Kidney Failure — AKI, CKD, ESRD — NCLEX Lesson A&P · Assessment · Renal & Genitourinary · Kidney Failure Condition Lesson · NCLEX-PN / NCLEX-RN

When kidneys fail, everything backs up — fluid, potassium, acid, waste, and blood pressure. AKI is sudden and often reversible if you find the cause fast. CKD is slow, silent, and irreversible. ESRD needs dialysis or transplant to live.

In this lesson

Lesson Objectives
Why This Matters
Disease Overview
Pathophysiology
Risk Factors
Signs & Symptoms
Nursing Assessment
Diagnostic Tests
Laboratory Tests
Medications
Nursing Interventions
Potential Complications
Patient Education
Clinical Judgment
Clinical Connections
NCLEX High-Yield
Memory Aids
Case Study
Practice Questions — RANDOMIZED ANSWERS
Key Takeaways
References

Lesson Objectives

Differentiate AKI, CKD, and ESRD by cause, timeline, reversibility, and clinical course and explain WHY each distinction matters for nursing care.
Explain how loss of filtration, reabsorption, secretion, and hormonal functions causes fluid overload, hyperkalemia, metabolic acidosis, uremia, anemia, and mineral bone disease.
Identify early, late, and emergency findings of kidney failure including hyperkalemia ECG changes and fluid overload.
Interpret labs: BUN, creatinine, eGFR, GFR staging, electrolytes K+, Ca, Phos, Mg, ABGs, CBC, and urine findings.
Prioritize safe care: fluid and electrolyte management, dialysis indications AEIOU, access protection, nephrotoxic med avoidance, and patient teaching for diet and dialysis adherence.

Why This Disease Matters

Prevalence: CKD affects 37 million Americans, 15% of adults, 90% unaware. AKI affects 10-15% of hospitalized patients and 50% of ICU patients. ESRD affects 800,000 Americans, 70% on dialysis. Leading causes CKD: diabetes 40% and hypertension 25%. Black adults 3x more likely to develop ESRD.

Patient safety: Kidneys fail → K+ rises → peaked T waves → VT/VF cardiac arrest. Fluid overload → pulmonary edema → hypoxia. Uremia → pericarditis, encephalopathy, bleeding from platelet dysfunction. Missed nephrotoxic meds (NSAIDs, aminoglycosides, contrast) worsen AKI. Giving magnesium antacids or K+ in ESRD can kill. In dialysis patients, crushing AV fistula or taking BP in fistula arm can clot fistula and lose access.

NCLEX importance: Top tested renal topic. AKI phases oliguric <400mL/day → diuretic → recovery, causes prerenal/intrarenal/postrenal, indications for dialysis AEIOU (Acidosis, Electrolytes K+ high, Ingestions, Overload fluid, Uremia), hyperkalemia management calcium first to stabilize heart, fluid restriction, daily weight same scale/time, I&O hourly, nephrotoxic avoidance, dialysis diet low K+ low Phos low Na high protein? Actually low protein CKD not ESRD, high protein ESRD on dialysis, phosphate binders with meals.

Why nurses encounter them: Every med-surg, ICU, ED, cardiac, diabetes clinic sees AKI/CKD. Heart failure patients on diuretics/ACE, diabetics, elderly on NSAIDs, post-op with hypotension, contrast studies all risk AKI. CKD patients frequent admissions for fluid overload, hyperkalemia, access infection.

Connecting to prior lessons From A&P: Nephron filters blood at glomerulus GFR ~120mL/min, reabsorbs water/Na in tubules, secretes K+/H+, produces EPO for RBCs, activates vitamin D for Ca absorption, regulates acid-base via H+ excretion and HCO3 reabsorption. From assessment: I&O hourly, daily weight same scale/time/clothing is best fluid indicator 1L = 1kg = 2.2lb, BP trends, edema 1-4+, urine color/clarity, bladder scan for retention vs true oliguria, CVA tenderness, crackles for overload.

Disease Overview

Condition	Timeline	Reversible?	Core problem
AKI	Hours to days sudden rise Cr ≥0.3 or 1.5x baseline and/or oliguria <0.5mL/kg/hr 6hr	Often reversible if cause removed early	Sudden drop in GFR → cannot excrete fluid/K+/acid/waste → fluid overload, hyperkalemia, acidosis, uremia
CKD	Months to years, GFR <60 for >3 months or kidney damage albuminuria	Not reversible, progressive	Gradual nephron loss → HTN, anemia low EPO, mineral bone disease high Phos low Ca low Vit D, metabolic acidosis
ESRD	G5 GFR <15, requires dialysis or transplant to live	Irreversible without replacement	Uremia, fluid overload, electrolyte emergencies, need renal replacement therapy

