Nursing Care Plans Nursing Care Plan for Acute Renal Failure (AKI): 7 Sample Plans & Priority Diagnoses
Building a nursing care plan for acute renal failure can feel overwhelming — the labs move fast, the electrolytes are dangerous, and your instructor wants a priority diagnosis backed by solid rationales. If that’s where you are right now, you’re not behind. You just need the pattern.
Here’s the good news: once you can sort acute renal failure by why the kidneys failed and what that does to fluid, electrolytes, perfusion, and the heart, the care plan almost writes itself. One quick terminology note before we start — “acute renal failure (ARF)” is the older name for what clinicians and the NCLEX now call acute kidney injury (AKI). They mean the same thing, so we’ll use both terms the way you’ll see them in practice and on exams.
This guide covers everything you need for a nursing care plan for acute renal failure: a fast pathophysiology refresher, cause-focused assessment and labs, the priority nursing diagnosis options, and 7 complete sample care plans with goals, interventions, rationales, and evaluation.
Scope note. This is educational content for nursing students. It is not a substitute for your facility’s policies, provider orders, or your instructor’s guidance. Always confirm lab reference ranges and treatment protocols with your institution.
Quick answer — what’s the priority? Acute renal failure is now more commonly called acute kidney injury (AKI) — a sudden decline in kidney function over hours to days that disrupts waste clearance and fluid, electrolyte, and acid–base balance. Nursing priorities are to assess ABCs and perfusion, monitor urine output, creatinine, potassium and ECG, and acid–base and fluid status, identify reversible causes (hypovolemia, sepsis, nephrotoxins, obstruction), prevent complications like dysrhythmias and pulmonary edema, and escalate promptly for refractory hyperkalemia, acidosis, uremic complications, fluid overload, or possible dialysis. Hyperkalemia is a top life-threatening risk — especially in oliguric AKI — but it is not always the single first priority.
At a glance: the 3 types of acute renal failure
| Type | What’s going wrong | Common examples |
|---|---|---|
| Prerenal | Reduced blood flow to the kidney (hypoperfusion) | Hypovolemia, hypotension, sepsis, hemorrhage, heart failure |
| Intrinsic (intrarenal) | Direct damage inside the kidney | Acute tubular necrosis (ischemia, nephrotoxins), glomerulonephritis, interstitial nephritis |
| Postrenal | Obstruction after the kidney | BPH, kidney stones, pelvic tumor, solitary kidney, bilateral obstruction |
Two clarifications students miss: Prerenal AKI can progress to intrinsic (acute tubular) injury if hypoperfusion isn’t corrected — so restoring perfusion early matters. And postrenal AKI is quickly reversible if caught: check catheter patency, do a bladder scan per protocol, and escalate for urgent evaluation (often ultrasound) when obstruction is suspected.
Common mistakes to avoid. ① Treating every AKI patient as fluid overloaded — prerenal AKI may need perfusion restored, not fluids restricted. ② Missing hyperkalemia or ECG changes. ③ Forgetting obstruction — check catheter patency and bladder scan, and escalate for suspected postrenal AKI. ④ Relying on a single creatinine or eGFR instead of trends, urine output, and clinical status. ⑤ Continuing nephrotoxins or skipping a renal-dose medication review. ⑥ Using diuretics as if they treat AKI rather than fluid overload. ⑦ Discharging without a medication review, a repeat kidney-function plan, and clear follow-up.
In this guide
- What is acute renal failure (AKI)?
- Signs, symptoms & risk factors
- Nursing assessment
- Diagnostic studies & key labs
- Priority nursing diagnoses
- Nursing goals & expected outcomes
- Nursing interventions & rationales
- 7 sample acute renal failure nursing care plans
- Escalation: red flags, dialysis & nephrology
- Discharge & patient teaching
- Practice question
- FAQs
- Related resources
- References
What is acute renal failure (AKI)?
Acute renal failure is a sudden, rapid drop in kidney function that develops over hours to days. The kidneys stop clearing nitrogenous waste (so BUN and creatinine climb) and lose control of fluid, electrolyte, and acid–base balance.
