AKI nursing: KDIGO staging, causes, and NCLEX tips

Acute kidney injury (AKI) is a sudden decline in kidney function that occurs over hours to days. It affects roughly 10–15% of hospitalized patients, and the multinational AKI-EPI study found it in 57% of ICU patients during their first ICU week. Mortality climbs with severity: in AKI-EPI the adjusted odds of hospital death were about 3 times higher at KDIGO stage 2 and about 7 times higher at stage 3, and 45% of patients died in a Madrid study of hospital-diagnosed acute renal failure. The 2012 KDIGO (Kidney Disease: Improving Global Outcomes) guideline provides the diagnostic and staging framework used in clinical practice today. KDIGO released a draft AKI and acute kidney disease (AKD) guideline update for public comment in March 2026 (the comment window was extended to May 11, 2026); until the final version is published, the 2012 staging criteria below remain the operative standard.

This reference page is organized as a fast-access clinical resource: KDIGO staging criteria first, then the three AKI categories with comparison tables, then diagnostics, medical management, nursing interventions, and high-yield NCLEX scenarios. Use it alongside the nursing lab values cheat sheet and the electrolyte imbalances reference for complete renal coverage.

KDIGO AKI staging criteria

The KDIGO system defines AKI as any of the following: serum creatinine rise ≥0.3 mg/dL within 48 hours, serum creatinine ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 hours. Once AKI is diagnosed, staging uses whichever criterion – creatinine or urine output – assigns the higher stage.

Key staging points:

• Stage 1 captures the 0.3 mg/dL absolute rise – this catches early AKI even when the percentage increase is small (e.g., creatinine 0.8 → 1.1 mg/dL within 48 hours meets Stage 1)
• Any patient requiring dialysis is automatically Stage 3, regardless of creatinine level
• When creatinine and urine output criteria disagree, assign the higher stage
• Urine output calculation requires the patient’s weight: for a 70 kg patient, the oliguria threshold is 35 mL/h

AKI classification: prerenal, intrinsic, and postrenal

Prerenal AKI

Prerenal AKI accounted for 70% of community-acquired cases in Kaufman’s prospective study of patients admitted with AKI. The kidneys themselves are healthy – they receive insufficient perfusion pressure to filter effectively. The intact tubules respond appropriately, reabsorbing sodium and water aggressively to compensate. This produces concentrated, low-sodium urine. If perfusion is restored within 24–72 hours, creatinine returns to baseline. Prolonged hypoperfusion causes ischemic tubular cell death, converting prerenal AKI to ATN.

Intrinsic AKI (ATN)

Acute tubular necrosis (ATN) is the most common form of intrinsic AKI and the most common cause of hospital-diagnosed acute renal failure (45% of episodes in the Madrid multicenter study, versus 21% prerenal). Damaged tubular cells cannot concentrate urine or reabsorb sodium – producing dilute, high-sodium urine with the pathognomonic muddy brown granular casts. ATN progresses through four phases:

1. Onset: initial insult (ischemia, nephrotoxin)
2. Oliguric phase: urine output <400 mL/day for 1–3 weeks; highest risk for hyperkalemia, metabolic acidosis, and fluid overload
3. Diuretic phase: urine output rises to 3–6 L/day as tubules recover function but cannot yet concentrate; risk shifts to dehydration and hypokalemia
4. Recovery phase: gradual GFR restoration over weeks to months; some patients have permanent GFR reduction

Other intrinsic causes: acute interstitial nephritis (AIN – drug-induced, typically penicillins, NSAIDs, PPIs; may present with WBC casts, fever, and rash, though the full triad is uncommon and urine eosinophils are an unreliable test), acute glomerulonephritis (RBC casts), renal vascular injury (HUS/TTP, renal artery thrombosis).

Postrenal AKI

Obstruction downstream from the kidneys raises collecting-system pressure, opposing GFR. Serum creatinine usually rises only with bilateral obstruction, obstruction of a single functioning kidney, or unilateral obstruction on top of existing CKD. Once relieved, recovery is typically rapid. After relief of chronic obstruction, a post-obstructive diuresis may occur – monitor closely for volume depletion.

Clinical presentation

Fluid and urine output changes

• Oliguria: urine output <0.5 mL/kg/h (KDIGO threshold) or <400 mL/day – the earliest clinical indicator of AKI
• Anuria: urine output <100 mL/day – severe; suggests Stage 3 or complete obstruction
• Fluid overload: peripheral edema, pulmonary crackles, orthopnea, hypertension, JVD, weight gain (1 kg ≈ 1 L fluid)
• Tea-colored or brown urine: myoglobinuria in rhabdomyolysis, or hemoglobinuria; signals pigment nephropathy
• Foamy urine: significant proteinuria indicating glomerular damage

Electrolyte disturbances

Hyperkalemia is the most immediately life-threatening complication of AKI. Potassium rises because impaired GFR reduces renal excretion, and cellular injury releases intracellular potassium. The classic EKG progression is tall peaked T waves → PR prolongation and P-wave flattening → widened QRS → sine-wave pattern → ventricular fibrillation or asystole, but changes do not track the potassium level reliably and a patient can deteriorate without passing through each step. Potassium ≥6.5 mEq/L, or any hyperkalemic EKG change, needs urgent treatment.

