Acute Kidney Injury

Basics

Description

  • “Renal failure” is an outdated term
  • Acute kidney injury (AKI) is newly defined by the Kidney Disease Improving Global Outcomes (KDIGO) classification as:
    • Serum creatinine increase ≥0.3 mg/dL within 48 hr; or
    • Serum creatinine increase to ≥1.5 × baseline, occurring within prior 7 d; or
    • Urine volume <0.5 mL/kg/hr for 6 hr
  • Serum creatinine or urine volume maximum changes determine AKI stage
  • KDIGO staging:
    • Stage 1: Increase in Cr by 0.3 mg/dL or 1.5–1.9 × baseline or Urine output (UO) <0.5 mg/kg/hr for ≥6 hr
    • Stage 2: Increase in Cr by 2–2.9 × baseline or UO <0.5 mg/kg/hr for ≥12 hr
    • Stage 3: Increase in Cr by 4 mg/dL or 3 × baseline or UO <0.3 mg/kg/hr for ≥24 hr or initiation of renal replacement therapy
  • AKI consequences include:
    • Waste product accumulation
    • Electrolyte disturbances
    • Fluid accumulation
    • Reduced immunity
    • Other organ dysfunction
  • AKI leads to increased morbidity and mortality
  • AKI biomarkers may become increasingly important for early diagnosis and prognosis.

Etiology

  • Prerenal AKI:
    • Caused by renal hypoperfusion
    • Renal tissue remains normal unless severe/prolonged hypoperfusion
  • Intrarenal AKI:
    • Caused by renal parenchymal diseases
  • Iatrogenic AKI, causes include:
    • Aminoglycoside antibiotics
    • NSAIDs
    • ACE inhibitors
    • Angiotensin receptor blockers
    • IV contrast may be a risk in patients with significant preexisting disease
  • Postrenal AKI:
    • Due to urinary tract obstruction (eg, prostatic hypertrophy, prostatitis)

Diagnosis

Signs And Symptoms

  • Often asymptomatic, commonly diagnosed/suspected based on routine lab screening
  • Oliguria (<400 mL/d urine production)
  • Fluid overload:
    • Dyspnea
    • Hypertension
    • Jugular venous distention
    • Pulmonary and peripheral edema
    • Ascites
    • Pericardial and pleural effusion
  • Nausea/vomiting
  • Pruritus/skin changes
  • Altered mental status

Prerenal Aki

  • Absolute or relative intravascular fluid deficit
  • Dry mucous membranes
  • Hypotension
  • Tachycardia
  • Low cardiac output
  • Congestive heart failure
  • Systemic vasodilation (eg, sepsis, anaphylaxis)

Intrinsic Aki

  • Acute interstitial nephritis:
    • Fever
    • Rash
    • Arthralgias
    • Recent myocardial infarction
  • Renal vein thrombosis:
    • Nephrotic syndrome
    • Can be associated with pulmonary embolus
    • Flank or abdominal pain
  • Thrombotic thrombocytopenic purpura (TTP):
    • Mild BUN/Cr elevation
    • Fever
    • Altered mental status
    • Anemia and thrombocytopenia
    • Neurologic: Coma, seizure, headache, altered mental status

Postrenal Aki

  • Abdominal or flank pain
  • Distended bladder
  • Oliguria or anuria

Aki Complications

  • Uremic syndrome:
    • Altered mental status
    • Asterixis
    • Reflex abnormalities
    • Focal neurologic deficits
    • Seizures
    • Restless leg syndrome
    • Pericarditis
    • Pericardial effusion/cardiac tamponade
    • Ileus
    • Platelet dysfunction
    • Pruritus
  • Hematologic disorders:
    • Anemia
    • Increased bleeding time and platelet dysfunction
    • Leukocytosis

History

  • Prior AKI history
  • AKI risk factors: CHF, DM, HTN
  • Medication or nephrotoxin exposure
  • Weight change

Physical Exam

  • Vital signs: Hypotension, HTN, fever, tachycardia
  • Altered mental status
  • Eyes: Fundoscopy
  • CV exam: Jugular venous distention, gallop
  • Lungs: Rales
  • Abdomen: Flank tenderness, palpable kidneys
  • Edema
  • Integument: Excoriations, “uremic frost,” dry mucous membranes

