Kidney Injury, Acute

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 at least 1.5 times baseline that is known or presumed to have occurred within 7 days

• Characterized as oliguric if urine production is < roughly 400–500 mL/day

• 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: 3.0-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

Symptoms and Signs

• Nausea, vomiting

• Malaise

• Hypertension

• Pericardial friction rub, effusions, and cardiac tamponade

• Ventricular tachycardia and other tachyarrhythmias

• 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

    • 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

    • 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

    • Beta-lactams

    • Sulfa

    • Diuretics

    • NSAIDs

    • Rifampin

    • Phenytoin

    • Allopurinol

  • Infections

    • Streptococcus

    • Leptospirosis

    • Cytomegalovirus

    • Histoplasmosis

    • Rocky Mountain spotted fever

  • Immune

    • SLE

    • Sjögren syndrome

    • Sarcoidosis

    • Cryoglobulinemia

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 acute interstitial nephritis

• Hyperkalemia

• Anion gap metabolic acidosis

• Hyperphosphatemia

• Hypocalcemia

• Anemia

• Fractional excretion of sodium (FE_Na) can be useful in oliguric states:

  • FE_Na = clearance of Na⁺/GFR = clearance of Na⁺/creatinine clearance

  • FE_Na = (urine_Na /serum_Na)/(urine_Cr/ serum_Cr) × 100%

• FE_Na low (< 1%) in prerenal insults; high (> 1%) in acute tubular necrosis; variable in postrenal causes, acute interstitial nephritis, acute glomerulonephritis

Imaging Studies

• Renal ultrasonography to exclude obstruction or other anatomic abnormalities; check renal size and echotexture

• CT or MRI if retroperitoneal fibrosis from tumor or radiation suspected

Diagnostic Procedures

• ECG: peaked T waves, PR prolongation, and QRS widening in hyperkalemia, long QT interval with hypocalcemia

Therapeutic Procedures

• Prerenal insults

  • Treatment depends on cause

  • Achieve euvolemia

  • Monitor serum electrolytes

  • Avoid nephrotoxic drugs

• Postrenal causes: relieve obstruction if present

  • Place catheters or stents through an obstruction

  • Catheterize bladder if hydroureter, hydronephrosis and enlarged bladder on ultrasonography

• Intrinsic renal disease: treat underlying cause (see Tubular Necrosis, Acute); hold offending agents

• Indications for hemodialysis, peritoneal dialysis:

  • Uremic symptoms (eg, pericarditis, encephalopathy, or coagulopathy)

  • Fluid overload unresponsive to diuresis

  • Refractory hyperkalemia

  • Severe metabolic acidosis (pH < 7.20)

  • Neurologic symptoms (eg, seizures or neuropathy)

When to Refer

• If a patient has signs of acute kidney injury that have not reversed over 1–2 weeks, but no signs of acute uremia, the patient can usually be referred to a nephrologist rather than admitted

• If a patient has signs of persistent urinary tract obstruction, the patient should be referred to a urologist

When to Admit

• The patient should be admitted if there is sudden loss of kidney function resulting in abnormalities that cannot be handled expeditiously in an outpatient setting (eg, hyperkalemia, volume overload, uremia) or an acute intervention is needed, such as emergent urologic procedures or dialysis