👤 By the CinnaRN Clinical Content Team🕐 Updated 2026-08-23🏷️ Physiological Adaptation🔖 Free to read, print, and share
Also known as: AKI · acute renal failure · ARF · sudden kidney failure · kidneys shutting down
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Use this quick-reference guide to spot, treat, and prevent Acute Kidney Injury on the NCLEX. Keep it handy during review and on exam day!
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📒 The 1-minute cheat sheet
📌 Types
prerenal: ↓perfusion (hypovol, shock)
intrarenal: ATN, nephrotoxins
postrenal: obstruction (stones, BPH)
📌 Phases
oliguric: <400mL/day, ↑K+
diuretic: ↑↑ urine, watch dehydration
recovery: labs normalize
🧪 Labs
↑BUN ↑creatinine, ↓GFR
↑K+ = #1 deadly → dysrhythmias
metabolic acidosis, ↑phos
✅ Do
monitor I&O, daily weight
restrict K+, Na, fluids, protein
hold nephrotoxins (NSAIDs, contrast)
📚 Acute Kidney Injury — full study notes
The cheat sheet above is your quick recall card. These notes go deeper — what it is, what to do first, what must be reported, and what to teach.
Acute kidney injury is a sudden, often reversible loss of kidney function over hours to days, causing buildup of waste and fluid/electrolyte imbalance. Causes are grouped as prerenal (decreased perfusion: hypovolemia, hypotension, heart failure), intrarenal (direct damage: acute tubular necrosis, nephrotoxins, contrast dye), and postrenal (obstruction: stones, BPH, tumor). It matters because rising potassium and fluid overload can be rapidly life-threatening.
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Key points
Understand these first
AKI classically progresses through four phases (onset, oliguric, diuretic, recovery) in intrinsic AKI/ATN; note that not all AKI is oliguric (non-oliguric AKI is common). Oliguric phase: urine under 400 mL/day for 1-3 weeks; diuretic phase: large urine output with risk of dehydration and hypokalemia.
BUN and creatinine rise while urine output typically falls; creatinine is the more reliable marker of kidney function.
Hyperkalemia is the most dangerous electrolyte change and can cause fatal dysrhythmias.
Fluid overload causes hypertension, edema, crackles, jugular vein distention, and risk of pulmonary edema.
Metabolic acidosis develops as the kidneys fail to excrete hydrogen ions and retain bicarbonate.
Prerenal causes show a high BUN-to-creatinine ratio and concentrated urine because the kidneys are reabsorbing sodium and water.
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Nursing priorities
What to do, in order
Monitor strict intake and output and daily weights (1 kg gain equals about 1 L fluid retained).
Assess for hyperkalemia and continuous cardiac monitoring for peaked T waves and widening QRS.
Restrict fluids, potassium, sodium, and protein as ordered; correct the underlying cause (fluids for prerenal, relieve obstruction for postrenal).
Hold or avoid nephrotoxic agents (NSAIDs, aminoglycosides, contrast dye) and adjust drug doses.
Prepare for dialysis if severe hyperkalemia, fluid overload, acidosis, or uremia are present.
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Red flags — report now
Escalate immediately
Serum potassium above 6.0 mEq/L or peaked T waves, widened QRS, or bradycardia - report and treat immediately.
Urine output less than 30 mL/hr - report; indicates inadequate perfusion or worsening failure.
Never give nephrotoxic drugs or IV contrast without checking renal function first.
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Labs & values
Numbers to know
Creatinine: normal 0.6-1.2 mg/dL (rises in AKI)
BUN: normal 10-20 mg/dL (elevated)
Potassium: normal 3.5-5.0 mEq/L (often high)
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Patient teaching
What patients must know
Report decreased urination, swelling, or weight gain promptly.
Avoid over-the-counter NSAIDs and herbal supplements that can harm the kidneys.
Follow the prescribed fluid, sodium, potassium, and protein restrictions.
❓ Acute Kidney Injury: NCLEX FAQs
What are the priority nursing interventions for Acute Kidney Injury?
Monitor strict intake and output and daily weights (1 kg gain equals about 1 L fluid retained). Assess for hyperkalemia and continuous cardiac monitoring for peaked T waves and widening QRS. Restrict fluids, potassium, sodium, and protein as ordered; correct the underlying cause (fluids for prerenal, relieve obstruction for postrenal). Hold or avoid nephrotoxic agents (NSAIDs, aminoglycosides, contrast dye) and adjust drug doses.
What are the warning signs of Acute Kidney Injury a nurse must report?
Serum potassium above 6.0 mEq/L or peaked T waves, widened QRS, or bradycardia - report and treat immediately. Urine output less than 30 mL/hr - report; indicates inadequate perfusion or worsening failure. Signs of pulmonary edema (sudden dyspnea, frothy sputum, crackles) require immediate escalation. Never give nephrotoxic drugs or IV contrast without checking renal function first.
What do I need to know about Acute Kidney Injury for the NCLEX?
AKI classically progresses through four phases (onset, oliguric, diuretic, recovery) in intrinsic AKI/ATN; note that not all AKI is oliguric (non-oliguric AKI is common). Oliguric phase: urine under 400 mL/day for 1-3 weeks; diuretic phase: large urine output with risk of dehydration and hypokalemia. BUN and creatinine rise while urine output typically falls; creatinine is the more reliable marker of kidney function. Hyperkalemia is the most dangerous electrolyte change and can cause fatal dysrhythmias. Fluid overload causes hypertension, edema, crackles, jugular vein distention, and risk of pulmonary edema.
What patient teaching is important for Acute Kidney Injury?
Report decreased urination, swelling, or weight gain promptly. Avoid over-the-counter NSAIDs and herbal supplements that can harm the kidneys. Follow the prescribed fluid, sodium, potassium, and protein restrictions.
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Quick Tip
AKI classically progresses through four phases (onset, oliguric, diuretic, recovery) in intrinsic AKI/ATN; note that not all AKI is oliguric (non-oliguric AKI is common). Oliguric phase: urine under 400 mL/day for 1-3 weeks; diuretic phase: large urine output with risk of dehydration and hypokalemia.