According to the KDIGO clinical practice guideline, AKI is diagnosed when any of these is present: a rise in serum creatinine of at least 0.3 mg/dL within 48 hours, a rise to at least 1.5 times baseline within the prior 7 days, or urine output under 0.5 mL/kg/hr for 6 hours. The big-picture takeaway for your care plan: AKI is often reversible if you catch the cause early — but if it isn’t corrected, it can progress to chronic kidney disease or even end-stage renal disease.
Causes: prerenal, intrinsic, postrenal
Think of it as a plumbing problem — flow in, the kidney itself, or flow out.
- Prerenal (before the kidney): anything that drops perfusion — dehydration, hemorrhage, hypotension, sepsis, or heart failure. Most common type and the most reversible if you restore fluid volume and perfusion quickly. Left uncorrected, it can tip into intrinsic tubular injury.
- Intrinsic (inside the kidney): acute tubular necrosis from prolonged ischemia or nephrotoxins (contrast dye, aminoglycosides, NSAIDs), or glomerular/interstitial disease.
- Postrenal (after the kidney): obstruction from an enlarged prostate, kidney stones, or tumors backing urine up into the kidney. Screen with catheter patency and a bladder scan; escalate for urgent imaging when obstruction is suspected.
Phases of AKI
Classic teaching pattern for acute tubular injury/ATN — not universal. Some cases of acute tubular necrosis are taught in three phases, but not every patient follows this. AKI may be oliguric, nonoliguric, or anuric depending on the cause, severity, medications, hemodynamics, and obstruction status.
- Oliguric phase — urine output drops (often under 400 mL/day). Highest risk for hyperkalemia and fluid overload.
- Diuretic phase — urine output surges. Risk flips to dehydration and low potassium; watch for hypovolemia.
- Recovery phase — kidney function gradually normalizes over weeks to months.
Signs, symptoms & risk factors
AKI can be silent early — in hospitalized patients, a rising creatinine or a falling urine output is often the first sign, before the patient feels anything. When symptoms do appear, they track with retained fluid and waste:
- Decreased urine output (oliguria) or none at all (anuria) — though some AKI is nonoliguric
- Weight gain, edema, and crackles from fluid retention
- Fatigue, nausea, and loss of appetite from rising uremia
- Confusion or altered mental status — uremic encephalopathy (acute confusion)
- Shortness of breath if fluid backs up into the lungs
Risk factors worth flagging in your assessment (these should trigger a closer look): older age (≥65), pre-existing CKD, diabetes, heart failure, sepsis, hypovolemia, recent surgery, urologic obstruction symptoms, and exposure to nephrotoxic drugs or IV contrast.
Nursing assessment
A strong acute renal failure nursing care plan starts with focused, repeated assessment — and the single most important judgment call is volume status, because it decides whether the patient needs fluids restricted or restored.
- Assess for both hypovolemia and overload: orthostatic changes, mucous membranes, skin turgor, heart rate, blood pressure, JVD, edema, lung sounds (crackles), oxygen need, and daily weight trends.
- Strict intake and output (I&O) and daily weights (same scale, time, and clothing) are core bedside measures of fluid balance — trends are more useful than any single number, and I&O is often imperfect.
- Check catheter patency and consider a bladder scan per protocol when urine output suddenly drops — a quick way to catch postrenal obstruction.
- Vital signs and hemodynamics; respiratory and cardiac status (heart for dysrhythmias).
- Neuro checks — rising uremia clouds mental status.
- Labs and ECG trends (see below); review the med list for nephrotoxins. This whole sequence follows the nursing process — assess before you plan.