Hyponatremia can develop from water retention proportionally exceeding sodium retention, or from administration of hypotonic fluids. Monitor serum sodium daily and correct cautiously (rapid correction risks osmotic demyelination syndrome).

Metabolic acidosis develops because impaired kidneys cannot excrete hydrogen ions or regenerate bicarbonate. Patients compensate with Kussmaul respirations (deep, labored breathing). Severe acidosis (pH <7.1) depresses myocardial contractility.

Hyperphosphatemia arises from reduced renal phosphorus excretion. Elevated phosphorus binds calcium, producing hypocalcemia – monitor for Chvostek’s sign (facial twitch with CN VII tap) and Trousseau’s sign (carpopedal spasm with BP cuff inflation).

BUN and creatinine rise

BUN and creatinine accumulate as GFR falls. At steady state, a doubling of creatinine from the patient’s baseline (for example 1.0 → 2.0 mg/dL) reflects roughly a 50% fall in GFR; in evolving AKI, creatinine lags behind the true fall in GFR. BUN rises faster than creatinine in prerenal AKI (ratio >20:1) because intact tubules reabsorb urea along with water; in ATN the rise is proportional (ratio 10–15:1).

Uremic symptoms

As BUN exceeds 80–100 mg/dL, uremic toxins affect multiple organ systems: nausea, vomiting, metallic taste, anorexia, fatigue, confusion, asterixis (flapping hand tremor with wrists extended), pericardial friction rub (uremic pericarditis – a dialysis emergency), pruritus (more typical of chronic uremia; the cause is multifactorial), and platelet dysfunction causing bleeding tendency.

Diagnostics

Laboratory panel

FENa formula: FENa (%) = (urine Na × plasma Cr) / (plasma Na × urine Cr) × 100

FENa caveats: Results are unreliable in patients receiving loop diuretics (diuretics force natriuresis regardless of tubular function). Important exceptions where FENa may be <1% despite intrinsic AKI: contrast-induced nephropathy, myoglobinuria (rhabdomyolysis), early obstructive AKI, and acute glomerulonephritis.

Imaging

Renal ultrasound is the first-line imaging study for AKI. It evaluates kidney size (normal or enlarged = AKI; small/shrunken = CKD), identifies hydronephrosis (post-renal obstruction), and rules out structural lesions. A post-void residual bladder scan is performed if lower urinary tract obstruction (BPH, stricture) is suspected.

Renal biopsy

Indicated when the diagnosis remains unclear after clinical evaluation and imaging – particularly when intrinsic causes other than ATN are suspected (glomerulonephritis, vasculitis, thrombotic microangiopathy). Uncorrected coagulopathy and uncontrolled hypertension are contraindications to percutaneous biopsy; a solitary kidney is a relative contraindication that pushes the team toward an open or transjugular approach. Post-procedure monitoring: bedrest, serial vital signs, urine color checks, CBC at 4–6 hours.

Medical management

Prerenal AKI: fluid resuscitation

Isotonic crystalloid (0.9% normal saline or lactated Ringer’s) is administered IV to restore renal perfusion. Monitor urine output response – improvement within hours suggests prerenal etiology. Fluid challenges in heart failure must be given cautiously to avoid precipitating pulmonary edema; in these patients, small boluses (250–500 mL) with reassessment are preferred over large-volume resuscitation.

Intrinsic/oliguric AKI: fluid restriction and diuretics

Patients with established ATN and fluid overload require restriction (typically prior day’s output + 500 mL for insensible losses) and loop diuretics. Furosemide (Lasix) is first-line; may be given as IV bolus or continuous infusion. KDIGO recommends against using diuretics to prevent AKI (1B) and suggests against using them to treat AKI except to manage volume overload (2C); their role is fluid-balance control, since they do not change the course of AKI.

Contrast-induced AKI: prevention protocol

Contrast-associated AKI typically shows a creatinine rise that peaks 48–72 hours post-contrast and resolves within about a week in most patients. The 2020 ACR–National Kidney Foundation consensus notes that the risk from IV iodinated contrast has historically been overstated, because older studies lacked control groups. Prevention:

• IV volume expansion with isotonic saline (or isotonic bicarbonate) for patients at increased risk (KDIGO 1A); ACR–NKF says prophylaxis is indicated for patients with AKI or eGFR <30 mL/min/1.73 m² who are not on dialysis. A common regimen is 1 mL/kg/h for 6–12 hours before and after contrast
• Hold nephrotoxins before the procedure: NSAIDs, aminoglycosides
• Metformin (FDA label): stop at the time of or before iodinated contrast if eGFR is 30–60, with liver disease, alcoholism, or heart failure, or with intra-arterial contrast; recheck eGFR at 48 hours and restart if kidney function is stable. Metformin is contraindicated below eGFR 30
• Use the lowest possible contrast dose and iso-osmolar or low-osmolar agents in high-risk patients (KDIGO)

Rhabdomyolysis AKI: aggressive hydration

Myoglobin released from damaged muscle is directly nephrotoxic, causing pigment nephropathy and tubular obstruction. Management:

