Acute Kidney Injury NCLEX Questions | Chronic Kidney Disease

Practice Acute Kidney Injury NCLEX Questions to help you master AKI concepts, improve clinical reasoning, and boost your NCLEX exam readiness with real-world patient care scenarios.

These NCLEX-style questions on Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD) are designed to strengthen your clinical reasoning and exam readiness. While focused on the NCLEX, they also reflect real-world patient care scenarios, helping you connect theory to practice.

Acute Kidney Injury NCLEX Practice Questions

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Question 1

A 72-year-old client is admitted with sepsis secondary to pneumonia. Urine output over the last 6 hours is 90 mL. BP is 86/50 mmHg, HR 118, and serum creatinine has risen from 0.9 to 1.8 mg/dL in 24 hours. Which mechanism is most likely causing this client’s acute kidney injury?

A	Immune-mediated glomerular destruction
B	Obstruction of urine flow in the ureters
C	Renal hypoperfusion leading to ischemic tubular injury
D	Nephrotoxic effect of inflammatory cytokines on the bladder

Question 1 Explanation:

This client is in septic shock with hypotension and tachycardia, causing decreased renal perfusion. Prolonged hypoperfusion leads to acute tubular necrosis (ATN), the most common cause of intrinsic AKI. The rising creatinine and oliguria support this. There is no evidence of obstruction (B) or immune glomerular disease (A). Cytokines contribute to systemic inflammation but the primary injury is ischemic tubular damage.

Question 2

A client with AKI is in the oliguric phase. Which assessment finding requires the nurse’s immediate action?

A	BUN 58 mg/dL
B	Serum potassium 6.3 mEq/L
C	Phosphorus 5.8 mg/dL
D	Hemoglobin 10.8 g/dL

Question 2 Explanation:

Hyperkalemia is the most life-threatening complication of AKI due to reduced potassium excretion. A potassium level above 6.0 can cause fatal cardiac dysrhythmias (peaked T waves, ventricular arrhythmias). Elevated BUN and phosphorus are expected, and mild anemia is common from hemodilution and decreased erythropoietin, but they are not immediately life-threatening.

Question 3

A postoperative client develops AKI after receiving IV contrast for a CT scan. Which finding best indicates contrast-induced nephropathy?

A	Hematuria and flank bruising
B	Gradual rise in creatinine 24–48 hours after contrast exposure
C	Sudden anuria within 1 hour of the scan
D	Decreased urine specific gravity below 1.005

Question 3 Explanation:

Contrast-induced AKI typically presents as a delayed rise in serum creatinine within 24–48 hours after exposure due to renal vasoconstriction and tubular toxicity. Immediate anuria suggests obstruction or vascular catastrophe. Low specific gravity suggests concentrating defects but is not specific. Hematuria/bruising point more toward trauma.

Question 4

A client in the diuretic phase of AKI has urine output of 4,500 mL in 24 hours. Which complication is the nurse’s priority concern?

A	Fluid volume overload
B	Metabolic acidosis
C	Uremic pericarditis
D	Hypovolemia and electrolyte loss

Question 4 Explanation:

During the diuretic phase, the kidneys begin excreting large volumes of dilute urine but cannot yet concentrate or conserve electrolytes. This places the client at high risk for dehydration, hypotension, hyponatremia, and hypokalemia. Fluid overload and severe uremia are more typical of the oliguric phase.

Question 5

A client with AKI has the following ABG results: pH 7.28, PaCO₂ 32 mmHg, HCO₃⁻ 16 mEq/L. Which interpretation is correct?

A	Metabolic acidosis with respiratory compensation
B	Respiratory acidosis
C	Metabolic alkalosis
D	Respiratory alkalosis

Question 5 Explanation:

AKI commonly causes metabolic acidosis due to retention of hydrogen ions and inability to excrete acids. The low pH and low bicarbonate confirm metabolic acidosis. The decreased PaCO₂ indicates the lungs are compensating via hyperventilation to blow off CO₂.

Question 6

A client with rhabdomyolysis after a crush injury develops dark cola-colored urine. Labs show CK 18,000 U/L, K⁺ 5.8 mEq/L, creatinine 2.1 mg/dL. Which intervention helps prevent worsening AKI?

A	Restrict IV fluids to prevent overload
B	Start sodium bicarbonate infusion as prescribed
C	Administer IV calcium gluconate
D	Give loop diuretics immediately

Question 6 Explanation:

Rhabdomyolysis releases myoglobin, which obstructs renal tubules and causes oxidative damage. Aggressive hydration and urine alkalinization (bicarbonate) help reduce myoglobin precipitation in tubules. Calcium gluconate treats cardiac membrane instability from hyperkalemia but doesn’t protect kidneys. Fluid restriction worsens injury. Diuretics without adequate perfusion are harmful.

Question 7

A client in the oliguric phase of AKI has these findings: weight gain 2 kg in 24 hrs, crackles in lungs, BP 168/94, Na⁺ 130 mEq/L. Which prescription should the nurse question?