Diagnostic studies & key labs
These labs track severity and complications:
| Test | Typical normal range | AKI finding |
|---|---|---|
| BUN | 10–20 mg/dL | ↑ Elevated |
| Serum creatinine | 0.6–1.2 mg/dL | ↑ ≥1.5× baseline (trend it) |
| eGFR | ≥90 mL/min/1.73m² | May read low, but interpret cautiously in AKI — creatinine isn’t at steady state. Trend creatinine, urine output, and clinical course instead of relying on one eGFR. |
| Potassium (K⁺) | 3.5–5.0 mEq/L | ↑ Hyperkalemia — high-priority |
| Sodium | 135–145 mEq/L | Variable |
| Bicarbonate / CO₂ | 22–28 mEq/L | ↓ Metabolic acidosis |
| Phosphorus | 2.5–4.5 mg/dL | ↑ Retained |
| Calcium | 8.5–10.2 mg/dL | ↓ Often low |
| Magnesium | 1.7–2.2 mg/dL | ↑ Possible |
| ABG/VBG (if severe) | pH 7.35–7.45 | Metabolic acidosis |
| Urine output | ≥0.5 mL/kg/hr | <0.5 mL/kg/hr for 6 hr (or nonoliguric) |
High-yield teaching point: In AKI, creatinine can lag behind the actual injury, and low muscle mass (older or frail patients) can make creatinine look deceptively “not that bad.” Trend it alongside urine output and volume status — don’t trust a single value.
These tests help identify the cause, not just the severity — order or anticipate them early:
| Cause-focused test | Why it matters |
|---|---|
| Urinalysis / dipstick (blood, protein, leukocytes, nitrites, glucose) | Screens for nephritis, infection, or glomerular disease — check as soon as AKI is suspected |
| Urine microscopy / sediment | Differentiates tubular injury, glomerular disease, and infection |
| Bladder scan / catheter patency check | Rapid bedside screen for retention or lower-tract obstruction |
| Renal / urinary tract ultrasound | Evaluates obstruction or hydronephrosis when the cause is unclear or obstruction risk exists (urgent if infected obstruction is suspected) |
| CK / urine myoglobin (if rhabdomyolysis suspected) | Identifies muscle breakdown as an AKI driver |
| Medication / toxin review ± drug levels | Identifies nephrotoxins and dosing problems |
For the deeper dive on sorting out electrolytes, see our guide to electrolyte imbalance.
Priority nursing diagnoses for acute renal failure
Below are common nursing-diagnosis options often used in AKI care plans, paraphrased into plain language. Verify the exact current NANDA-I label and code in the edition your program or facility requires before you submit — labels and wording change between editions.
- Deficient Fluid Volume — in prerenal AKI from hypovolemia, hemorrhage, or GI losses.
- Excess Fluid Volume — when the kidneys can’t excrete fluid (often oliguric AKI).
- Risk for Electrolyte Imbalance — especially hyperkalemia from reduced potassium excretion.
- Risk for Decreased Cardiac Output — high potassium and fluid overload strain the heart.
- Imbalanced Nutrition: Less Than Body Requirements — anorexia, nausea, dietary restrictions, catabolism.
- Risk for Infection — uremia and invasive lines (including dialysis access).
- Deficient Knowledge — about diagnosis, diet, medications, and follow-up.
Risk vs. actual — a wording trap. Use a risk diagnosis only when the complication hasn’t happened yet. If potassium is already 6.8 mEq/L, that’s an actual clinical/collaborative problem, not a “risk” — don’t write “Risk for Electrolyte Imbalance as evidenced by K⁺ 6.8” (a risk diagnosis has no “as evidenced by”). Document the actual hyperkalemia as a collaborative problem and pair it with the best-fit nursing diagnosis (e.g., risk for dysrhythmia / decreased cardiac output) per your required taxonomy.
Which is priority? It depends on the presentation. Assess ABCs and perfusion first; the immediate life threat may be shock/hypovolemia, sepsis, pulmonary edema, severe acidosis, obstruction, uremic complications, or a dysrhythmia. Hyperkalemia is a top-priority risk — potassium can rise fast and stop the heart, especially in oliguric AKI — but it isn’t the only possible first priority.
Nursing goals & expected outcomes
Good goals in an acute renal failure nursing care plan are specific and measurable. The client will:
- Maintain serum potassium within 3.5–5.0 mEq/L (or facility reference range) with no ECG signs of hyperkalemia.