• Early, aggressive IV isotonic crystalloid as ordered (commonly started at several hundred mL/hr, adjusted to response and volume status)
• Urine output goal commonly 200–300 mL/hr (to flush myoglobin); watch closely for fluid overload if oliguria persists
• Monitor urine color – tea or cola color indicates myoglobinuria; clears as myoglobin is flushed
• Serial CK, potassium, and creatinine monitoring
• Urinary alkalinization (sodium bicarbonate in IV fluids) may reduce myoglobin precipitation in tubules, though evidence is mixed

Dialysis indications: AEIOU mnemonic

Renal replacement therapy (RRT) is initiated when conservative management is insufficient. KDIGO says to start RRT emergently for life-threatening fluid, electrolyte, and acid-base changes, and to weigh the whole clinical picture and lab trends rather than single BUN or creatinine thresholds. Starting earlier does not help without such an indication: in the STARRT-AKI trial (3,019 critically ill patients), an accelerated strategy did not lower 90-day mortality (43.9% vs 43.7%) and left more survivors dialysis-dependent at 90 days (10.4% vs 6.0%).

• A – Acidosis: severe metabolic acidosis refractory to medical therapy (pH <7.1 is a commonly quoted threshold)
• E – Electrolytes: life-threatening hyperkalemia unresponsive to medical management
• I – Intoxication/Ingestion: dialyzable toxins – methanol, ethylene glycol, lithium, salicylates
• O – Overload: pulmonary edema or severe fluid overload unresponsive to IV diuretics
• U – Uremia: symptomatic uremia – encephalopathy, pericarditis (uremic pericarditis is an absolute indication), platelet dysfunction with bleeding

Nursing assessment and interventions

Priority assessments

Hourly intake and output (I&O) is the most important nursing action in AKI. Urine output <0.5 mL/kg/h for 6 hours meets KDIGO Stage 1 criteria. Calculate the threshold by weight: a 70 kg patient must produce >35 mL/h to stay below the Stage 1 threshold. Document every drain, emesis, and insensible loss source.

Daily weights are performed at the same time with the same scale and same clothing. A 1 kg weight gain = 1 L fluid retained. Sudden weight gain signals fluid accumulation; sudden weight loss during the diuretic phase signals dehydration risk.

Fluid status assessment each shift:

• Auscultate lungs: crackles indicate pulmonary edema
• Inspect for peripheral edema: grade 1+ (slight) to 4+ (deep, non-pitting)
• Assess JVD with patient at 45 degrees
• Check vital signs: hypertension (fluid overload) vs hypotension/tachycardia (dehydration in prerenal AKI)
• Skin turgor and mucous membranes for hydration status

Electrolyte monitoring and hyperkalemia management

Monitor potassium with each lab draw. When potassium exceeds 5.5 mEq/L, perform a 12-lead EKG to assess for cardiac changes and notify the provider. Place the patient on continuous cardiac monitoring at K+ ≥6.5 mEq/L or with any hyperkalemic EKG change (UK Kidney Association 2026).

Hyperkalemia management sequence:

1. Calcium gluconate IV – given when EKG changes are present; improves the EKG within about 3 minutes and lasts 30–60 minutes; does NOT lower potassium
2. Insulin (regular) + dextrose IV – shifts K+ intracellularly; potassium starts to fall within 15 minutes, with a peak fall of about 0.6–1.0 mEq/L at 30–60 minutes that lasts up to about 2 hours. Hypoglycemia is the main risk, so check glucose repeatedly for up to 6 hours
3. Sodium bicarbonate IV – not routine for lowering potassium (UK Kidney Association 2026); considered when significant metabolic acidosis coexists
4. Potassium binders – GI potassium removal. Sodium zirconium cyclosilicate acts within about 1 hour, patiromer takes 4–7 hours, and sodium polystyrene sulfonate (Kayexalate) is slow and unpredictable and carries a labeled risk of intestinal necrosis (concomitant sorbitol is not recommended). All three US labels state they should not be used as emergency treatment for life-threatening hyperkalemia, so none substitutes for calcium, insulin/dextrose, or dialysis.
5. Dialysis – definitive removal when refractory or when other AEIOU indications coexist

Review the electrolyte imbalances reference for full hyperkalemia management detail.

Nephrotoxin avoidance

Review the medication administration record at each shift and flag:

• Aminoglycosides (gentamicin, tobramycin, amikacin) – KDIGO suggests avoiding them unless no less nephrotoxic alternative exists; monitor drug levels and adjust doses in AKI
• NSAIDs (ibuprofen, ketorolac, naproxen) – reduce prostaglandin-mediated afferent arteriolar dilation; worsen prerenal AKI
• ACE inhibitors and ARBs – reduce efferent arteriolar tone; decrease GFR in states of low renal perfusion (hold in acute hypoperfusion)
• IV contrast – flag any planned contrast study so the team can weigh risk and order prophylaxis; recheck creatinine at 48–72 hours in high-risk patients
• Metformin – hold when kidney function is falling (lactic acidosis risk) and around iodinated contrast per the FDA label criteria
• Amphotericin B – directly nephrotoxic; use lipid formulations when possible

Collaborate with pharmacy for dose adjustments on renally cleared medications (antibiotics, anticoagulants, digoxin, opioids).