Pathophysiology

Normal physiology: GFR 90-120 mL/min filters 180L/day, 99% reabsorbed. Tubules reabsorb water/Na, secrete K+/H+, excrete waste BUN/Cr. Produces EPO → RBCs, activates vitamin D → Ca absorption, makes renin → BP control, regulates HCO3 and acid. Urine output 0.5-1.5mL/kg/hr 30-60mL/hr adult. ↓ AKI — What goes wrong: Prerenal: ↓ perfusion (hypovolemia bleeding, hypotension, HF, NSAIDs vasoconstrict afferent, ACE/ARBs vasodilate efferent ↓ GFR) → kidneys not getting blood → BUN/Cr ↑ ratio >20:1, FENa <1%, urine concentrated but oliguric. Reversible with fluids/pressors if early. Intrarenal: direct nephron injury ATN from prolonged prerenal, nephrotoxic drugs aminoglycosides/vancomycin/cisplatin/contrast, rhabdomyolysis myoglobin, glomerulonephritis. Cells slough → muddy brown casts. FENa >2%. Postrenal: obstruction BPH, stones, tumor, clots, kinked Foley → urine backs up → hydronephrosis. Reversible if obstruction relieved quickly. All three → GFR falls → oliguria <400mL/day, fluid overload, K+ high, H+ high acidosis, BUN/Cr high, waste high uremia. ↓ How AKI causes symptoms: Cannot excrete water → edema, weight gain, crackles, dyspnea, HTN. Cannot excrete K+ → hyperkalemia muscle weakness, paresthesias, peaked T → VT/VF. Cannot excrete H+ or make HCO3 → metabolic acidosis Kussmaul breathing. Cannot excrete waste → uremia nausea/vomiting, confusion, pericardial rub, pruritus. Cannot make concentrated urine → initially dilute or oliguric. ↓ AKI phases: Initiation hours-days cause happening but Cr may still normal. Oliguric <400mL/day 1-3 weeks worst — fluid overload, hyperkalemia, acidosis, uremia highest risk. Diuretic output ↑ 1-5L/day but tubules still not working → still waste high + risk hypokalemia and dehydration — not recovery yet. Recovery weeks-months Cr slowly returns toward baseline GFR improves. ↓ CKD — What goes wrong: Diabetes high sugar damages glomerular basement membrane → albumin leaks; HTN high pressure damages arterioles → nephrosclerosis; chronic GN, PKD, NSAIDs. Nephrons destroyed slowly → remaining nephrons hyperfilter → further damage. Consequences WHY: Water retention → HTN + edema + HF. K+ retention → hyperkalemia. H+ retention + low HCO3 → metabolic acidosis. Urea retention → uremia nausea/vomiting, pericarditis, encephalopathy, bleeding (platelet dysfunction). No EPO → anemia fatigue pallor. No vitamin D activation → Ca low, Phos high (cannot excrete), PTH high secondary hyperparathyroidism → renal osteodystrophy bone pain fractures. ↓ ESRD: GFR <15 → need dialysis or transplant. Uremic toxins affect all systems: neuro confusion, asterixis, seizures; cardiac pericarditis, HTN, HF; GI nausea/vomiting/anorexia; hematologic anemia + bleeding; metabolic hyperkalemia, acidosis, high Phos low Ca, high Mg.

Risk Factors

Non-modifiable	Modifiable / Preventable	High-risk populations
Age >60, family history PKD, male, Black/Native American/Hispanic higher ESRD, history AKI, low birth weight	Diabetes #1 cause CKD, HTN #2 cause, NSAID overuse, aminoglycosides, vancomycin, cisplatin, contrast dye without hydration, dehydration, hypotension, HF, sepsis, urinary obstruction BPH/stones, smoking, obesity, high protein/high sodium diet, recurrent UTIs, lupus, gout, hyperlipidemia	Diabetics, hypertensives, heart failure, elderly on NSAIDs/diuretics/ACE, ICU with sepsis/hypotension, post-op, post-contrast, BPH men, kidney stones, autoimmune lupus, Black adults 3x ESRD

