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Key Features

Essentials of Diagnosis

  • Acute kidney injury

  • Ischemia or toxic insult or underlying sepsis

  • Pigmented granular casts and renal tubular epithelial cells in urine sediment are pathognomonic but not always present

General Considerations

  • Acute kidney injury as a result of tubular damage

  • Accounts for approximately 85% of intrinsic acute kidney injury

  • Two major causes are ischemia and nephrotoxin exposure

  • Renal tubular damage with low effective arterial blood flow to the kidney can result in tubular necrosis and apoptosis

  • Ischemic acute kidney injury occurs in prolonged hypotension or hypoxemia such as with volume depletion, shock, and sepsis and after major surgical procedures

  • Exogenous nephrotoxins more commonly cause damage than endogenous nephrotoxins

Exogenous nephrotoxins

  • Aminoglycosides

  • Vancomycin, intravenous acyclovir, several cephalosporins

  • Radiographic contrast media

  • Antineoplastics, such as cisplatin and organic solvents (eg, etoposides, paclitaxel), and heavy metals (mercury, cadmium, and arsenic)

Endogenous nephrotoxins

  • Myoglobinuria as a consequence of rhabdomyolysis

  • Hemoglobinuria as a consequence of massive intravascular hemolysis

  • Hyperuricemia

  • Bence Jones proteinuria, paraproteins

Clinical Findings

Symptoms and Signs

  • See Kidney Injury, Acute

Differential Diagnosis

  • Prerenal azotemia (eg, dehydration)

  • Postrenal azotemia (eg, benign prostatic hyperplasia)

  • Renal causes of acute kidney injury

    • Acute glomerulonephritis: immune complex (eg, IgA nephropathy), pauci-immune (eg, granulomatosis with polyangiitis [formerly Wegener granulomatosis]), antiglomerular basement membrane disease

    • Acute interstitial nephritis: drugs (eg, β-lactams), infections (eg, Streptococcus), immune (eg, systemic lupus erythematosus)

Diagnosis

Laboratory Tests

  • BUN:creatinine ratio < 20:1

  • Hyperkalemia and hyperphosphatemia are commonly present

  • Urinalysis

    • May show evidence of acute tubular damage

    • Urine sediment may be brown

    • On microscopic examination, an active sediment may show renal tubular epithelial cells, epithelial cell casts, and pigmented granular ("muddy brown") casts

  • Fractional excretion of sodium or FENa = clearance of Na+/GFR = clearance of Na+/creatinine clearance

  • FENa = (urineNa/serumNa)/(urineCr/serumCr) × 100%

  • FENa is high (> 1%) in acute tubular necrosis

Treatment

Medications

  • Stop offending agent and correct ischemia

  • Furosemide

    • Intravenous use can minimize disabling side effects of supranormal dosing

    • Starting dose of 0.1–0.3 mg/kg/h is appropriate

      • Increase to a maximum of 0.5–1 mg/kg/h

      • A bolus of 1–1.5 mg/kg should be administered with each dose escalation

  • Thiazide diuretics can be used to augment urinary output; reasonable choices include

    • Metolazone: 2.5–5 mg orally every 12–24 hours

      • Less expensive than intravenous chlorothiazide

      • Reasonable bioavailability

    • Chlorothiazide at doses of 250–500 mg intravenously every 8–12 hours

  • Phosphate-binding agents

    • Aluminum hydroxide, 500 mg orally with meals

    • Calcium carbonate, 500–1500 mg three times daily orally

    • Calcium acetate, 667 mg 2–3 tablets orally before meals

    • Sevelamer carbonate, 800–1600 mg three times daily orally

    • Lanthanum carbonate, ...

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