Skin and fluid assessment

Fluid overload causes skin to become taut, shiny, and fragile over edematous areas. Pressure injury risk increases substantially. Reposition every 2 hours, use pressure-redistributing mattresses, protect bony prominences, and apply barrier cream to intertriginous areas. Uremia can also cause dry, itchy skin – apply emollient lotions and teach the patient to avoid scratching.

Diet and fluid modifications

• Fluid restriction (if oliguric/fluid-overloaded): calculate allowance based on prior day output + 500 mL; distribute across meals and medication administrations
• Potassium restriction (when hyperkalemic): limit high-potassium foods such as bananas, oranges, tomatoes, and potatoes, and avoid potassium-based salt substitutes; the dietitian individualizes the limit
• Phosphorus restriction (when hyperphosphatemic): limit processed foods with phosphate additives, cola drinks, and processed meats; administer phosphate binders (calcium carbonate, sevelamer) with meals
• Sodium restriction: <2 g/day to reduce fluid retention
• Protein: do not restrict protein to delay dialysis (KDIGO 2D). KDIGO suggests 0.8–1.0 g/kg/day for non-catabolic AKI without dialysis, 1.0–1.5 g/kg/day on RRT, and up to 1.7 g/kg/day on CRRT or when hypercatabolic, with 20–30 kcal/kg/day total energy and the enteral route preferred

AKI vs CKD: key distinctions

Key pearl: A renal ultrasound showing bilaterally small kidneys strongly supports CKD, while normal or enlarged kidneys are more consistent with an acute process. Baseline creatinine records are invaluable – AKI requires a change from baseline; CKD is a chronic, stable elevation. For full CKD management, see the CKD and ESRD nursing reference.

NCLEX scenarios

Scenario 1: prerenal AKI from dehydration

A 68-year-old patient is admitted from a long-term care facility with three days of vomiting and diarrhea. Vital signs: BP 88/54, HR 118, dry mucous membranes. Labs: creatinine 2.4 mg/dL (baseline 0.9 mg/dL), BUN 72 mg/dL, urine sodium 14 mEq/L, urine specific gravity 1.028, FENa 0.6%.

Which intervention takes priority?

IV isotonic fluid resuscitation. The elevated BUN:creatinine ratio (30:1), low urine sodium, concentrated urine, and low FENa all point to prerenal AKI from volume depletion. Healthy tubules are aggressively retaining sodium and water. The priority is restoring renal perfusion – fluids, not restriction. Monitor for urine output improvement within 6–12 hours; persistent oliguria after adequate resuscitation suggests progression to ATN.

Scenario 2: rhabdomyolysis AKI

A 25-year-old is brought to the ED after being found unresponsive at home following suspected drug overdose. He has been on a hard floor for an estimated 18 hours. Labs: CK 42,000 U/L, creatinine 3.1 mg/dL, potassium 6.2 mEq/L. Urine is tea-colored.

What is the nursing priority?

Aggressive IV fluid resuscitation to flush myoglobin from the renal tubules. The goal urine output is 200–300 mL/hr to clear the pigment. Tea-colored urine suggests myoglobinuria (a heme-positive dipstick with few or no RBCs on microscopy supports it). Potassium of 6.2 mEq/L requires an immediate 12-lead EKG, continuous monitoring, and hyperkalemia management (calcium gluconate first if the EKG shows hyperkalemic changes). Serial CK and creatinine monitoring every 4–6 hours. Position change every 2 hours given immobility duration. Watch for compartment syndrome in crush injury patients.

Scenario 3: contrast-induced AKI

A 72-year-old patient with hypertension and diabetes has a CT angiogram with IV contrast. Creatinine before the procedure was 1.3 mg/dL. At 48 hours post-procedure, creatinine is 1.9 mg/dL; at 72 hours it is 2.2 mg/dL.

What nursing actions are indicated?

This presentation – creatinine peak at 48–72 hours post-contrast – is the classic timing of contrast-induced AKI. Nursing actions: hold nephrotoxins (NSAIDs, metformin if not already held), maintain IV fluid hydration as ordered, monitor creatinine daily until trending downward, monitor urine output and restrict nephrotoxins in subsequent care. Metformin stays on hold until the provider confirms kidney function is stable again (the FDA label calls for an eGFR recheck 48 hours after contrast before restarting). Most cases resolve within about a week without requiring dialysis.

Scenario 4: hyperkalemia management in AKI

A patient with ATN from aminoglycoside nephrotoxicity has potassium 6.8 mEq/L. The EKG shows widened QRS complexes and peaked T waves. The provider orders: calcium gluconate IV, regular insulin with D50W IV, sodium bicarbonate IV, and sodium polystyrene sulfonate oral.

In what order do the nurse administer these?

1. Calcium gluconate first – immediate cardiac membrane stabilization given EKG changes (widened QRS). Acts within minutes. Does not lower potassium – it protects the heart while other agents work.
2. Insulin with D50W – shifts potassium intracellularly; K+ starts to fall within 15 minutes, with a peak fall of about 0.6–1.0 mEq/L at 30–60 minutes. Check blood glucose repeatedly afterward.
3. Sodium bicarbonate – an adjunct when metabolic acidosis is present; its potassium-lowering effect on its own is weak.
4. Sodium polystyrene sulfonate – removes potassium from the body via GI excretion over hours; the slowest-acting of the four.