Signs and Symptoms

Category	Finding & WHY
Early — AKI	Oliguria <30mL/hr or <400mL/day (WHY: GFR ↓), slight weight gain, BP ↑ mild, BUN/Cr ↑ but may still be normal early, fatigue, nausea. Prerenal: thirst, orthostatic hypotension, dry mucosa. Intrarenal: muddy brown urine, recent nephrotoxic exposure. Postrenal: suprapubic bulge, no urine despite urge, flank pain if stones.
Early — CKD	Often asymptomatic until GFR <30. Nocturia (WHY: cannot concentrate urine early), polyuria then oliguria, foamy urine (proteinuria), mild fatigue, HTN. WHY silent: remaining nephrons compensate until 70% lost.
Expected — both as failure worsens	Fluid overload: weight gain 1kg=1L, periorbital then dependent edema 1-4+, JVD, crackles, dyspnea, orthopnea, HTN. WHY: cannot excrete Na/water. Electrolytes: hyperkalemia muscle weakness, paresthesias, cramps, peaked T on ECG. WHY: cannot excrete K+. Acidosis: Kussmaul deep rapid breathing, fatigue, confusion. WHY: cannot excrete H+ or make HCO3. Uremia: nausea/vomiting/anorexia, metallic taste, pruritus with excoriations (WHY: urea crystals deposit skin), fatigue. Anemia: pallor, weakness, exertional dyspnea (WHY: no EPO). Mineral bone: bone pain, fractures, muscle cramps (WHY: low Ca high Phos high PTH). Urine: oliguria, tea-colored, low specific gravity CKD cannot concentrate 1.010 fixed.
Late — CKD/ESRD	Uremic frost (urea crystals skin), pericardial friction rub (WHY: uremic pericarditis), confusion, asterixis flap, seizures, bleeding (epistaxis, gum bleed, prolonged bleeding after venipuncture) WHY: platelet dysfunction from uremia, not low count. Anemia Hgb 7-9, HTN resistant, HF, pericarditis.
Emergency	Hyperkalemia K+ >6.5 + muscle weakness + peaked T + widened QRS + bradycardia → VT/VF arrest. Fluid overload pulmonary edema: severe dyspnea, crackles all fields, SpO2 <90%, pink frothy sputum, HTN then hypotension. Uremic pericarditis: chest pain with friction rub + hypotension + JVD = tamponade. Encephalopathy: confusion, seizures, coma. Metabolic acidosis pH <7.1 + Kussmaul. Anuria <100mL/24hr + rising Cr + K+ + overload = need dialysis now.

Nursing Assessment

Subjective: fluid intake/output, urine color/amount changes oliguria/polyuria/nocturia, hematuria, foamy urine, dysuria, flank/suprapubic pain, edema, weight gain, dyspnea orthopnea/PND, fatigue, nausea/vomiting, anorexia, metallic taste, pruritus, muscle cramps/weakness/paresthesias, confusion, bleeding, bone pain. History: diabetes, HTN, HF, kidney stones, BPH, recurrent UTIs, NSAID use frequency, aminoglycosides, contrast recent, chemotherapy cisplatin, recent hypotension/surgery/bleeding, urinary obstruction, family history PKD/CKD/dialysis, smoking, diet protein/Na/K+/Phos, meds ACE/ARB/diuretics, supplements K+/Mg, herbal NSAIDs.

Objective: vitals including orthostatics, HR, BP (HTN CKD, hypotension prerenal AKI), RR, SpO2, temp, pain, weight daily same scale/time/clothing, I&O hourly if AKI, urine color/clarity/odor/amount, specific gravity. Skin: pallor (anemia), edema periorbital/ankle/sacral 1-4+, turgor dry, uremic frost, excoriations, bruises/petechiae bleeding tendency, cap refill. Neuro: alert/orientation, asterixis, confusion, fatigue, muscle strength. Cardiac: JVD, crackles, S3 HF, pericardial rub, ECG for hyperkalemia peaked T wide QRS bradycardia. Abdomen: suprapubic bulge retention, flank CVA tenderness, bladder scan, abdominal girth. Extremities: edema, pulses, muscle weakness. Labs: BUN/Cr trend, eGFR, electrolytes K+/Na/Ca/Phos/Mg, HCO3, ABGs, CBC Hgb/Hct, albumin, urinalysis protein/blood.

Diagnostic Tests

Test	Purpose / Why / Findings / Nursing
Urinalysis + microscopy	Screen kidney damage. Proteinuria albuminuria = glomerular damage diabetes, hematuria RBCs = GN/stones, WBCs infection, casts: muddy brown granular ATN intrinsic AKI, RBC casts GN, WBC casts pyelonephritis. Specific gravity fixed 1.010 CKD cannot concentrate. Prep clean catch midstream.
Bladder scan + Kidney ultrasound	Differentiate obstruction vs intrinsic, measure size. AKI: normal size, hydronephrosis if postrenal obstruction. CKD: small echogenic shrunken <9cm irreversible. Bladder scan residual >100 abnormal >300 retention.
CT without contrast (stone) vs with contrast caution	CT without contrast gold standard stone obstruction. CT with contrast can cause AKI — need hydration and hold nephrotoxins, check BUN/Cr before.
ECG	Hyperkalemia: peaked T → wide QRS → sine wave → VT/VF. Hypocalcemia: prolonged QT. Pericarditis: diffuse ST elevation.

Laboratory Tests

Lab	Purpose / Normal / Abnormal / Trend / Priority
BUN 7-20 mg/dL, Creatinine 0.6-1.2 mg/dL, eGFR >90, BUN/Cr ratio 10-20:1	AKI: Cr ↑ ≥0.3 or 1.5x baseline within 48hr-7 days, BUN ↑. CKD: Cr slowly ↑, eGFR <60 >3 months = CKD, G1 ≥90 to G5 <15 ESRD. Ratio >20:1 prerenal, <10:1 intrarenal. Trend Cr most reliable. Priority: Cr ↑ 0.3 is AKI even if still normal range.
Electrolytes: K+ 3.5-5.0, Na 135-145, Ca 8.5-10.5, Phos 2.5-4.5, Mg 1.7-2.2	AKI/CKD: K+ high >5.5 cannot excrete → peaked T → VT/VF emergency. Ca low, Phos high, Mg high. Priority: K+ >5.5 notify STAT especially >6.5 + ECG changes.
ABGs: pH 7.35-7.45, HCO3 22-28	Metabolic acidosis from H+ retention and low HCO3. AKI/CKD pH low <7.35 HCO3 <22. Priority: pH <7.2 severe, prepare bicarbonate/dialysis.
CBC: Hgb 12-16F 14-18M	Anemia from low EPO and uremic bleeding, Hgb 7-9 CKD, normocytic. Platelet count normal but dysfunction.