- Achieve the prescribed fluid-balance target — balanced I&O and stable daily weight (or ordered goal).
- Have clear lung sounds, no worsening edema, and an adequate oxygen saturation / work of breathing.
- Stay free of infection (no fever, access site clean/dry/intact; WBC alone is nonspecific).
- Verbalize their diet, medication, and follow-up plan before discharge, confirmed by teach-back.
Nursing interventions & rationales
| Intervention | Rationale |
|---|---|
| Monitor strict I&O and daily weights | Earliest, most reliable trend for fluid status and AKI phase |
| Monitor potassium trends; place on telemetry/continuous ECG for hyperkalemia, ECG changes, rapid K⁺ rise, or severe AKI (per protocol) | Detects dangerous hyperkalemia before lethal dysrhythmias — targeted rather than universal telemetry |
| Individualize fluids by volume status, hemodynamics, urine output, cardiac function, and AKI cause | Restrict fluids/sodium if overloaded or at risk of pulmonary edema; restore intravascular volume if hypovolemia/poor perfusion is driving prerenal AKI |
| Administer loop diuretics such as furosemide only as ordered for fluid overload/edema | Diuretics manage overload; they do not treat AKI itself or “restart” the kidneys |
| Give protocol-based hyperkalemia therapy (see table below); monitor glucose after insulin | Emergency treatment is stepwise, not a single drug |
| Provide a renal diet with a renal dietitian (limit potassium, phosphorus, sodium; protein per provider) | Reduces electrolyte/waste load while avoiding protein malnutrition in catabolic illness |
| Review and flag nephrotoxins and renal-dose medications; notify provider/pharmacy | Prevents further tubular injury (hold only per order/protocol) |
| Use strict aseptic technique with all lines and access | Lowers infection risk in an immunocompromised client |
| Identify and treat the reversible cause (perfusion, sepsis, obstruction) | Reversing the cause is the definitive fix for prerenal and postrenal AKI |
| Prepare for dialysis/KRT if indicated | Removes waste and corrects severe, refractory derangements (see escalation below) |
Hyperkalemia therapy — stabilize → shift → remove. This is the framework to memorize:
| Goal | Examples | Teaching point |
|---|---|---|
| Stabilize the myocardium | IV calcium gluconate/chloride (for ECG changes or severe hyperkalemia) | Protects the heart; does not lower serum potassium |
| Shift potassium into cells | Insulin + dextrose; nebulized beta-agonist; bicarbonate selectively (esp. metabolic acidosis) | Temporizing — potassium can rebound; monitor glucose after insulin for delayed hypoglycemia |
| Remove potassium from the body | Loop diuretics (if making urine), newer potassium binders (patiromer, sodium zirconium cyclosilicate), dialysis/KRT | Definitive removal; depends on renal function and patient status |
Sodium polystyrene sulfonate may still appear in some facilities, but it carries serious GI risks and is no longer the highlighted first-line emergency intervention. For a deeper, step-by-step breakdown of each action, see our companion guide on acute renal failure nursing interventions — part of the broader set of nursing interventions you plan across any care plan.
7 sample acute renal failure nursing care plans
Below are 7 sample plans you can adapt. Each nursing care plan for acute renal failure follows the same structure: diagnosis, goals, interventions with rationales, and evaluation. Build yours from a clean care plan template, and verify each NANDA-I label against your required edition.
Care plan #1 — Deficient Fluid Volume (prerenal AKI)
Nursing diagnosis: Deficient Fluid Volume related to excessive losses or reduced intake (e.g., vomiting, diarrhea, hemorrhage, sepsis) causing renal hypoperfusion, as evidenced by hypotension, tachycardia, dry mucous membranes, poor skin turgor, low urine output, and rising creatinine.
- Goal: The client will restore adequate perfusion (BP/MAP at target, urine output ≥0.5 mL/kg/hr) within the ordered timeframe.