Scenario 5: dialysis indications in AKI (AEIOU)

A patient with Stage 3 AKI has the following: pH 7.06, bicarbonate 10 mEq/L, potassium 7.2 mEq/L despite two rounds of insulin/dextrose and sodium polystyrene sulfonate, urine output <20 mL over the past 12 hours, and a new pericardial friction rub on auscultation.

What action does the nurse anticipate?

Emergent renal replacement therapy. This patient meets multiple AEIOU indications simultaneously: severe metabolic acidosis (pH 7.06 < 7.1), refractory hyperkalemia (7.2 mEq/L despite medical management), anuria (Stage 3 urine output criterion), and uremic pericarditis (absolute indication – pericardial friction rub). The nurse should notify nephrology immediately, prepare the patient for vascular access, and document all current hemodynamic status. Uremic pericarditis carries a risk of cardiac tamponade – urgent dialysis is the only definitive treatment.

Scenario 6: AKI vs CKD differentiation

A 55-year-old patient with type 2 diabetes presents with creatinine 4.8 mg/dL. The chart shows a creatinine of 4.2 mg/dL from two years ago. Renal ultrasound shows bilateral kidneys measuring 8 cm (normal 9–12 cm). Hemoglobin is 9.1 g/dL.

Is this AKI, CKD, or AKI-on-CKD?

This presentation is most consistent with CKD, with possible AKI-on-CKD if a specific precipitant exists. Evidence for CKD: bilaterally small kidneys on ultrasound, normocytic anemia (decreased erythropoietin), and chronically elevated creatinine from records two years prior. The current creatinine is only modestly elevated above the prior value, making an acute-on-chronic process possible – a new precipitant (infection, dehydration, contrast exposure, new nephrotoxin) could explain the incremental rise. Management: identify and correct any acute precipitant, avoid nephrotoxins, and assess for CKD complications. See the CKD and ESRD nursing reference for full CKD management.

Common confusions

FENa <1% does NOT always mean prerenal. Several intrinsic causes can produce a low FENa: contrast-induced AKI, myoglobinuria (rhabdomyolysis), acute glomerulonephritis, and early obstruction. FENa must always be interpreted in clinical context. In patients receiving diuretics, FENa is unreliable – use FEUrea <35% to identify prerenal etiology instead.

Oliguria vs anuria thresholds:

• Oliguria = urine output <400 mL/day (or <0.5 mL/kg/h)
• Severe oliguria = <100–200 mL/day
• Anuria = <100 mL/day in most nursing texts (some sources use <50 mL/day); KDIGO’s Stage 3 criterion is anuria for ≥12 hours without a volume cutoff
• Anuria is more commonly postrenal (obstruction) or end-stage ATN; true anuria from prerenal AKI is rare

Calcium gluconate does not lower potassium. It stabilizes the cardiac membrane by raising the action potential threshold. The question “which intervention lowers potassium the fastest?” – the answer is insulin with dextrose (intracellular shift, onset within 15 min, peak 30–60 min) or dialysis (for immediate removal). Calcium gluconate is given first in emergencies but it is not a potassium-lowering agent.

BUN:Cr ratio >20:1 can occur without AKI. High-protein diet, GI bleeding, and catabolic states all elevate BUN disproportionately without necessarily indicating prerenal kidney injury. Use the ratio in context: the patient must have rising creatinine (meeting AKI criteria) for the ratio to be interpretively useful.

Diuretic phase of ATN is a high-risk period. Nursing students often focus on the oliguric phase as the danger zone, but the diuretic phase (urine output 3–6 L/day) carries its own risks: severe volume depletion and hypokalemia. Replace fluids and electrolytes as ordered and monitor for orthostatic hypotension, muscle cramps, and dysrhythmias.

NANDA-I nursing care plans for AKI

The following care plans address the five most clinically significant nursing diagnoses in acute kidney injury. Each diagnosis is grounded in AKI-specific pathophysiology – oliguria thresholds, KDIGO staging, electrolyte emergencies, and nephrotoxin mechanisms – rather than generic renal content. Interventions include the clinical rationale behind each action.

1. Impaired urinary elimination

NANDA-I label: Impaired urinary elimination (Domain 3, Class 1) Related to: Reduced glomerular filtration rate from ischemic, nephrotoxic, or obstructive injury to the renal tubules As evidenced by: Urine output below KDIGO threshold (<0.5 mL/kg/hr for ≥6 hours), oliguria (<400 mL/day), anuria (<100 mL/day), elevated serum creatinine, tea-colored or foamy urine, altered urine specific gravity

Short-term goal: Patient will achieve and maintain urine output ≥0.5 mL/kg/hr within 24 hours of initiation of AKI management interventions. Long-term goal: Patient will demonstrate return to baseline creatinine and normal urine output pattern prior to discharge, with understanding of self-monitoring signs requiring provider contact.