Medications

Class / Meds	Mechanism & Nursing
Loop diuretics: Furosemide	Blocks Na/K/Cl in loop → water loss reduces edema/HTN. Only if fluid overloaded not prerenal hypotensive. Side hypokalemia hypoMg hypotension ototoxicity. Nursing I&O hourly daily weight orthostatics lung sounds K+/Mg/BP.
Hyperkalemia: Calcium gluconate/chloride, Insulin+glucose, bicarbonate, Kayexalate, Patiromer, Zirconium, Albuterol, Diuretics, Dialysis	Calcium stabilizes myocardium first does NOT lower K+ but protects heart. Insulin+glucose shifts K+ into cells. Bicarbonate shifts if acidotic. Kayexalate removes via GI delayed risk bowel necrosis. Dialysis definitive. Nursing continuous ECG vitals K+ q1-4h glucose checks calcium first if ECG changes.
Phosphate binders: Calcium carbonate/acetate, Sevelamer, Lanthanum — WITH meals	Binds Phos in gut excreted stool lowers Phos. Take WITH meals or within 30min. If taken empty fails. Monitor Ca/Phos/PTH.
ESA: Epoetin alfa, Darbepoetin + Iron	Stimulates RBC production. Target Hgb 10-11 not >11 ↑ death/MI/stroke black box. Need iron ferritin/TSAT. Side HTN clot.

Nursing Interventions

Priority	Intervention & WHY
Airway / Breathing	O2 if SpO2 <94% crackles pulmonary edema fluid overload, semi-Fowler, monitor RR/lung sounds, daily weight best fluid indicator, I&O hourly.
Circulation / Fluids & Electrolytes	Vitals orthostatics BP HR JVD edema daily weight same scale/time/clothing I&O hourly check Foley patency kinks/clots bladder scan if anuria differentiate retention vs true oliguria. Prerenal isotonic fluids NS small bolus reassess if hypovolemic. Intrinsic avoid nephrotoxins hydrate before contrast hold ACE/ARB if hypotensive. Postrenal relieve obstruction. Fluid restriction if overloaded CKD 1-1.5L/day low Na 2g. Hyperkalemia continuous ECG stop K+ sources calcium gluconate first if ECG changes then insulin/glucose. Protect AV fistula no BP/venipuncture in fistula arm check bruit/thrill q shift.
Safety	Avoid nephrotoxins adjust renally cleared drugs per CrCl, bleeding precautions uremic platelet dysfunction pressure 10min after venipuncture soft toothbrush electric razor no NSAIDs, infection sterile dialysis technique, fall weakness.

Potential Complications

Complication	Early signs	Nursing response
Hyperkalemia cardiac arrest	Muscle weakness peaked T wide QRS brady K+ >6.5	Continuous ECG vitals stop K+ sources calcium gluconate first then insulin/glucose dialysis check K+ q1-4h low K+ diet hold ACE/ARB
Fluid overload pulmonary edema	Weight gain >1kg/day edema 2-4+ crackles dyspnea JVD HTN SpO2 <90%	O2 semi-Fowler vitals I&O hourly daily weight lung sounds low Na fluid restriction diuretics if making urine dialysis AEIOU
Uremic pericarditis → tamponade	Chest pain friction rub hypotension JVD muffled sounds pulsus paradoxus >10	O2 vitals q15min continuous ECG notify STAT prepare pericardiocentesis dialysis emergently avoid anticoag type & cross

Patient Education

AKI sudden often reversible if cause fixed fast, CKD slow silent irreversible, ESRD GFR <15 needs dialysis/transplant.
Stop NSAIDs unless provider says ok, quit smoking, control diabetes A1c <7 HTN <130/80.
Take BP meds but hold if sick hypotensive vomiting per provider, take phosphate binders WITH meals, take ESA + iron, no K+ salt substitutes KCl, no Mg antacids, no NSAIDs.
Diet: CKD not dialysis low protein 0.6-0.8g/kg, ESRD dialysis high protein 1.2g/kg, low Na 2g low K+ low Phos low fluid 1-1.5L if overloaded.
Home: I&O log daily weight same scale/time BP log check edema skin care, protect AV fistula no BP/venipuncture in that arm check bruit/thrill daily.
Emergency: Anuria <100/day oliguria <30/hr x6h weight gain >1kg/day dyspnea crackles SpO2 <90% chest pain with rub confusion/seizures muscle weakness/paresthesias peaked T wide QRS K+ high.

