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INTRODUCTION

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Patients with acute kidney injury (AKI) present with a wide variety of manifestations depending on the underlying etiology. AKI can be caused by hypovolemia, nephrotoxic medications, and anatomic problems of the genitourinary tract. Additional etiologies include cardiac, vascular, thrombotic, glomerular, and renal tubular disorders.

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CLINICAL FEATURES

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Deterioration in renal function leads to an excessive accumulation of nitrogenous waste products in the serum and significant electrolyte abnormalities. Patients usually have signs and symptoms of their underlying causative disorder but eventually develop stigmata of renal failure. Volume overload, hypertension, pulmonary edema, mental status changes or neurologic symptoms, nausea and vomiting, bone and joint problems, anemia, and increased susceptibility to infection (a leading cause of death) can occur as patients develop more chronic uremia.

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DIAGNOSIS AND DIFFERENTIAL

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History and physical examination usually provide clues to the etiology. Signs and symptoms of the underlying causative disorder should be vigorously sought. Physical examination should assess vital signs and volume status, establish urinary tract patency and output, and search for signs of chemical intoxication, drug usage, muscle damage, infection, or associated systemic disease. Diagnostic studies include urinalysis, blood urea nitrogen and creatinine levels, serum electrolytes, urinary sodium and creatinine, and urinary osmolality. Analysis of these tests allows most patients to be categorized as prerenal, renal, or postrenal. Fractional excretion of sodium can be calculated to help in this categorization (Table 50-1). Normal urinary sediment may be seen in prerenal and postrenal failure, hemolytic-uremic syndrome, and thrombotic thrombocytopenic purpura. The presence of albumin may indicate glomerulonephritis or malignant hypertension. Granular casts are seen in acute tubular necrosis. Albumin and red blood cell casts are found in glomerulonephritis, malignant hypertension, and autoimmune disease. White blood cell casts are seen in interstitial nephritis and pyelonephritis. Crystals can be present with renal calculi and certain drugs (sulfas, ethylene glycol, and radiocontrast agents). Renal ultrasound is the radiologic procedure of choice in most patients with renal failure when upper tract obstruction and hydronephrosis are suspected. Color-flow Doppler can assess renal perfusion and facilitate the diagnosis of large vessel causes of renal failure. Bedside sonography can quickly diagnose some treatable causes and give guidance for fluid resuscitation; inspiratory collapse of the intrahepatic inferior vena cava (IVC) can give a good measure of volume status and fluid responsiveness (Fig. 50-1).

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Figure 50-1

Ultrasound of the inferior vena cava. A. Dilated inferior vena cava (arrows) with little respiratory variation as might be expected in volume overload. B. An almost fully collapsed inferior vena cava at inspiration (arrows) and expiration (arrowheads) as might be expected in prerenal acute kidney injury. Used with permission from Michael B, Stone, MD, RDMS.

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