- Goal: The client’s creatinine will trend downward toward baseline.
| Intervention | Rationale |
|---|---|
| Assess volume status (BP, HR, orthostatics, mucous membranes, skin turgor, JVP) | Distinguishes prerenal hypovolemia from overload — the key decision |
| Administer ordered isotonic IV fluids; monitor response | Restoring perfusion is the treatment for prerenal AKI |
| Monitor I&O, daily weights, urine output, and creatinine trend | Tracks response and catches developing overload |
| Reassess frequently for overload, especially in older adults or heart failure | Over-resuscitation can cause pulmonary edema |
| Identify/treat the cause (bleeding, sepsis, GI losses); avoid nephrotoxins | Reversing the cause reverses prerenal AKI |
Evaluation: BP/HR normalized; urine output ≥0.5 mL/kg/hr; creatinine trending down; no overload.
Care plan #2 — Excess Fluid Volume
Nursing diagnosis: Excess Fluid Volume related to compromised renal regulatory mechanism (decreased GFR with sodium and water retention), as evidenced by edema, weight gain, decreased urine output, and crackles.
- Goal: The client will achieve the prescribed fluid-balance target within 48 hours.
- Goal: The client will show reduced edema and clear lung sounds by discharge.
| Intervention | Rationale |
|---|---|
| Monitor I&O and daily weights | A 1 kg gain ≈ 1 L of retained fluid |
| Assess for edema, crackles, JVD, and oxygen need | Detects worsening overload early |
| Restrict fluids and sodium per orders (when overloaded) | Limits further accumulation in volume-overloaded AKI |
| Administer loop diuretics as ordered; monitor response | Manages overload when the kidney is responsive |
Evaluation: Fluid-balance target met; weight stable; lungs clear; edema reduced.
Care plan #3 — Risk for Electrolyte Imbalance (hyperkalemia)
Nursing diagnosis: Risk for Electrolyte Imbalance related to decreased renal excretion of potassium. (If hyperkalemia is already present, document it as an actual/collaborative problem instead of a risk.)
- Goal: The client will maintain potassium within 3.5–5.0 mEq/L (or facility range).
- Goal: The client will remain free of ECG changes associated with hyperkalemia.
| Intervention | Rationale |
|---|---|
| Monitor potassium and ECG; place on continuous monitoring for elevated/rising K⁺ | Peaked T waves and widened QRS signal dangerous hyperkalemia |
| Limit dietary potassium | Reduces the load the kidney can’t clear |
| Give protocol-based therapy: calcium (stabilize) → insulin+dextrose / beta-agonist (shift) → binders/dialysis (remove) | Stepwise emergency management (see framework above) |
| Monitor blood glucose after insulin/dextrose | Insulin-treated hyperkalemia can cause delayed hypoglycemia, especially in renal impairment |
Evaluation: Potassium normalized; no dysrhythmias. See electrolyte imbalance for the full work-up.
Care plan #4 — Risk for Decreased Cardiac Output
Nursing diagnosis: Risk for Decreased Cardiac Output related to electrolyte imbalance (hyperkalemia) and fluid overload.
- Goal: The client will maintain stable vital signs and a normal sinus rhythm.
- Goal: The client will show no signs of decreased perfusion.
| Intervention | Rationale |
|---|---|
| Continuous cardiac monitoring | Hyperkalemia and overload can trigger dysrhythmias |
| Assess perfusion (BP, pulses, LOC, cap refill) | Detects falling cardiac output early |
| Correct potassium and fluid status promptly | Removes the main threats to the myocardium |
Evaluation: Normal sinus rhythm; stable hemodynamics; adequate perfusion.
Care plan #5 — Imbalanced Nutrition: Less Than Body Requirements
Nursing diagnosis: Imbalanced Nutrition: Less Than Body Requirements related to anorexia, nausea, and dietary restrictions, as evidenced by poor intake and weight changes.
- Goal: The client will meet prescribed nutritional intake within 3 days.
- Goal: The client will maintain or improve toward target weight without protein malnutrition.
| Intervention | Rationale |
|---|---|
| Provide small, frequent renal-appropriate meals | Improves intake despite nausea and anorexia |
| Collaborate with a renal dietitian | Balances calories/protein against electrolyte limits and avoids malnutrition |
| Administer antiemetics as ordered | Controls nausea so the client can eat |
Evaluation: Improved intake; stable weight. More at imbalanced nutrition.