A	IV furosemide
B	Fluid restriction to 800 mL/day
C	0.9% NS at 125 mL/hr
D	Daily weights

Question 7 Explanation:

This client shows fluid volume overload (weight gain, hypertension, crackles, dilutional hyponatremia). Continuous isotonic saline would worsen pulmonary edema and hypertension. Diuretics, restriction, and daily weights are appropriate.

Question 8

A client with AKI has peaked T waves and widened QRS complexes on telemetry. Which medication should the nurse administer first?

A	Regular insulin with dextrose
B	Sodium polystyrene sulfonate
C	Albuterol nebulizer
D	IV calcium gluconate

Question 8 Explanation:

ECG changes indicate severe hyperkalemia affecting cardiac conduction. Calcium gluconate stabilizes cardiac membranes immediately. Insulin and albuterol shift potassium intracellularly but do not protect the heart first. Kayexalate removes potassium slowly.

Question 9

A client recovering from AKI suddenly develops confusion, pericardial friction rub, and platelet count 95,000/mm³. Which complication does the nurse suspect?

A	Fluid overload
B	Uremic syndrome
C	Electrolyte depletion
D	Sepsis

Question 9 Explanation:

Uremia causes neurologic changes (confusion), uremic pericarditis (friction rub), and platelet dysfunction leading to thrombocytopenia and bleeding risk. This indicates severe toxin buildup and possible need for dialysis.

Question 10

A client with AKI has urine sodium 60 mEq/L and fractional excretion of sodium (FENa) 3%. What type of AKI is most likely?

A	Intrinsic (acute tubular necrosis)
B	Prerenal
C	Postrenal
D	Obstructive nephropathy

Question 10 Explanation:

In intrinsic renal injury like ATN, damaged tubules cannot reabsorb sodium, so urine sodium >40 mEq/L and FENa >2%. Prerenal AKI shows low urine sodium (<20) and FENa <1% because kidneys conserve sodium.

Question 11

A client with septic shock develops AKI. Current labs: BUN 68 mg/dL, creatinine 3.2 mg/dL, K⁺ 5.6 mEq/L, urine output 12 mL/hr. CVP is low, MAP 58 mmHg. Which action is the priority to prevent further renal damage?

A	Administer IV regular insulin with dextrose
B	Increase IV isotonic fluid infusion as prescribed
C	Prepare for emergent dialysis
D	Administer IV furosemide

Question 11 Explanation:

This is prerenal AKI from hypoperfusion (low MAP, low CVP, oliguria). Restoring renal perfusion with fluids is the priority. Insulin treats hyperkalemia but does not address the cause. Dialysis is premature unless refractory complications occur. Diuretics without perfusion worsen injury.

Question 12

A client in the oliguric phase of AKI has ABG: pH 7.28, HCO₃⁻ 16 mEq/L, PaCO₂ 30 mmHg. Which mechanism explains this acid-base imbalance?

A	Loss of bicarbonate through kidneys
B	Excessive respiratory compensation
C	Increased lactic acid from tissue hypoxia only
D	Retention of metabolic acids due to decreased filtration

Question 12 Explanation:

AKI reduces excretion of hydrogen ions and organic acids, causing metabolic acidosis. The low CO₂ reflects respiratory compensation. The kidneys are not “losing” bicarbonate; they are failing to regenerate and retain it.

Question 13

A client with AKI reports nausea and metallic taste. The nurse notes ecchymoses and oozing at IV sites. Which lab result explains these findings?

A	Platelets 88,000/mm³
B	Calcium 7.8 mg/dL
C	Sodium 129 mEq/L
D	Magnesium 3.1 mg/dL

Question 13 Explanation:

Uremia causes platelet dysfunction and decreased platelet count, leading to bleeding tendencies. GI symptoms are also classic uremic effects. Electrolyte imbalances do not directly explain bleeding and oozing.

Question 14

A client recovering from AKI enters the diuretic phase. Urine output is 4,000 mL/day. Which electrolyte imbalance is the highest risk during this phase?

A	Hyperkalemia
B	Hypermagnesemia
C	Hypokalemia
D	Hyperphosphatemia

Question 14 Explanation:

During the diuretic phase, kidneys excrete large amounts of water and electrolytes but still cannot concentrate urine. Massive potassium loss leads to hypokalemia, causing dysrhythmias and muscle weakness.

Question 15

A client with contrast-induced AKI is scheduled for another imaging study. Which order should the nurse question?

A	IV normal saline before procedure
B	N-acetylcysteine as prescribed
C	Monitoring creatinine after procedure
D	Metformin continuation

Question 15 Explanation:

Metformin should be held in AKI or before contrast exposure because renal impairment increases risk of lactic acidosis. Hydration and renal monitoring are protective measures.

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*Disclaimer:

These questions are designed for NCLEX exam preparation and to enhance understanding of Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD). They are educational only and not a substitute for professional medical judgment in real patient care. Always follow evidence-based guidelines and consult licensed healthcare providers.