Acute Kidney Injury (AKI): Stages, Causes, and Nursing Management

Acute kidney injury (AKI) is a high-yield topic on nursing exams because it develops quickly, can be reversed with early recognition, and carries life-threatening complications such as hyperkalemia and fluid overload. This guide reviews the definition, staging, causes, clinical phases, diagnostics, and priority nursing interventions.

What Is Acute Kidney Injury?

• A sudden decrease in kidney function occurring over hours to days.
• Characterized by a rapid rise in serum creatinine, a decrease in urine output, or both.
• Often reversible if identified and treated early.
• Increases risk of chronic kidney disease and mortality.

Stages of AKI (KDIGO Criteria)

• Stage 1: Serum creatinine 1.5–1.9× baseline OR increase ≥0.3 mg/dL within 48 hours; urine output <0.5 mL/kg/hour for 6–12 hours.
• Stage 2: Serum creatinine 2.0–2.9× baseline; urine output <0.5 mL/kg/hour for ≥12 hours.
• Stage 3: Serum creatinine 3.0× baseline OR increase ≥4.0 mg/dL OR initiation of RRT; urine output <0.3 mL/kg/hour for ≥24 hours OR anuria for ≥12 hours.

Mnemonic: Stage 1 = small rise; Stage 2 = double; Stage 3 = triple or dialysis.

Causes and Classification

• Prerenal — decreased blood flow to the kidneys: hypovolemia, heart failure, shock, sepsis, NSAIDs, ACE inhibitors.
• Intrinsic — direct damage to kidney tissue: acute tubular necrosis (ATN), glomerulonephritis, interstitial nephritis, nephrotoxins.
• Postrenal — obstruction of urine flow: BPH, kidney stones, tumors, strictures.

Pathophysiology

• Prerenal AKI: reduced renal perfusion lowers glomerular filtration.
• If hypoperfusion persists, ischemia progresses to intrinsic damage (acute tubular necrosis).
• Intrinsic AKI: direct injury to tubular cells, glomeruli, or interstitium.
• Postrenal AKI: obstruction creates back pressure that damages nephrons.

Clinical Phases

Phase 1: Oliguric Phase

• Lasts 1–2 weeks with urine output <400 mL/day.
• Fluid overload: edema, hypertension, crackles, JVD.
• Electrolyte imbalances: hyperkalemia, hyperphosphatemia, hypocalcemia.
• Metabolic acidosis as kidneys cannot excrete acids.
• Uremic symptoms: nausea, anorexia, fatigue, confusion.

Phase 2: Diuretic Phase

• Urine output increases to 1–3 L/day.
• Kidneys excrete waste but cannot concentrate urine.
• Monitor closely for dehydration and hypokalemia.

Phase 3: Recovery Phase

• Renal function returns toward baseline over weeks to months.

Diagnostic Tests

• Serum creatinine: a rise indicates AKI.
• Urinalysis: identifies cause — casts, protein, RBCs, WBCs.
• Fractional Excretion of Sodium (FENa): <1% = prerenal; >2% = intrinsic.
• Renal ultrasound: rules out obstruction; hydronephrosis suggests postrenal cause.

Hyperkalemia Management

• Hyperkalemia is the most urgent complication of AKI.
• ECG changes progress from peaked T waves → widened QRS → sine wave pattern.
• Calcium gluconate: stabilizes cardiac membranes (does not lower K+).
• Insulin with glucose: shifts potassium into cells.
• Sodium polystyrene sulfonate (Kayexalate): removes potassium from the gut.
• Hemodialysis: definitive treatment for rapid removal.

Fluid Management

• Strict intake and output (I&O) monitoring is essential.
• Daily weight is the most accurate indicator of fluid status.
• Fluid restriction may be ordered: 400–600 mL plus insensible losses.
• Signs of fluid overload: edema, hypertension, crackles, dyspnea.

Renal Replacement Therapy (RRT)

Indications for Dialysis — AEIOU:

• Acidosis (pH <7.2)
• Electrolytes (refractory hyperkalemia)
• Ingestion (toxins/drugs)
• Overload (fluid overload/pulmonary edema)
• Uremia (BUN >100, pericarditis, encephalopathy)

Nursing Care

Assessment

• Monitor I&Os; report urine output <0.5 mL/kg/hour.
• Weigh patient daily at the same time.
• Assess for fluid overload: edema, crackles, JVD.
• Monitor ECG for hyperkalemia changes.

Interventions

• Restrict fluids as ordered; offer ice chips.
• Avoid nephrotoxic medications (NSAIDs, aminoglycosides).
• Provide skin care for edema.
• Maintain aseptic technique to prevent infection.

Patient Teaching

• Avoid NSAIDs (ibuprofen, naproxen).
• Follow fluid and dietary restrictions (low potassium and sodium).
• Report decreased urine output or swelling immediately.

Common Exam Traps

• Prerenal: FENa <1%; Intrinsic: FENa >2%.
• Calcium gluconate protects the heart but does not lower potassium.
• Daily weight is more accurate than I&O for fluid status.
• Oliguria = <400 mL/day; Anuria = <50 mL/day.
• Contrast dye is a major cause of intrinsic AKI — hydrate the patient first.

Key takeaways

• AKI is a sudden loss of function classified as prerenal (perfusion), intrinsic (damage), or postrenal (blockage).
• Hyperkalemia is the killer — watch for peaked T waves and treat with calcium gluconate, insulin/glucose, Kayexalate, or dialysis.
• Use the AEIOU mnemonic for dialysis indications.
• Daily weights and strict I&Os are the priority nursing assessments.
• Differentiate prerenal vs. intrinsic AKI using FENa (<1% vs. >2%).
• Prevent AKI by avoiding nephrotoxins and hydrating before contrast studies.