Clinical Judgment

Recognize: 68yo CKD G4 baseline Cr 2.8 eGFR 18 now vomiting diarrhea poor intake ibuprofen lisinopril furosemide, BP 88/56 HR 108 orthostatic, UOP 10mL/hr anuria 60mL/24hr, K+ 6.8 peaked T wide QRS, BUN 68 Cr 5.2 eGFR 8 HCO3 16 pH 7.22.
Analyze: CKD G4 + AKI on CKD prerenal hypovolemia + NSAID afferent constriction + ACE efferent dilation + diuretic volume depletion → ATN if prolonged, true oliguria bladder scan empty not retention, hyperkalemia + acidosis + uremia.
Prioritize: #1 Hyperkalemia with ECG changes arrest risk #2 AKI on CKD anuria #3 Acidosis uremia.
Solutions: O2 monitor vitals q15min I&O hourly daily weight bladder scan type & cross labs K+ q1-2h BUN/Cr ABGs hold nephrotoxins small NS bolus 250mL reassess calcium gluconate first for ECG then insulin+glucose dialysis AEIOU nephrology.
Take Action: Call rapid STAT cardiac monitor vitals q15min IV NS 250mL bolus reassess bladder scan 50mL empty hold ibuprofen/lisinopril/furosemide per order calcium gluconate 1g IV first then insulin 10U+glucose 25g monitor glucose K+ q1-2h.
Evaluate: Calcium ECG less peaked QRS narrows K+ 6.8→5.4 UOP 10→30 BP 88→102 HR 108→88 pH 7.22→7.32, continue hold nephrotoxins I&O weight BUN/Cr K+ trend teach NSAID avoidance sick day rules diet low K+/Na/Phos dialysis teaching.

Clinical Connections

Feature	Prerenal AKI	Intrarenal ATN	Postrenal AKI	CKD/ESRD
Lab hallmark	BUN/Cr >20:1 FENa <1% urine Na <20 osmolality high >500	BUN/Cr <10-20 FENa >2% Na >40 osmolality low <350 muddy brown casts	Hydronephrosis on US bladder scan full >300	BUN/Cr both high eGFR <60 >3mo SG fixed 1.010 proteinuria small shrunken kidneys <9cm Ca low Phos high PTH high K+ high HCO3 low anemia
Treatment	Fluids NS if hypovolemic hold NSAID/ACE	Stop nephrotoxin hydrate before contrast dialysis if AEIOU	Relieve obstruction Foley BPH meds stone removal	Control diabetes HTN ACE/ARB if not AKI SGLT2 low Na 2g low protein CKD high protein ESRD low K+/Phos fluid restriction binders with meals ESA+iron dialysis AEIOU transplant

NCLEX High-Yield Review

AKI sudden reversible vs CKD slow irreversible Cr ↑ ≥0.3 or 1.5x + oliguria <0.5mL/kg/hr 6hr. Small kidneys <9cm CKD vs normal AKI.
Prerenal >20:1 FENa <1% vs intrarenal <10-20 FENa >2%
Hyperkalemia emergency Calcium first then insulin+glucose, hold ACE/ARB.
Dialysis AEIOU Acidosis pH <7.1 Electrolytes K+ >6.5 Ingestions Overload Uremia.
Phosphate binders WITH meals
Daily weight same scale/time 1kg=1L best fluid marker

Memory Aids

Prerenal Perfusion low, Intrarenal direct Injury, Postrenal Plug — PIP
Pre 20/1 FENa <1% vs Intra 2% FENa >2% muddy brown
AEIOU dialysis, C BIG K Drop calcium first
Phos binder WITH meals
Protect fistula: No BP/No venipuncture/No labs in fistula arm check bruit/thrill

Case Study

Patient: Mr. Jackson 62 diabetes HTN CKD G4 baseline Cr 2.6 eGFR 22 on lisinopril metformin ibuprofen daily, 3 days diarrhea vomiting poor PO intake, fatigue nausea vomiting oliguria 100mL/24hr weight loss 1.5kg dry mucosa poor turgor BP 90/58 orthostatic HR 110 no suprapubic bulge bladder scan 30mL empty labs BUN 58 Cr 5.0 from 2.6 eGFR 9 K+ 6.2 HCO3 18 pH 7.26 Hgb 9.0 ECG peaked T BUN/Cr ratio 11.6.

Recognize true oliguria not retention, orthostatic hypo dry mucosa weight loss prerenal but ratio 11.6 intrarenal now ATN after prolonged prerenal, hyperkalemia peaked T emergency. Prioritize hyperkalemia and AKI on CKD. Take action small NS bolus 250mL reassess hold ibuprofen/lisinopril/metformin calcium gluconate first then insulin+glucose monitor K+ glucose, I&O hourly daily weight BUN/Cr ABGs. Evaluate K+ down UOP up BP up pH up.

