Kidney Injury, Acute

Key Features

Essentials of Diagnosis

• Rapid increase in serum creatinine

• Oliguria may be present

• Symptoms and signs depend on cause

General Considerations

• Defined as an absolute increase in serum creatinine by ≥ 0.3 mg/dL within 48 hours or relative increase to ≥ 1.5 times baseline that is known or presumed to have occurred within 7 days

• Characterized as oliguric if urine production is < 400–500 mL/day or < 20 mL/h

• Clinically, characterized by an inability to maintain acid-base, fluid, and electrolyte balance and to excrete nitrogenous wastes

• The 2012 KDIGO Clinical Practice Guidelines for AKI describes three progressive stages based on the elevation in serum creatinine or decline in urinary output

  • Stage 1: 1.5- to 1.9-fold increase in serum creatinine or a decline in urinary output to 0.5 mL/kg/h over 6–12 hours

  • Stage 2: 2.0–2.9 increase in serum creatinine or a decline in urinary output to 0.5 mL/kg/h over > 12 hours

  • Stage 3: 3-fold or greater increase in serum creatinine, an increase in serum creatinine to ≥ 4 mg/dL, or a decline in urinary output to < 0.3 mL/kg/h for ≥ 24 hours, anuria for ≥ 12 hours, or initiation of renal replacement therapy

• Serum creatinine concentration can typically increase by 1.0–1.5 mg/dL daily

Demographics

• 5% of hospital admissions and 30% of ICU admissions have acute kidney injury

• 25% of hospitalized patients develop acute kidney injury

Clinical Findings

Symptoms and Signs

• Nausea, vomiting

• Malaise

• Hypertension

• Pericardial friction rub, effusions, and cardiac tamponade

• Arrhythmias

• Rales

• Abdominal pain and ileus

• Bleeding secondary to platelet dysfunction

• Encephalopathy, altered sensorium, asterixis, seizures

• Oliguria, defined as urinary output < 500 mL/day or < 20 mL/h

Differential Diagnosis

PRERENAL CAUSES

• Dehydration

• Hemorrhage (eg, gastrointestinal bleeding)

• Heart failure

• Renal artery stenosis, including fibromuscular dysplasia

• Nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme inhibitors

POSTRENAL CAUSES

• Obstruction (eg, benign prostatic hyperplasia, bladder tumor)

INTRINSIC RENAL DISEASE

• Acute tubular necrosis

  • Toxins

    • NSAIDs

    • Antibiotics

    • Intravenous contrast

    • Plasma cell myeloma (formerly multiple myeloma)

    • Rhabdomyolysis

    • Hemolysis

    • Chemotherapy

    • Hyperuricemia

    • Cyclosporine

  • Ischemia (eg, prolonged prerenal insults)

• Acute glomerulonephritis

  • Immune complex

    • IgA nephropathy

    • Endocarditis

    • Systemic lupus erythematosus (SLE)

    • Cryoglobulinemia

    • Postinfectious

    • Membranoproliferative

  • Pauci-immune (ANCA-positive)

    • Granulomatosis with polyangiitis (formerly Wegener granulomatosis)

    • Eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome)

    • Microscopic polyarteritis

  • Antiglomerular basement membrane (anti-GBM)

    • Goodpasture disease

    • Anti-GBM glomerulonephritis

• Vascular

  • Malignant hypertension

  • Thrombotic thrombocytopenia purpura

  • Atheroembolism

• Acute interstitial nephritis

  • Drugs

    • β-Lactams

    • Sulfa

    • Diuretics

    • NSAIDs

    • Rifampin

    • Phenytoin

    • Allopurinol

  • Infections

    • Streptococcus

    • Leptospirosis

    • Cytomegalovirus

    • Histoplasmosis

    • Rocky Mountain spotted fever

  • Immune

    • SLE

    • Sjögren syndrome

    • Sarcoidosis

    • Cryoglobulinemia

Diagnosis

Laboratory Tests

• Serum creatinine and BUN elevated

• BUN–creatinine ratio > 20:1 in prerenal and postrenal causes, and acute glomerulonephritis; < 20:1 in acute tubular necrosis and ...