2. Excess fluid volume

NANDA-I label: Excess fluid volume (Domain 2, Class 5) Related to: Inability of injured kidneys to excrete sodium and water in oliguric AKI; impaired GFR reducing urinary output As evidenced by: Weight gain >1 kg/day, peripheral edema (graded 1+ to 4+), pulmonary crackles on auscultation, elevated blood pressure, jugular venous distension (JVD), decreased serum sodium (dilutional hyponatremia), SpO2 decline

Short-term goal: Patient will demonstrate no new evidence of pulmonary edema (clear breath sounds, SpO2 ≥94%) within 8 hours of diuretic or fluid-restriction intervention. Long-term goal: Patient will maintain fluid balance within ±1 kg of dry weight by discharge, with verbalized understanding of fluid restriction rationale and daily self-weighing.

3. Risk for electrolyte imbalance

NANDA-I label: Risk for electrolyte imbalance (Domain 2, Class 5) Related to: Impaired renal excretion of potassium, phosphorus, and hydrogen ions; inability to regenerate bicarbonate; accumulation of uremic metabolites Risk factors: Oliguric or anuric AKI, KDIGO Stage 2–3, rhabdomyolysis, metabolic acidosis, potassium >5.5 mEq/L, EKG changes, total body potassium release from cellular injury

Short-term goal: Patient will maintain serum potassium 3.5–5.0 mEq/L, with no severe acidemia (pH above 7.20), and remain free of cardiac arrhythmia during hospitalization. Long-term goal: Patient will verbalize dietary potassium and phosphorus restrictions and identify foods to avoid prior to discharge.

4. Risk for infection

NANDA-I label: Risk for infection (Domain 11, Class 1) Related to: Uremia-related immune suppression, indwelling urinary catheter providing a portal of entry, skin integrity compromise from edema, and altered phagocyte function from uremic toxin accumulation Risk factors: Indwelling Foley catheter for I&O monitoring, prolonged hospitalization, elevated BUN (>80 mg/dL) indicating uremic immune dysfunction, peripheral edema creating skin breakdown risk, IV access sites, malnutrition from anorexia

Short-term goal: Patient will remain afebrile and without signs of catheter-associated urinary tract infection (CAUTI) or IV site infection throughout hospitalization. Long-term goal: Patient will verbalize signs of infection requiring provider notification and demonstrate correct hand hygiene technique before discharge.

5. Deficient knowledge

NANDA-I label: Deficient knowledge (Domain 5, Class 4) Related to: Unfamiliarity with AKI pathophysiology, nephrotoxin avoidance, contrast precautions, fluid and dietary restrictions, follow-up creatinine monitoring, and MAKE-90 outcomes As evidenced by: Patient questions about medication safety in kidney injury, incorrect beliefs about salt substitutes, unawareness of contrast-AKI risk, no established follow-up plan for creatinine monitoring

Short-term goal: Patient will verbalize three nephrotoxins to avoid, signs requiring emergency care, and the purpose of follow-up creatinine checks before discharge. Long-term goal: Patient will attend follow-up nephrology or primary care visit within 30 days of discharge and demonstrate understanding of MAKE-90 monitoring goals (creatinine trend, dialysis avoidance, survival).

Frequently asked questions

What is the priority nursing intervention for AKI?

The priority intervention depends on AKI type and current clinical status. In all AKI, accurate hourly intake and output monitoring – including urine output against the KDIGO threshold of 0.5 mL/kg/hr – is the most fundamental assessment action. For hyperkalemia with EKG changes (peaked T waves, widened QRS), administering calcium gluconate IV for cardiac membrane stabilization is the immediate clinical priority regardless of fluid status. In prerenal AKI, IV isotonic fluid resuscitation to restore renal perfusion takes priority over fluid restriction. The first-priority question is always: what is the AKI type, and what is threatening the patient most right now?

What are the most common NANDA nursing diagnoses for AKI?

The five NANDA-I diagnoses most relevant to AKI are: (1) Impaired urinary elimination, related to reduced GFR and tubular injury; (2) Excess fluid volume, related to inability to excrete sodium and water in oliguric AKI; (3) Risk for electrolyte imbalance, related to impaired excretion of potassium, phosphorus, and hydrogen ions; (4) Risk for infection, related to uremia-induced immune suppression and indwelling Foley catheter; and (5) Deficient knowledge, related to nephrotoxin avoidance, contrast precautions, and follow-up creatinine monitoring. In rhabdomyolysis-related AKI, Acute pain may apply; in patients awaiting dialysis decision, Anxiety is also appropriate.

How is AKI staged using the KDIGO criteria?

KDIGO 2012 defines three AKI stages based on serum creatinine and urine output. Stage 1: creatinine rises ≥0.3 mg/dL within 48 hours, or 1.5–1.9× baseline within 7 days, or urine output <0.5 mL/kg/hr for 6–12 hours. Stage 2: creatinine 2.0–2.9× baseline or urine output <0.5 mL/kg/hr for ≥12 hours. Stage 3: creatinine ≥3× baseline, or ≥4.0 mg/dL absolute, or initiation of RRT; urine output criterion is <0.3 mL/kg/hr for ≥24 hours or anuria for ≥12 hours. Assign the higher stage when creatinine and urine output criteria disagree. Any patient requiring dialysis is automatically Stage 3.

How should hyperkalemia be managed in AKI?

