Acute Kidney Injury

Key Points

  • Acute kidney injury (AKI) is the sudden loss of kidney function over hours to days — reversible if detected and treated early.
  • Three pathophysiological categories: prerenal (reduced blood flow to kidneys), intrarenal (direct kidney tissue damage), and postrenal (urinary outflow obstruction).
  • Critical lab indicators: rising serum creatinine, elevated BUN, decreased GFR, and hyperkalemia — hyperkalemia is the most immediately life-threatening electrolyte implication.
  • Priority nursing goal: urine output ≥30 mL/hour; oliguria (<400 mL/day) or anuria (<50 mL/day) signals severe impairment.
  • Management: treat underlying cause, IV fluids (prerenal), eliminate nephrotoxins, electrolyte correction, and dialysis in severe cases.

Pathophysiology

Three Categories of AKI

TypeMechanismExamples
PrerenalReduced renal blood flow → decreased glomerular perfusionHypovolemia, hemorrhage, sepsis, cardiogenic shock, severe heart failure, vascular obstruction
IntrarenalDirect damage to renal tubules or nephronsProlonged ischemia, nephrotoxic drugs (aminoglycosides, NSAIDs, contrast media), rhabdomyolysis (myoglobin), hemolysis (hemoglobin)
PostrenalMechanical obstruction of urinary outflow → urine backflow damages kidneyBenign prostatic hyperplasia (BPH), prostate cancer, kidney stones, urethral stricture, pelvic tumors

Prerenal causes also include severe burns and other high-volume fluid-loss states. Intrarenal injury may occur with interstitial nephritis, vasculitic or malignant-hypertension vascular injury, and selected heavy-metal toxic exposure.

High-risk populations: older adults (natural decline in renal reserve), clients with CKD, diabetes, hypertension, heart failure, liver disease, autoimmune disease, dehydration, blood-loss/trauma burden, severe infection, or recent exposure to nephrotoxins or contrast dye.

Nursing Assessment

NCLEX Focus

Hyperkalemia in AKI is the priority electrolyte emergency — the kidneys cannot excrete potassium, and elevated levels cause fatal cardiac dysrhythmias. Always correlate potassium levels with ECG changes (peaked T waves, wide QRS, sine wave pattern).

Clinical manifestations by system:

SystemManifestations
RenalOliguria (<30 mL/hr), anuria, uremia (elevated BUN/creatinine, uremic frost in severe cases)
CardiovascularHypertension (fluid overload), pitting edema, heart failure, arrhythmias from hyperkalemia, pericarditis
RespiratoryDyspnea from pulmonary edema, Kussmaul breathing (severe metabolic acidosis)
NeurologicalConfusion, asterixis (flapping tremor), peripheral neuropathy, seizures
GINausea, vomiting, anorexia, gastritis, GI bleeding
HematologicAnemia (↓ erythropoietin), bleeding tendencies
IntegumentaryPruritus, pallor, dry skin, ecchymosis, uremic frost (severe)
EndocrineHyperkalemia, hyponatremia, metabolic acidosis, insulin resistance

Priority laboratory findings:

  • Serum creatinine: elevated (primary indicator)
  • BUN: elevated (creatinine:BUN ratio helps identify prerenal vs intrarenal)
  • GFR: decreased
  • Potassium: hyperkalemia — most urgent
  • Sodium: hyponatremia (dilutional)
  • Arterial blood gas: metabolic acidosis (low pH, low HCO₃)
  • CBC: anemia, elevated WBC if infection is cause
  • Urinalysis and renal ultrasound: evaluate structural causes, obstruction, and infection contributors

Nursing Interventions

Identify and treat the underlying cause:

  • Prerenal: restore circulating volume with IV fluids (isotonic crystalloids) — improve renal perfusion
  • Intrarenal: identify and discontinue nephrotoxins; medications that affect renal blood flow (NSAIDs, ACE inhibitors) may need to be held
  • Postrenal: relieve obstruction (urethral catheter for BPH, nephrostomy tube for stone/tumor)

Fluid and electrolyte management:

  • Monitor urine output hourly — target ≥30 mL/hour; insert indwelling catheter for accurate measurement
  • Hyperkalemia management: insulin + dextrose (shifts K⁺ into cells), sodium bicarbonate, kayexalate (removes K⁺ from body), cardiac monitoring — check ECG for peaked T waves, widened QRS
  • Fluid restriction if oliguric to prevent fluid overload
  • Sodium and fluid restriction as prescribed; dietary phosphorus and protein restriction in established AKI

Dialysis indications (severe AKI): refractory fluid overload, severe hyperkalemia, symptomatic uremia, metabolic acidosis unresponsive to treatment — hemodialysis (acute), peritoneal dialysis, or continuous renal replacement therapy (CRRT) for hemodynamically unstable clients.

  • If dialysis is started, coordinate pre-treatment medication review because some medications are dialyzable or can worsen intradialytic hypotension.

Medication safety:

  • Avoid or dose-adjust all renally cleared medications (digoxin, antibiotics, NSAIDs, contrast dye)
  • Hold ACE inhibitors, ARBs, diuretics in prerenal AKI until volume restored
  • Consult pharmacy for renal dosing adjustments
  • Ensure intake/output is measured and documented accurately each shift and trended over 24 hours.
  • Monitor daily weights to support fluid-balance decisions, especially during dialysis care windows.

Acute Oliguria

A urine output <0.5 mL/kg/hour for more than 6 consecutive hours is a criterion for AKI and requires immediate provider notification. Do not wait for laboratory confirmation — act on clinical cues.

Self-Check

  1. How do you differentiate prerenal from intrarenal AKI based on clinical history and laboratory values?
  2. A client with AKI has a potassium level of 6.8 mEq/L and is showing peaked T waves on the ECG. What is the priority nursing action?
  3. When should a nurse hold IV fluid administration for a client with AKI, and what assessment finding would guide this decision?