Geriatric Considerations

  • Prone to prerenal AKI
  • Cr varies with muscle mass, so “normal” Cr may represent an elevation
  • Increased risk for contrast- and medication-induced AKI

Pediatric Considerations

  • Prerenal AKI a concern in neonates
  • Anatomic abnormalities (renal dysplasia, agenesis, cysts)

Pregnancy Considerations

  • Intrinsic renal azotemia
  • Pre-eclampsia/eclampsia
  • Ischemia: Postpartum hemorrhage, abruptio placentae, amniotic fluid embolus
  • Direct toxicity of illegal abortifacients
  • Postpartum TTP, hemolytic uremic syndrome (HUS)

Essential Workup

  • Electrolytes including Ca, Mg, PO4
  • BUN/Cr
  • Urinalysis (UA):
    • Centrifuged specimen helps to distinguish different etiologies of AKI
    • Exam for casts, blood, WBCs, and crystals
  • Fractional excretion (FE) of Na and/or urea
  • CBC: Anemia common with chronic disease
  • Postvoid residual volume (>100 mL suggests obstruction) OR US to rule out obstruction—especially in older men (eg, prostatic hypertrophy, prostatitis)
  • ECG—but CAUTION: Insensitive indicator for potentially lethal hyperkalemia
  • Biomarkers (likely clinically available in the near future)—NGAL, KIM-1, IL-18, L-FABP, cystatin-C all studied in ED populations

Diagnostic Tests And Interpretation

Lab

Prerenal

  • UA:
    • Specific gravity >1.018
    • Osmolality >500 mmol/kg
    • Sodium <10 mmol/L
    • Hyaline casts
    • BUN/Cr ratio >20
    • Fractional excretion of sodium (FENa) <1%
    • Rapid renal function recovery when renal perfusion normalized

Intrarenal

  • BUN/Cr ratio <10–15
  • FENA >2%
  • Glomerulonephritis, vasculitis:
    • UA with red cell or granular casts
    • Complement and autoimmune antibodies
  • HUS or TTP:
    • UA normal
    • Anemia
    • Thrombocytopenia
    • Schistocytes on blood smear
  • Nephrotoxic acute tubular necrosis (ATN):
    • UA:
      • Brown granular or epithelial cell casts
      • Specific gravity = 1.010
      • Urine osmolality <350 mmol/kg
      • Urine Na >20 mmol/L
  • Ethylene glycol ingestion:
    • UA: Calcium oxalate crystals
    • Anion gap metabolic acidosis
    • Osmolar gap
  • Rhabdomyolysis:
    • Elevated serum K+, PO4, myoglobin, creatine phosphokinase, uric acid
    • Decreased serum Ca2+
  • Acute interstitial nephritis:
    • UA with WBC casts, WBCs, RBCs, and proteinuria
    • Peripheral eosinophilia

Postrenal

UA:

  • Usually normal
  • May have some hematuria but no casts or protein
  • FENA often >4%
  • Urine osmolality usually <350 mmol/kg

Imaging

  • US:
    • 98% sensitive for detecting hydronephrosis
  • CT scan:
    • Noncontrast sensitive for obstruction
    • May detect intrarenal abnormalities
  • Duplex scan for:
    • Renal artery or vein thrombosis
  • Renal arteriogram:
    • Definitive diagnosis of renal artery thrombosis, renal infarction
  • Inferior vena cava and renal vessel venogram for renal vein thrombosis
  • IV pyelogram (rarely performed)

Diagnostic Procedures/Surgery

ECG:

  • Hypertension secondary to volume overload may cause ischemia
  • May detect acute electrolyte changes, but poorly sensitive for potentially life-threatening hyperkalemia

Treatment

Prehospital

  • Airway, breathing, and circulation (ABCs):
    • Supplemental oxygen for hypoxia
  • IV crystalloid for volume depletion

Initial Stabilization/Therapy

  • ABCs:
    • Supplemental oxygen for hypoxia
    • IV crystalloid for volume depletion
    • Correct electrolyte disturbances
  • Emergent dialysis indications (discuss with nephrologist):
    • Hypervolemia with pulmonary edema
    • Severe hyperkalemia (serum K >6.5 mEq/L), hyperkalemia with symptoms (cardiac conduction abnormalities, muscle weakness), or hyperkalemia >5.5 mEq/L with ongoing tissue breakdown (rhabdomyolysis) or ongoing K absorption (large volume blood transfusion)
    • Uremic encephalopathy, bleeding, or pericarditis
    • Intractable metabolic acidosis (pH <7.1)
  • Avoid nephrotoxic drugs
  • Monitor UO
  • Cardiac monitoring