Hyperkalemia management in AKI follows a four-step sequence based on urgency. First, obtain a 12-lead EKG whenever K+ ≥5.5 mEq/L. If EKG changes are present (peaked T waves, widened QRS), administer calcium gluconate IV (1–2 g over 5–10 minutes) immediately for cardiac membrane stabilization – this does not lower potassium but protects against arrhythmia for 30–60 minutes while other agents work. Second, administer regular insulin 10 units IV with 25 g dextrose (D50W) to shift K+ intracellularly (onset within 15 minutes, peak fall of about 0.6–1.0 mEq/L at 30–60 minutes), then monitor glucose for up to 6 hours. Third, IV sodium bicarbonate is reserved for patients with significant metabolic acidosis; it is not a routine potassium-lowering drug. Fourth, a potassium binder removes potassium through the gut (sodium zirconium cyclosilicate within about 1 hour, patiromer 4–7 hours), and dialysis removes it definitively. Emergency threshold is any hyperkalemic EKG change, or K+ ≥6.5 mEq/L regardless of EKG.

What is the difference between pre-renal, intrinsic, and post-renal AKI?

Pre-renal AKI (70% of community-acquired cases in one prospective study) is caused by reduced renal perfusion – the nephrons are intact, producing concentrated, low-sodium urine (FENa <1%, specific gravity >1.020, BUN:Cr ratio >20:1). It responds to fluid resuscitation within 24–72 hours. Intrinsic AKI (ATN is most common, 45% of hospital-diagnosed episodes in the Madrid study) results from direct tubular cell damage; tubules cannot concentrate urine or reabsorb sodium (FENa >2%, specific gravity <1.010, muddy brown granular casts). It does not improve with fluids alone. Post-renal AKI results from obstruction below the kidneys – ureteral, bladder outlet, or urethral – and requires obstruction relief rather than fluid management. Nursing assessment focus: pre-renal patients are volume-depleted (dry mucous membranes, tachycardia, low BP); intrinsic AKI patients may appear euvolemic or hypervolemic; post-renal patients may have suprapubic distension, a history of BPH, or bilateral flank pain.

When should a nurse call the provider in AKI?

Contact the provider immediately for any of the following: urine output <0.5 mL/kg/hr for ≥6 hours (KDIGO Stage 1 threshold met); potassium ≥5.5 mEq/L (obtain 12-lead EKG before calling); any EKG change (peaked T waves, PR prolongation, widened QRS) in a patient with known or suspected AKI; blood pressure <90/60 mmHg or MAP <65 mmHg (hypoperfusion worsening pre-renal AKI); new pulmonary crackles or SpO2 <94% (pulmonary edema from fluid overload); pH <7.2 or bicarbonate <15 mEq/L on ABG (severe metabolic acidosis that may need bicarbonate or RRT); creatinine rise of ≥0.3 mg/dL within 48 hours (Stage 1 met if not yet recognized); or any new pericardial friction rub (uremic pericarditis – an absolute dialysis indication).

What lab values indicate AKI is worsening?

Rising serum creatinine is the primary indicator – a rise of ≥0.3 mg/dL in 48 hours or to ≥1.5 times baseline within 7 days confirms AKI, and doubling marks stage 2; continued upward trend indicates progression. Falling bicarbonate (normal 22–26 mEq/L) indicates worsening metabolic acidosis from accumulating H+ ions. Rising potassium above 5.5 mEq/L signals declining ability to excrete potassium. A BUN rising faster than creatinine (>20:1 ratio) in established ATN suggests new catabolic stress, GI bleeding, or inadequate nutrition. Falling hemoglobin may indicate dilution from fluid retention or uremia-related platelet dysfunction causing occult bleeding. Declining urine output despite adequate fluid management or diuretics indicates progression toward dialysis-dependent AKI. MAKE-90 tracking at 30 and 90 days post-discharge confirms recovery trajectory.

How is fluid management approached in oliguric vs anuric AKI?

In oliguric AKI (urine output <400 mL/day), fluid management balances the need for adequate perfusion against the risk of fluid overload the kidneys cannot excrete. Fluid restriction to prior day output + 500 mL insensible losses is the standard formula. Loop diuretics (furosemide) may generate additional output if tubular function remains partially intact. In anuric AKI (urine output <100 mL/day), diuretics are ineffective – the tubules are too damaged to respond. Strict fluid restriction is mandatory. Any fluid given must have a specific clinical indication (medication administration, maintenance of vascular access). Anuric AKI with concurrent indications from the AEIOU mnemonic (acidosis pH <7.1, refractory electrolyte abnormalities, intoxication, volume overload unresponsive to diuretics, uremic symptoms) requires renal replacement therapy – conservative fluid management alone is insufficient.