NCLEX Practice Questions — Rationale

1. A client with AKI has K+ 6.8 mEq/L, peaked T waves, wide QRS, muscle weakness. What is the first nursing action?

Give sodium polystyrene sulfonate orally
Give calcium gluconate IV per order to stabilize myocardium
Give insulin with glucose to shift K+ into cells
Restrict fluids to 1L/day

Rationale

Answer: 2. Why 2 is correct: Hyperkalemia with ECG changes peaked T wide QRS = emergency risk VT/VF. Calcium gluconate/chloride first stabilizes myocardium — does NOT lower K+ but protects heart. WHY it works: raises threshold potential, counteracts excitability from high K+. Then insulin+glucose shifts K+ into cells, bicarb if acidotic, kayexalate removes, dialysis definitive. Why others wrong: 1. Kayexalate delayed and removes K+ but not first for ECG changes, risk bowel necrosis. 3. Insulin is second after calcium, not first. 4. Fluid restriction does not treat hyperkalemia emergency.

2. A client with CKD has Ca 7.2 low, Phos 6.8 high, PTH high. Which teaching is correct about phosphate binders?

Take calcium carbonate on empty stomach at bedtime
Take calcium acetate 2 hours after meals
Eat high phosphate foods dairy cola nuts beans to raise phosphate
Take phosphate binder with meals or within 30 minutes of meals to bind food phosphate

Rationale

Answer: 4. Why 4 is correct: Phosphate binders calcium carbonate/acetate/sevelamer/lanthanum must be WITH meals or within 30min to bind food Phos in gut → excreted stool lowers Phos. WHY: if taken empty, no food Phos to bind, fails. Why others wrong: 1. Empty stomach at bedtime fails and causes hypercalcemia without benefit. 2. 2 hours after meals misses food Phos window. 3. High Phos foods worsen high Phos low Ca high PTH bone disease — need low Phos diet.

3. A client with prerenal AKI from hypovolemia has BUN 42 Cr 1.4 ratio 30:1 FENa <1% orthostatic hypotension dry mucosa. Which intervention is priority?

Give isotonic fluids NS small bolus per order reassessing lung sounds/JVD/daily weight and hold nephrotoxins
Give furosemide 40mg IV to increase urine output
Restrict fluids to 500mL/day
Prepare for dialysis immediately without fluids

Rationale

Answer: 1. Why 1 is correct: Prerenal AKI from ↓ perfusion hypovolemia BUN/Cr >20:1 FENa <1% concentrated urine orthostatic hypotension dry mucosa needs fluids isotonic NS small bolus reassess lung sounds/JVD/weight for overload, hold nephrotoxins NSAIDs/ACE per provider — can reverse if early before ATN. Why others wrong: 2. Furosemide worsens hypovolemia prerenal — would drop perfusion further. 3. Fluid restriction worsens prerenal. 4. Dialysis not first — fluids may reverse prerenal if early.

4. A client with ESRD on hemodialysis has an AV fistula in left arm. Which action is correct?

Take blood pressure and draw labs from left arm with fistula for convenience
Deep palpate fistula to assess for clot daily
Check bruit and thrill over fistula each shift, no BP/venipuncture/labs in fistula arm, no tight clothing, no sleeping on arm
Give 2L NS bolus quickly in fistula arm to keep it open

Rationale

Answer: 3. Why 3 is correct: Protect AV fistula — check bruit auscultate whoosh and thrill palpate vibration q shift indicates patency, no BP/venipuncture/labs in fistula arm, no tight jewelry/clothing, no sleeping on arm, no carrying heavy. WHY: pressure or venipuncture can clot and lose access. Why others wrong: 1. BP/labs in fistula arm can clot fistula lose access. 2. Deep palpation can damage, gentle thrill check only. 4. Bolus in fistula arm not routine.

5. A client with AKI is in diuretic phase output 3000mL/day BUN/Cr still high. What should the nurse monitor?

No monitoring needed because diuresis means recovery
Hypokalemia, dehydration, hypotension, and still elevated BUN/Cr — diuretic phase not recovery yet
Fluid overload and hyperkalemia only
Give NSAIDs to improve urine output

Answer: 2. Why 2 is correct: Diuretic phase UOP ↑ 1-5L/day but tubules still not concentrating waste → BUN/Cr still high, risk hypokalemia K+ lost, dehydration hypotension. Not recovery yet — recovery weeks-months Cr returns toward baseline. WHY: tubules still dysfunctional. Monitor I&O hourly daily weight orthostatics electrolytes K+/Na/Mg BUN/Cr lung sounds. Why others wrong: 1. No monitoring false diuresis does not mean recovery. 3. Overload/hyperkalemia is oliguric phase, diuretic phase opposite risk hypoK dehydration. 4. NSAIDs nephrotoxic worsens AKI.

