Renal failure is defined as the inability of the kidney tomaintain homeostasis leading to azotemia or theaccumulation of nitrogenous wastes; however, exactbiochemical or clinical criteria for this diagnosis are notdefined clearly. “Renal failure” is distinguished from“renal insufficiency,” where renal function is abnormalbut capable of sustaining essential bodily functions .Renal failure is defined as anuric when urine volume isless than 50 ml for 24 hours; oliguric when the volume isless than 500 ml for 24 hours; and nonoliguric when thevolume is from 500-6,000 ml for 24 hours. Urine outputabove 6,000 ml is designated polyuric .

　　Causes of renal failure are conventionally separated intothree categories: prerenal, intrarenal, and postrenal.Hypoperfusion is the cause of prerenal failure (fluid loss,fluid sequestration, low cardiac output, renal arterystenosis [RAS]). Causes of intrarenal failure include acutetubular necrosis (ATN) and interstitial, glomerular, orsmall–vessel disease. Obstruction is the usual postrenalcause of failure (also, distal renal tubular obstruction).Distinction between acute renal failure (ARF) and chronicrenal failure (CRF) can often be made clinically .However, many patients are first seen with markedlyelevated serum creatinine of unknown duration, so thatclassification into ARF or CRF is not possible.

　　There are significant limitations in using serum creatinineas an accurate measure of renal function, includingdecreased muscle mass and poor nutritional status [4].Creatinine clearance measures the ability of theglomerulus to filter creatinine from the plasma andapproximates the glomerular filtration rate (GFR); there isa reasonable correlation between the 2-hour and 24-hourcreatinine clearance ( r=0.85), but the error in calculationmay vary from 10%-27%. Creatinine clearance of lessthan 60 ml/min may be termed renal insufficiency; lessthan 30 ml/min is renal failure. End-stage renal disease(ESRD) implies CRF of a degree (ie, GFR <10-12ml/min) such that life cannot be sustained long-termwithout dialysis. In ARF, the creatinine clearance isusually less than 25 ml/min. Unfortunately, creatinineclearance is often not helpful when the creatinine value ischanging.

　　ARF can be broadly defined as a sudden decrease in renalfunction resulting in azotemia. It can develop in thesetting of pre-existing renal insufficiency or can developin a patient with previously normal kidneys . In apatient with previously undiagnosed renal failure, initialevaluation of renal size by gray-scale ultrasonography(US) is most helpful. If the kidneys are small andechogenic, the process of long-standing evaluation by UShelps to identify a correctable cause of renal failure suchas obstruction. If hydronephrosis is present, retrograde orantegrade relief of the obstruction is usually undertaken.If no hydronephrosis is evident and the patient does nothave hypertension or other history to suggest RAS,further workup of small, echogenic kidneys is notwarranted. Conversely, if the kidneys are of normal sizewith or without increased echogenicity, this may representreversible renal failure, most often ARF, and a moreextensive evaluation is initiated. It should be noted that,as with all modalities and procedures, the yield of gray-scale sonography in the detection of hydronephrosis islow among patients without a high pretest probability for urinary obstruction (eg, flank pain, urolithiasis, pelvicmasses, etc), and, therefore is of little value in patientmanagement [6]. Scintigraphy with a tubular secretionagent (eg, MAG-3) can help assess the level of renalfunction as well as the potential reversibility of theprocess causing the renal failur e. Therefore, in addition tothe history, physical examina tion, and laboratory analysisof serum and urine, US and radionuclide scintigraphy areimaging tools that are used early in the evaluation of thepatient with previously undiagnosed renal failure. If RASor occlusion is suspected, magnetic resonanceangiography (MRA) techniques may be used to avoidnephrotoxic iodinated contrast media.

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