Care plan #6 — Risk for Infection
Nursing diagnosis: Risk for Infection related to invasive lines and dialysis access and uremia-related immune suppression.
- Goal: The client will remain free of infection (no fever, normal WBC).
- Goal: The access site will stay clean, dry, and intact.
| Intervention | Rationale |
|---|---|
| Use strict aseptic technique with all access | Prevents introduction of pathogens |
| Monitor temperature, WBC, and access site | Detects early signs of infection |
| Limit unnecessary invasive devices | Fewer entry points means lower risk |
Evaluation: No fever or infection; access site intact.
Care plan #7 — Deficient Knowledge
Nursing diagnosis: Deficient Knowledge related to unfamiliarity with AKI, medications, and follow-up needs, as evidenced by questions or inaccurate statements about self-care.
- Goal: Before discharge, the client will teach back their medications, nephrotoxin avoidance, warning signs, and follow-up plan.
| Intervention | Rationale |
|---|---|
| Teach nephrotoxin avoidance (no NSAIDs unless approved) and medication reconciliation | Prevents recurrent AKI |
| Teach daily weights (if prescribed), the individualized hydration plan, and reporting oliguria/swelling/dyspnea | Enables early detection of recurrence or overload |
| Teach the client to mention AKI history before contrast studies or new medications | Prevents avoidable nephrotoxic exposure |
| Use teach-back; provide written instructions with the follow-up creatinine/eGFR plan | Confirms understanding |
Evaluation: Client correctly teaches back the plan and verbalizes warning signs and follow-up.
Escalation: red flags, dialysis & nephrology
Call the provider right away for any of these:
| Red flag | Why it matters |
|---|---|
| Potassium ≥6.0 mEq/L or peaked T waves / widened QRS | Imminent risk of lethal dysrhythmia |
| Anuria (no urine output) | Severe obstruction or shutdown |
| SpO₂ drop, crackles, pink frothy sputum | Pulmonary edema from fluid overload |
| Declining level of consciousness | Worsening uremic encephalopathy |
| Severe metabolic acidosis | Kidneys failing to clear acid load |
Possible urgent dialysis / renal replacement therapy (KRT/RRT) indications in AKI: refractory hyperkalemia, refractory metabolic acidosis, pulmonary edema or fluid overload not responding to medical therapy, uremic encephalopathy or pericarditis, certain toxin ingestions, or severe AKI with worsening clinical status. The decision is based on the whole clinical picture — not a single urea, creatinine, or potassium value. Escalate to nephrology/critical care per facility protocol.
Discuss with nephrology promptly for stage 3 AKI, unclear cause, inadequate response to treatment, AKI complications, renal transplant, advanced CKD (stage 4/5), suspected glomerulonephritis / vasculitis / interstitial nephritis / myeloma, or any possible need for renal replacement therapy.
Discharge & patient teaching
| Topic | Teach the client to… |
|---|---|
| Medications | Avoid NSAIDs and other nephrotoxins unless specifically approved; take meds exactly as prescribed; complete a medication reconciliation |
| Diet | Follow potassium, phosphorus, sodium, and protein limits per the provider/dietitian |
| Fluids | Follow the individualized prescribed fluid plan; weigh daily (if prescribed) and report rapid gain — do not self-increase fluids if on a fluid restriction |
| Contrast studies | Tell the team about prior AKI, CKD, dialysis, transplant, heart failure, and current meds; follow the prescriber’s individualized hydration/medication instructions (don’t assume “drink more water”) |
| Monitoring | Track urine output and report swelling, decreased urine, or shortness of breath |
| Follow-up | Discharge instructions should identify the AKI episode, suspected cause, medication changes, pending labs, and who is responsible for follow-up. A clinical review (with medication review and repeat creatinine/eGFR) should occur within ~3 months, sooner if recovery is incomplete or high-risk. AKI can progress to CKD. |
Practice question
A client with acute kidney injury has a serum potassium of 6.8 mEq/L. Which action should the nurse take first?