6. SATA. Which are indications for dialysis AEIOU? Select all that apply.

Mild BUN 22 Cr 1.1 with normal K+ and no symptoms
Metabolic acidosis pH <7.1 refractory to bicarbonate, hyperkalemia K+ >6.5 refractory with ECG changes, fluid overload pulmonary edema unresponsive to diuretics
Small kidney size <9cm on ultrasound alone
Uremia with pericarditis, encephalopathy, bleeding, and ingestions lithium/salicylate that are dialyzable
Anuria with rising BUN/Cr and uremic symptoms nausea/vomiting/confusion

Rationale

Answers: 2, 4, 5. Why these: Dialysis AEIOU: Acidosis pH <7.1 refractory, Electrolytes K+ >6.5 refractory with ECG changes, Ingestions lithium/salicylate dialyzable, Overload fluid pulmonary edema unresponsive diuretics, Uremia pericarditis/encephalopathy/bleeding/nausea. Anuria with rising BUN/Cr and uremic symptoms also needs dialysis. Why others wrong: 1. Mild BUN 22 Cr 1.1 normal K+ no symptoms not indication. 3. Small kidney size alone indicates CKD but not alone dialysis indication — need AEIOU criteria.

7. SATA. Which teaching is correct for CKD diet? Select all that apply.

Eat high potassium high phosphorus high sodium diet to replace losses
Take phosphate binders with meals to bind food phosphate and follow low phosphorus diet avoiding dairy cola nuts beans
Use salt substitutes with potassium chloride and take magnesium antacids daily
CKD not on dialysis low protein 0.6-0.8g/kg to reduce waste, ESRD on dialysis high protein 1.2g/kg because dialysis loses protein
Low sodium 2g and fluid restriction 1-1.5L/day if fluid overloaded, low potassium if hyperkalemia avoiding bananas oranges potatoes tomatoes salt substitutes KCl

Rationale

Answers: 2, 4, 5. Why these: Phosphate binders WITH meals binds food Phos low Phos diet avoid dairy cola nuts beans, CKD not dialysis low protein to reduce waste BUN but ESRD on dialysis high protein because dialysis loses protein, low Na 2g controls BP/edema fluid restriction 1-1.5L if overloaded low K+ if high K+ avoid bananas oranges potatoes tomatoes salt substitutes KCl high K+. Why others wrong: 1. High K+/Phos/Na diet worsens hyperkalemia fluid overload high Phos. 3. Salt substitutes KCl and Mg antacids dangerous in CKD/ESRD ↑ K+ and Mg.

8. Priority. The nurse has four clients with AKI. Who should be seen first?

Client with BUN 30 Cr 1.6 UOP 35mL/hr stable vitals
Client with K+ 5.0 BUN 24 Cr 1.3 UOP 40mL/hr no ECG changes stable
Client with anuria 50mL/24hr BUN 45 Cr 3.0 K+ 4.8 no ECG changes stable BP
Client with K+ 7.0 peaked T waves wide QRS muscle weakness UOP 10mL/hr BUN 68 Cr 5.0 pH 7.18

Rationale

Answer: 4. Why 4 first: K+ 7.0 high + peaked T wide QRS muscle weakness + oliguria 10mL/hr + acidosis pH 7.18 + high BUN/Cr = hyperkalemia cardiac arrest risk emergency needs calcium first then insulin/glucose dialysis AEIOU. WHY: cardiac arrest imminent. Others stable K+ normal or mildly high no ECG changes, anuria needs evaluation but not immediate cardiac arrest risk as hyperkalemia with ECG changes.

9. Delegation. Which task can the RN delegate to LPN/VN for a client with CKD on dialysis?

Check vital signs, I&O, daily weight same scale/time, lung sounds, report oliguria/edema/weight gain >1kg/day/K+ high/peaked T/pericardial rub, and reinforce low Na/K+/Phos diet and phosphate binders with meals per plan
Interpret BUN/Cr/eGFR/K+ and decide on dialysis need
Assess AV fistula bruit/thrill and manage hypotension during dialysis
Teach initial diagnosis of ESRD and transplant options

Rationale

Answer: 1. Why 1 is correct to delegate: LPN/VN can check vitals I&O daily weight same scale/time lung sounds give PO meds per order reinforce teaching per plan low Na/K+/Phos diet phosphate binders with meals report oliguria/edema/weight gain >1kg/day/K+ high/peaked T/pericardial rub. Why others RN only: 2. Interpreting BUN/Cr/eGFR/K+ deciding dialysis RN nephrology. 3. Assessing fistula bruit/thrill managing hypotension dialysis RN. 4. Initial teaching ESRD transplant RN.

10. NGN Case Study. A 70-year-old with diabetes HTN CKD G3b baseline Cr 1.8 eGFR 32 on lisinopril and ibuprofen daily reports 4 days vomiting diarrhea poor intake, fatigue, nausea, oliguria 80mL/24hr, weight loss 2kg, dry mucosa poor turgor orthostatic drop BP 86/54 HR 112, no suprapubic bulge bladder scan 20mL, labs BUN 62 Cr 4.8 from 1.8 eGFR 10, K+ 6.4 high, HCO3 17 low pH 7.24, ECG peaked T, Hgb 9.4.

a) What condition and cues support it? b) What are 3 priority actions and why? c) What indicates improvement and what teaching to prevent recurrence?