References

1. Kidney Disease: Improving Global Outcomes (KDIGO) AKI Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2(1):1–138.
2. Palevsky PM, Liu KD, Brophy PD, et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury. Am J Kidney Dis. 2013;61(5):649–672. doi:10.1053/j.ajkd.2013.02.349
3. Hoste EA, Bagshaw SM, Bellomo R, et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med. 2015;41(8):1411–1423. doi:10.1007/s00134-015-3934-7
4. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P; Acute Dialysis Quality Initiative workgroup. Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs. Crit Care. 2004;8(4):R204–R212. doi:10.1186/cc2872
5. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Kidney failure (ESRD) – diagnosis, treatment, and financial help. NIH NIDDK. Updated 2023. https://www.niddk.nih.gov/health-information/kidney-disease/kidney-failure
6. Perazella MA, Coca SG. Three feasible strategies to minimize kidney injury in ‘incipient AKI’. Nat Rev Nephrol. 2013;9(8):484–490. doi:10.1038/nrneph.2013.80
7. Ronco C, Bellomo R, Kellum JA. Acute kidney injury. Lancet. 2019;394(10212):1949–1964. doi:10.1016/S0140-6736(19)32563-2
8. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. 2024;105(4S):S117–S314. doi:10.1016/j.kint.2023.10.018
9. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31. doi:10.1186/cc5713
10. Bagshaw SM, George C, Bellomo R; ANZICS Database Management Committee. Changes in the incidence and outcome for early acute kidney injury in a cohort of Australian intensive care units. Crit Care. 2007;11(3):R68. doi:10.1186/cc5949
11. Uchino S, Kellum JA, Bellomo R, et al. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005;294(7):813–818. doi:10.1001/jama.294.7.813
12. Prowle JR, Bellomo R. Fluid administration and the kidney. Curr Opin Crit Care. 2010;16(4):332–336. doi:10.1097/MCC.0b013e32833be90b
13. Cerda J, Liu KD, Cruz DN, et al. Promoting kidney function recovery in patients with AKI requiring RRT. Clin J Am Soc Nephrol. 2015;10(10):1859–1867. doi:10.2215/CJN.01170215
14. Rewa O, Bagshaw SM. Acute kidney injury – epidemiology, outcomes and economics. Nat Rev Nephrol. 2014;10(4):193–207. doi:10.1038/nrneph.2013.282
15. Makris K, Spanou L. Acute kidney injury: definition, pathophysiology and clinical phenotypes. Clin Biochem Rev. 2016;37(2):85–98.
16. Liaño F, Pascual J; Madrid Acute Renal Failure Study Group. Epidemiology of acute renal failure: a prospective, multicenter, community-based study. Kidney Int. 1996;50(3):811–818. doi:10.1038/ki.1996.380
17. Kaufman J, Dhakal M, Patel B, Hamburger R. Community-acquired acute renal failure. Am J Kidney Dis. 1991;17(2):191–198. doi:10.1016/S0272-6386(12)81128-0
18. Davenport MS, Perazella MA, Yee J, et al. Use of intravenous iodinated contrast media in patients with kidney disease: consensus statements from the American College of Radiology and the National Kidney Foundation. Radiology. 2020;294(3):660–668. doi:10.1148/radiol.2019192094
19. US Food and Drug Administration. Metformin hydrochloride tablets and extended-release tablets: prescribing information (sections 2.4, 4, 5.1). DailyMed, revised September 2025. https://dailymed.nlm.nih.gov/
20. STARRT-AKI Investigators. Timing of initiation of renal-replacement therapy in acute kidney injury. N Engl J Med. 2020;383(3):240–251. doi:10.1056/NEJMoa2000741
21. Alfonzo A, Harrison A, Baines R, et al. Clinical practice guideline: management of hyperkalaemia in adults. UK Kidney Association; updated July 2026. https://www.ukkidney.org/sites/default/files/documents/FINAL%20VERSION%20-%20UKKA%20CLINICAL%20PRACTICE%20GUIDELINE%20-%20MANAGEMENT%20OF%20HYPERKALAEMIA%20IN%20ADULTS%20-%20UPDATED%20JULY%202026_0.pdf
22. US prescribing information (DailyMed): Lokelma (sodium zirconium cyclosilicate), rev. 02/2024; Veltassa (patiromer), rev. 01/2025; sodium polystyrene sulfonate for suspension, rev. 10/2025; calcium gluconate injection, rev. 11/2025. https://dailymed.nlm.nih.gov/
23. Fosset M, Pensier J, Jabaudon M, et al. Sodium bicarbonate therapy in severe metabolic acidemia: an individual patient data meta-analysis of the BICAR-ICU and BICAR-ICU2 trials. Crit Care. 2026;30(1):382. doi:10.1186/s13054-026-06206-3
24. Kalantar-Zadeh K, Gutekunst L, Mehrotra R, et al. Understanding sources of dietary phosphorus in the treatment of patients with chronic kidney disease. Clin J Am Soc Nephrol. 2010;5(3):519–530. doi:10.2215/CJN.06080809
25. Ikizler TA, Parikh CR, Himmelfarb J, et al. A prospective cohort study of acute kidney injury and kidney outcomes, cardiovascular events, and death. Kidney Int. 2021;99(2):456–465. doi:10.1016/j.kint.2020.06.032
26. Chawla LS, Davison DL, Brasha-Mitchell E, et al. Development and standardization of a furosemide stress test to predict the severity of acute kidney injury. Crit Care. 2013;17(5):R207. doi:10.1186/cc13015
27. Gould CV, Umscheid CA, Agarwal RK, Kuntz G, Pegues DA; HICPAC. Guideline for prevention of catheter-associated urinary tract infections 2009. Infect Control Hosp Epidemiol. 2010;31(4):319–326. doi:10.1086/651091
28. Centers for Disease Control and Prevention. CAUTI basics (background on catheter-associated urinary tract infections). Accessed October 13, 2026. https://www.cdc.gov/infection-control/hcp/cauti/background.html