Ed Treatment/Procedures

Prerenal AKI:

  • Treat hypoperfusion with IV crystalloid
  • Packed RBC for blood loss or anemia after lack of response after 2 boluses
  • Invasive cardiac monitoring if unable to assess cardiac failure vs hypovolemia
  • Response to crystalloid is good indicator of the degree to which hypovolemia is a factor
ALERT

Administer crystalloid fluid challenge cautiously to avoid fluid overload in liver failure with ascites Intrarenal AKI

  • Glomerulonephritis:
    • Glucocorticoids or plasma exchange
  • ATN:
    • Volume replacement
  • Hyponatremia: Free water restriction
  • Hyperkalemia:
    • For K+ >6.5 mEq/L or ECG abnormalities consistent with hyperkalemia:
      • Albuterol via nebulizer
      • Dextrose and insulin
      • Furosemide if patient not anuric
      • Calcium stabilizes myocardium in severe hyperkalemia; Calcium gluconate for stable patient, calcium chloride for patient without pulse
      • Dialysis for intractable hyperkalemia
  • Metabolic acidosis:
    • Consider sodium bicarbonate for pH <7.1 or HCO3 <15 mEq/L in chronic disease only
    • Hyperphosphatemia:
      • Calcium carbonate
      • Aluminum hydroxide
    • Myoglobinuria—aggressive fluid resuscitation with NS
ALERT
  • Calcium is only indicated by ECG for widened PR, QT, or QRS intervals. Peaked T-waves alone are not an indication
  • Sodium bicarbonate is a considerable sodium load; use caution in anuric/oliguric patients

Medication

  • Albuterol: Concentrated solution 10–20 mg via nebulizer
  • Aluminum hydroxide: 0.5–1.5 g PO
  • Calcium carbonate (Os-Cal): 0.25–3 g PO
  • Calcium gluconate: 10 mL of 10% solution over 5 min IV (may repeat q5min)
  • Calcium chloride: 5–10 mL of 10% solution-slow IVP (peds: 0.2–0.25 mL/kg)
  • Dextrose: D50W 1 amp (50 mL or 25 g) (peds: D25W 2 mL/kg) IV
  • Furosemide: 40–80 mg IV push
  • Insulin: 0.1 units/kg regular IV with IV dextrose (decrease dose by 50% for severe renal and/or liver disease)
  • Sodium bicarbonate: 1–2 mEq/kg IV
  • Sodium zirconium cyclosilicate 10 g PO
ALERT
  • Diuretics (in the absence of volume overload) and dopamine are not recommended in AKI
  • Sodium polystyrene sulfonate (Kayexalate) is no longer recommended

Follow-Up

Disposition

Admission Criteria

  • New-onset AKI
  • Hyperkalemia/significant electrolyte abnormalities
  • Fluid overload with hypoxia/congestive heart failure
  • Uremia
  • Altered mental status

Discharge Criteria

  • Stable
  • Normal electrolytes

Issues For Referral

Refer to primary physician for progressive AKI in an otherwise stable patient

Pearls And Pitfalls

  • Insulin dose for hyperkalemia should be reduced (half of normal dose) for significant liver or renal disease so as to avoid hypoglycemia
  • NSAIDs to be avoided with any degree of AKI

Additional Readings

  1. Gameiro J, Fonseca JA, Outerelo C, Lopes JA. Acute kidney injury: from diagnosis to prevention and treatment strategies. J Clin Med. 2020;9(6):1704.  [PMID:32498340]
  2. Ostermann M, Joannidis M. Acute kidney injury 2016: Diagnosis and diagnostic workup. Crit Care. 2016;20:299.  [PMID:27670788]
  3. Rahman M, Shad F, Smith MC. Acute kidney injury: A guide to diagnosis and management. Am Fam Physician. 2012;86(7):631–639.  [PMID:23062091]
  4. https://kdigo.org/

See Also (Topic, Algorithm, Electronic Media Element)

Authors

Robin Jin

Matthew N. Graber