will not necessarily cause the creatinine to be outside the normal range. Use of serum creatinine alone to define AKI, however, is problematic because creatinine is an inaccurate estimate of glomerular filtration rate (GFR) and can be removed by dialysis, and variable cut-off values for creatinine have been used in AKI. Therefore, the international classification system, Kidney Disease: Improving Global Outcomes (KDIGO) (Table 134–1), is preferred. The system uses creatinine and urine output criteria and can be applied to both children and adults, minimizing practice variation.3
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AKI is the result of nephrotoxic and/or hypoxic injury to the glomeruli and renal tubules.1 Reduced blood flow causes hypoxic injury and damages the proximal tubular cells. Common nephrotoxins include aminoglycosides, contrast agents, calcineurin inhibitors, amphotericin B, and nonsteroidal anti-inflammatory drugs.4 Inflammatory mediators intensify renal tubular damage.2
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AKI is frequently classified based on three major anatomic locations of injury: prerenal, renal, and postrenal disease. Prerenal disease is typically caused by inadequate renal perfusion and is the most common class of AKI. Prerenal AKI is typically due to hypovolemia (e.g., bleeding or GI losses such as vomiting and diarrhea), decreased renal artery blood flow, or reduction in effective circulation (e.g., heart failure, cardiogenic shock, third spacing in septic shock). Renal disease or intrinsic renal disease occurs when there is structural damage to the renal parenchyma. Common causes of renal disease include glomerular diseases (e.g., pyelonephritis, nephrotic syndrome, glomerulonephritis, Henoch-Schönlein purpura), vascular diseases (e.g., hemolytic-uremic syndrome, thrombosis, vasculitides), interstitial diseases (e.g., interstitial nephritis, infections), and tubular injuries (e.g., ischemia, nephrotoxins, hypotension). Lastly, postrenal disease is typically due to an obstruction caused by congenital or acquired anomalies to the lower urinary tract. Examples include nephrolithiasis, renal vein thrombosis, pelvic masses (e.g., lymphoma, rhabdomyosarcoma), and urethral obstruction (posterior ureteral valves).
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