Model answer

a) AKI on CKD prerenal → intrarenal ATN: CKD G3b baseline Cr 1.8, now vomiting diarrhea poor intake + NSAID ibuprofen constricts afferent + ACE lisinopril dilates efferent + volume depletion orthostatic hypotension dry mucosa weight loss = prerenal hypoperfusion, bladder scan 20mL empty true oliguria not retention, oliguria 80mL/24hr anuria, BUN 62 Cr 4.8 from 1.8 eGFR 10, K+ 6.4 high cannot excrete + ACE raises K+ + acidosis shifts K+ out, HCO3 17 pH 7.24 metabolic acidosis, ECG peaked T hyperkalemia emergency, Hgb 9 anemia CKD low EPO.

b) Priorities: 1) Hyperkalemia with ECG changes → cardiac monitor continuous, vitals q15min, calcium gluconate 1g IV per order first to stabilize myocardium, then insulin 10U + glucose 25g per order, bicarb per order, monitor glucose q1h K+ q1-2h, hold ACE/ARB/K+ sparing/K+ supplements/Mg antacids, low K+ diet. 2) AKI on CKD fluid management — small isotonic NS bolus 250mL reassess lung sounds/JVD/daily weight/I&O because hypovolemic but CKD risk overload, hold nephrotoxins ibuprofen/lisinopril/metformin per provider, check Foley patency, I&O hourly daily weight same scale/time, BUN/Cr trend, bladder scan already empty. 3) Acidosis and uremia → ABGs HCO3 trend, dialysis AEIOU acidosis pH <7.1 refractory + K+ >6.5 refractory + overload + uremia nausea, prepare type & cross, dialysis access, nephrology consult, teach sick day rules.

c) Improvement: K+ 6.4→5.0, ECG peaked T → normal T, HR 112→88, BP 86/54→102/68, UOP 80→400mL/24hr, weight stable, lung sounds clear, no crackles/JVD, BUN/Cr down, pH 7.24→7.34 HCO3 17→22, nausea improved. Teaching: avoid NSAIDs (constrict afferent ↓ GFR), sick day rules hold ACE/ARB/diuretics/metformin when vomiting/diarrhea/poor intake per provider, hydrate, low Na 2g low K+ low Phos diet, phosphate binders with meals, daily weight same scale/time, I&O log, BP log, no K+ salt substitutes KCl, no Mg antacids, no contrast without hydration, follow-up labs BUN/Cr/eGFR/K+, nephrology, dialysis teaching if ESRD progresses, protect future fistula arm.

Key Takeaways — Verified

AKI sudden Cr ↑ ≥0.3 or 1.5x + oliguria <0.5mL/kg/hr 6hr often reversible, CKD slow GFR <60 >3 months irreversible, ESRD GFR <15 needs dialysis/transplant.
Prerenal BUN/Cr >20:1 FENa <1% concentrated needs fluids, intrarenal ATN <10-20 FENa >2% muddy brown needs stop nephrotoxin, postrenal obstruction bladder scan full needs relieve obstruction.
Hyperkalemia emergency K+ >6.5 peaked T wide QRS → calcium first stabilizes heart then insulin+glucose shifts K+ then kayexalate/diuretics/dialysis definitive.
Dialysis AEIOU: Acidosis pH <7.1 Electrolytes K+ >6.5 Ingestions Overload Uremia pericarditis/encephalopathy. Protect fistula no BP/venipuncture in fistula arm check bruit/thrill.
Phosphate binders WITH meals, daily weight same scale/time 1kg=1L best fluid marker, I&O hourly.

References

Kidney Disease: Improving Global Outcomes. (2024). KDIGO clinical practice guideline for acute kidney injury. Kidney International.
Kidney Disease: Improving Global Outcomes. (2024). KDIGO clinical practice guideline for chronic kidney disease. Kidney International.
Lewis, S. L., Bucher, L., Heitkemper, M. M., & Harding, M. M. (2020). Medical-surgical nursing: Assessment and management of clinical problems (11th ed.). Elsevier.
Hinkle, J. L., Cheever, K. H., & Overbaugh, K. J. (2022). Brunner & Suddarth's textbook of medical-surgical nursing (15th ed.). Wolters Kluwer.
National Kidney Foundation. (2023). K/DOQI clinical practice guidelines for chronic kidney disease.
Silvestri, L. A., & Silvestri, A. E. (2023). Saunders comprehensive review for the NCLEX-RN examination (9th ed.). Elsevier.
Assessment Technologies Institute. (2023). ATI RN adult medical-surgical nursing review module (12th ed.). ATI Nursing Education.

Kidney Failure

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Welcome & Getting Started

Launch RN Simulator

Wellness Center

Nursing Foundations

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Pharmacology

Dosage Calculations

Leadership, Management & Delegation

Medical-Surgical Body Systems

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NCLEX Success Center

Clinical Judgment Practice

Prioritization Practice

Delegation Practice

Lab Values

Final Review