- A. Teach the client to restrict high-potassium foods
- B. Place the client on continuous cardiac monitoring and obtain/assess an ECG per protocol
- C. Encourage oral fluids
- D. Document the result and recheck potassium tomorrow
Answer: B. Potassium 6.8 mEq/L is severe hyperkalemia and can cause life-threatening dysrhythmias. The nurse should immediately assess cardiac rhythm/ECG status, notify the provider or rapid response team per protocol, and prepare for ordered emergency treatment (stabilize → shift → remove).
- A helps long-term but is far too slow for a critical potassium.
- C may be unsafe depending on volume status and does nothing for the immediate cardiac threat.
- D is unsafe — a critical value needs action now, not delayed reassessment.
Frequently asked questions
What is the priority for a nursing care plan for acute renal failure?
It depends on the presentation. Assess ABCs and perfusion first — the immediate threat may be shock, sepsis, pulmonary edema, severe acidosis, obstruction, uremic complications, or a dysrhythmia. Hyperkalemia is a top life-threatening risk (especially in oliguric AKI), but it isn’t always the single first priority.
What’s the difference between acute renal failure (ARF) and acute kidney injury (AKI)?
They’re the same condition. “Acute kidney injury” is the current standard term; “acute renal failure” is the older name you’ll still see in many textbooks and on the floor.
What are the 3 types of acute renal failure?
Prerenal (poor blood flow to the kidney), intrinsic/intrarenal (direct kidney damage such as acute tubular necrosis), and postrenal (obstruction of urine outflow).
What labs are monitored in AKI?
BUN, serum creatinine, eGFR (interpret cautiously), potassium and other electrolytes, bicarbonate/acid–base status, phosphorus, calcium, magnesium, urinalysis, and urine output. Trend creatinine and urine output rather than trusting one value.
What is the most dangerous electrolyte imbalance in acute renal failure?
Hyperkalemia (high potassium). It can trigger life-threatening cardiac dysrhythmias, which is why it’s a top nursing priority — managed as stabilize (calcium) → shift (insulin/dextrose) → remove (binders/dialysis).
Are all AKI patients oliguric?
No. AKI may be oliguric, nonoliguric, or anuric depending on the cause and severity. The classic oliguric → diuretic → recovery phases describe acute tubular necrosis but don’t fit every patient.
Related resources
Care-plan foundations
Related renal & fluid care plans
- Acute Renal Failure Nursing Interventions
- Chronic Kidney Disease (CKD)
- End-Stage Renal Disease (ESRD)
- SIADH
- Electrolyte Imbalance
References
- KDIGO. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements. 2012;2(1). kdigo.org
- NICE. Acute kidney injury: prevention, detection and management (NG148). National Institute for Health and Care Excellence. nice.org.uk/guidance/ng148
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH. Acute Kidney Injury. niddk.nih.gov
- Palmer BF, et al. Hyperkalemia: Diagnosis and Management. American Family Physician. 2023. aafp.org
- UK Kidney Association. Clinical Practice Guideline: Treatment of Acute Hyperkalaemia in Adults. ukkidney.org
- Herdman TH, Kamitsuru S, Lopes CT, eds. NANDA-I Nursing Diagnoses: Definitions & Classification 2024–2026, 13th ed. Thieme; 2024. thieme.com
- Lippincott Manual of Nursing Practice, current ed. Wolters Kluwer. shop.lww.com
- NCSBN. 2026 NCLEX-RN Examination Test Plan. ncsbn.org
Taxonomy and protocol note. Nursing-diagnosis labels vary by NANDA-I edition and program requirements — verify exact labels and codes in your required source. AKI lab reference ranges, fluid orders, medication protocols, and hyperkalemia algorithms vary by institution; always follow facility policy and provider orders. KDIGO 2012 remains the established AKI guideline cited here; KDIGO has released a 2026 AKI/AKD public-review draft — confirm whether the final version is published before relying on it.
