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Acute renal failure (ARF) is characterized by azotmeia that progresses over several hours or days, with or without oliguria. A consensus classification for acute renal failure has been proposed by the the Acute Dialysis Quality Initiative (ADQI) group to standardize the definition and severity categories of AKI. Acute renal failure is common, with a reported incidence of 2% to 5% of all patients admitted to general medical-surgical hospitals. Prerenal ARF, caused by underperfusion of an otherwise normal kidney, accounted for 21% of cases of ARF in a multicenter study in Madrid.2 The hallmark of prerenal failure is that it is quickly reversible with appropriate therapy.
Prerenal kidney failure can be a result of volume depletion from renal or extrarenal losses, fluid sequestration in liver failure or other edematous states, or inadequate perfusion pressure caused by heart failure. Treatment is imperative, because continued renal hypoperfusion can progress to intrinsic renal failure. Renal ultrasonography, when used to detect obstructions, has a sensitivity and specificity of 90% to 95%. Acute tubular necrosis (ATN), the most common type of intrinsic ARF, accounted for 45% of all cases of ARF.
In oliguric ATN, renal plasma flow declines, but the glomerular filtration rate declines even more.
The distribution of tubular necrosis in the kidneys is patchy, and the degree of necrosis does not correlate with the level of renal dysfunction. Intrinsic acute renal failure is the most common cause; acute tubular necrosis is the most common intrinsic acute renal failure. HIV patients are also at risk of ARF not only from the usual nephrotoxic insults but also from potential nephrotoxicity of protease inhibitors. The diagnosis of AKI traditionally has been based on functional parameters; an increase in serum creatinine is most commonly used as surrogate for impaired glomerular filtration rate (GFR). There is great interest in biomarkers of kidney injury that are elevated with ischemia and within hours of the event.
In addition, urine studies need to be performed, such as urinalysis and measurement of urine volume.
Treatment for intrinsic ARF is largely supportive, including adjusting medications, providing appropriate nutrition, and correcting volume status, hyperkalemia, and acidosis. With any patient with ARF, prescription and nonprescription medications should be reviewed immediately so that any potentially nephrotoxic drugs can be stopped.
If endogenous nephrotoxicity is diagnosed early enough, it can often be reversed with urinary alkalinization, which can prevent kidney failure and the need for dialysis.
Acute renal failure patients who make urine tend to have lower morbidity and mortality rates.
Dopamine in renal doses should probably be used sparingly, if at all, because data on its effectiveness and safety are scant.
The mortality rate in severe ARF is almost 50%, depending on the type of ARF and comorbidities of the patient.
Most deaths are not caused by the ARF itself but rather by the underlying disease or complications.

About 50% of people who survive ATN recover renal function completely and another 40% have an incomplete recovery. Using nonionic contrast agents can cut the overall risk of contrast nephropathy by 50%, from about 6% to 3%. Recently, the term acute kidney injury (AKI) has been popularized to increase awareness of milder degrees of renal impairment and to better describe the underlying pathobiology.
Up to 50% of patients who develop ARF die; survivors face marked increases in morbidity and prolonged hospitalization. Unfortunately, it is also highly operator-dependent, so it should be performed by a highly experienced radiologist. In Stoller JK, Michota, Mandell BF (eds): The Cleveland Clinic Intensive Review of Internal Medicine, 4th ed.
This dichotomy suggests that constriction of the afferent arterioles contributes to the pathophysiologic process.
This is because the medulla of the kidneys, containing the thick ascending limbs of Henle, is less well vascularized and perfused than the cortex and therefore is disproportionately affected by ischemia. Perioperative ATN can result from tumor lysis, sepsis, and nephrotoxins, including antibiotics and contrast agents.
However, estimation of GFR with creatinine in the setting of AKI is inaccurate due to lag time to steady state, as well as other changing determinants of serum creatinine such as volume and nutrition.
The medical history should be reviewed for possible nephrotoxic insults, such as exposure to contrast materials, medications, or hypotension.
In addition to contrast media, other nephrotoxic agents include aminoglycosides and amphotericin (see Box 1). For example, pigment nephropathy from myoglobin, hemoglobin, or methemoglobin can be treated with urinary alkalinization. They are at less risk of hypervolemia, there is room for bicarbonate and nutrition, and there is less likelihood of hyperkalemia.
In normal subjects, dopamine increases renal blood flow by approximately 40% and the glomerular filtration rate by approximately 10%, resulting in increases in salt and water excretion. This phenomenon has led to research with epidermal growth factor, insulin-like growth factor, and hepatocyte-type growth factor as therapy for ischemic ATN.
In a follow-up report of 16,000 patients who were studied by computed tomography with contrast, 183 developed ARF. Issues to consider are correcting volume status, avoiding exposure to nephrotoxins, and preparing for high-risk procedures, such as using contrast agents (Box 3). The spectrum of acute renal failure in the intensive care unit compared with that seen in other settings. Azotemia, on the other hand, signifies the accumulation of nitrogenous waste (urea) and other solutes. The high incidence and substantial morbidity and mortality of ARF demand a logical approach to its prevention and early diagnosis, prompt recognition, and management of its complications. Ultrasonography can yield false-negative results if the obstruction is caused by retroperitoneal fibrosis or certain malignancies that encase the entire system.

If a patient develops ATN while receiving medications, each medication must be reviewed for the possibility of nephrotoxicity. Ischemic injury to epithelial cells can lead to tubular back leak, which allows filtrate back into the bloodstream, and tubular obstruction. If ARF develops 10 to 16 days after transplantation, the most likely immediate cause is hepatic veno-occlusive disease that mimics acute hepatorenal syndrome.
In addition, significant renal impairment can occur with only subtle variation in serum creatinine due to renal reserve or increased secretion (or both). Anuria is a clue that ARF has one of three causes: urinary tract obstruction, a severe type of ATN called cortical necrosis, or a blood vessel blockage by a clot or another obstruction.
Outside the hospital, the main nephrotoxic agents are nonsteroidal anti-inflammatory drugs (NSAIDs). It is not clear whether these increases are caused by a direct effect on the kidneys or are the result of cardiac effects. Other researchers are investigating endothelium receptor blockers to address the ongoing vasoconstriction, and antiadhesion molecule antibodies to prevent vessel congestion by leukocytes.
The mortality rate among those with ARF was 34%, compared with only 7% in a matched cohort from the similarly exposed group.
Pretreating with acetylcysteine can reduce the rise of creatinine levels slightly but might have minor clinical impact. It might also fail to detect an obstruction in extremely volume-depleted patients who do not have enough fluid buildup to reveal the obstruction. Persistent vasoconstriction and congestion from white cells and cell debris lead to ongoing hypoxia and necrosis.
ARF developing 4 to 12 months after bone marrow transplantation may be caused by hemolytic uremic syndrome, perhaps related to cyclosporine or radiation therapy.
It is also prudent to screen for signs of systemic diseases that might affect kidney function, such as lupus erythematosus or Wegener's granulomatosis. Urinalysis, especially examination of the sediment, is fundamental to the evaluation (see Box 2). Patients can also be put at risk by angiotensin-converting enzyme (ACE) inhibitors, cisplatin, ifosfamide, and even Chinese herbal remedies.
Unfortunately, much of the literature on this subject is dated, the studies were poorly designed, and a beneficial effect on mortality is not clear. Low fractional excretion of sodium in a patient with acute oliguria is a classic sign of prerenal failure, and it is also associated with hepatorenal syndrome and acute glomerulonephritis.
However, some types of ATN also have low sodium excretion, specifically postcontrast ATN, rhabdomyolysis, and multisystem organ failure.

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