Acute kidney injury (AKI), previously known as acute renal failure, is characterized by the sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys. AKI is not a single disease but, rather, a designation for a heterogeneous group of conditions that share common diagnostic features: specifically, an increase in the blood urea nitrogen (BUN) concentration and/or an increase in the plasma or serum creatinine (SCr) concentration, often associated with a reduction in urine volume. AKI can range in severity from asymptomatic and transient changes in laboratory parameters of glomerular filtration rate (GFR), to overwhelming and rapidly fatal derangements in effective circulating volume regulation and electrolyte and acid-base composition of the plasma.
Changing the name of a syndrome as well known as "acute renal failure" does not occur frequently. We will summarize some of the reasons why the name was changed to "acute kidney injury." The term failure reflects only part of the spectrum of damage to the kidney that occurs clinically. In most cases of damage, the reduction in kidney function is modest. Nevertheless, this modest change has been documented to be associated with negative effects on outcome, albeit not nearly as ominous as seen with large decreases in kidney function associated with frank kidney failure that often requires acute dialysis therapies. Furthermore, the term renal is not well understood in the general population and this makes communication with patients and family more challenging; hence "kidney" has replaced "renal."
AKI complicates 5–7% of acute care hospital admissions and up to 30% of admissions to the intensive care unit. AKI is also a major medical complication in the developing world, particularly in the setting of diarrheal illnesses, infectious diseases like malaria and leptospirosis, and natural disasters such as earthquakes. The incidence of AKI has grown by more than fourfold in the United States since 1988 and is estimated to have a yearly incidence of 500 per 100,000 population, higher than the yearly incidence of stroke. AKI is associated with a markedly increased risk of death in hospitalized individuals, particularly in those admitted to the ICU where in-hospital mortality rates may exceed 50%.
AKI in the Developing World
The epidemiology of AKI differs tremendously between developed and developing countries, owing to differences in demographics, economics, geography, and comorbid disease burden. While certain features of AKI are common to both—particularly since urban centers of some developing countries increasingly resemble those in the developed world—many etiologies for AKI are region-specific such as envenomations from snakes, spiders, caterpillars, and bees; infectious causes such as malaria and leptospirosis; and crush injuries and resultant rhabdomyolysis from earthquakes.
The causes of AKI have traditionally been divided into three broad categories: prerenal azotemia, intrinsic renal parenchymal disease, and postrenal obstruction (Fig. 279-1).
Classification of the major causes of acute kidney injury. ACE-1, angiotensin-converting enzyme 1; ARB, angiotensin receptor blocker; NSAIDs, nonsteroidal anti-inflammatory drugs; TTP-HUS, thrombotic thrombocytopenic purpura-hemolytic uremic syndrome.
Prerenal azotemia (from "azo," meaning nitrogen, and "-emia") is the most common form of AKI. It is the designation for a rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration. The most common clinical conditions associated with prerenal azotemia are hypovolemia, decreased cardiac output, and medications that interfere with renal autoregulatory responses such as nonsteroidal anti-inflammatory drugs (NSAIDs) and inhibitors of angiotensin II (Fig. 279-2). Prerenal azotemia may coexist with other forms of intrinsic AKI. Prolonged periods of prerenal azotemia may lead to ischemic injury, often termed acute tubular necrosis, or ATN. By definition, prerenal azotemia involves no parenchymal damage to the kidney and is rapidly reversible once intraglomerular hemodynamics are restored.
Normal GFR is maintained in part by the relative resistances of the afferent and efferent renal arterioles, which determine the glomerular plasma flow and the transcapillary hydraulic pressure gradient that drive glomerular ultrafiltration. Mild degrees of hypovolemia and reductions in cardiac output elicit compensatory renal physiologic changes. Because renal blood flow accounts for 20% of the cardiac output, renal vasoconstriction and salt and water reabsorption occur as a homeostatic response to decreased effective circulating volume or cardiac output in order to maintain blood pressure and increase intravascular volume to sustain perfusion to the cerebral and coronary vessels. Mediators of this response include angiotensin II, norepinephrine, and vasopressin (also termed antidiuretic hormone). Glomerular filtration can be maintained despite reduced renal blood flow by angiotensin II–mediated renal efferent vasoconstriction, which maintains glomerular capillary hydrostatic pressure closer to normal ...