Acute kidney injury (AKI) is a sudden decline in kidney function that occurs over hours to days, affecting up to 15% of all hospitalized patients and more than 50% of ICU admissions. It carries a hospital mortality of 40–50% and represents one of the highest-stakes conditions in acute care nursing. The 2012 KDIGO (Kidney Disease: Improving Global Outcomes) guidelines provide the universal diagnostic and staging framework used in all clinical settings today.
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.
| Stage | Serum creatinine criterion | Urine output criterion | Clinical implication |
|---|---|---|---|
| Stage 1 | Rise ≥0.3 mg/dL within 48 h, OR 1.5–1.9× baseline within 7 days | <0.5 mL/kg/h for 6–12 h | Mild injury – optimize perfusion, remove nephrotoxins, monitor strict I&O |
| Stage 2 | 2.0–2.9× baseline | <0.5 mL/kg/h for ≥12 h | Moderate injury – nephrology consult, prepare for possible RRT |
| Stage 3 | ≥3.0× baseline, OR ≥4.0 mg/dL absolute value, OR initiation of RRT | <0.3 mL/kg/h for ≥24 h OR anuria for ≥12 h | Severe injury – high mortality, RRT often required |
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
| Feature | Prerenal | Intrinsic (ATN) | Postrenal |
|---|---|---|---|
| Mechanism | Decreased renal perfusion – nephrons intact | Direct parenchymal damage – nephrons injured | Urinary tract obstruction – back-pressure on GFR |
| Common causes | Hypovolemia, hemorrhage, [sepsis](/nursing-tips/sepsis-nursing/), heart failure, dehydration, burns | ATN (ischemic or nephrotoxic), rhabdomyolysis, AIN (drug-induced), glomerulonephritis | BPH, kidney stones, bladder tumor, retroperitoneal fibrosis, blood clots |
| BUN:Cr ratio | >20:1 | 10–15:1 (proportional rise) | Variable (often >20:1 early) |
| FENa | <1% (tubules reabsorbing Na) | >2% (tubules unable to reabsorb Na) | Variable |
| Urine sodium | <20 mEq/L | >40 mEq/L | Variable |
| Urine specific gravity | >1.020 (concentrated) | <1.010 (dilute, fixed) | Variable |
| Urine osmolality | >500 mOsm/kg | <350 mOsm/kg | Variable |
| Urine sediment | Bland – hyaline casts | Muddy brown granular casts (ATN); WBC casts (AIN); RBC casts (glomerulonephritis) | Normal or crystals/stones |
| Response to fluids | Creatinine improves within 24–72 h | No improvement with fluids alone | Improves after obstruction relief |
| Reversiblity | Fully reversible if caught early | Reversible if ischemia limited; risk of progression to CKD with prolonged ATN | Usually reversible once obstruction relieved |
Prerenal AKI
Prerenal AKI accounts for 60–70% of community-acquired cases. 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 (~45% of all cases). 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:
- Onset: initial insult (ischemia, nephrotoxin)
- Oliguric phase: urine output <400 mL/day for 1–3 weeks; highest risk for hyperkalemia, metabolic acidosis, and fluid overload
- Diuretic phase: urine output rises to 3–6 L/day as tubules recover function but cannot yet concentrate; risk shifts to dehydration and hypokalemia
- 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; presents with eosinophiluria, WBC casts, fever, rash), 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. Bilateral obstruction (or unilateral in a single-kidney patient) is required to raise serum creatinine. 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. EKG changes progress in sequence: tall peaked T waves → PR prolongation → widened QRS → sine-wave pattern → ventricular fibrillation. Any potassium above 6.0 mEq/L with EKG changes is a medical emergency.
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. A creatinine of 2.0 mg/dL represents approximately 50% reduction in GFR from normal. 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 from phosphate crystal deposition, and platelet dysfunction causing bleeding tendency.
Diagnostics
Laboratory panel
| Test | What it measures | AKI interpretation |
|---|---|---|
| Serum creatinine | GFR surrogate (muscle metabolism byproduct) | Rises as GFR falls; 2.0 mg/dL ≈ 50% GFR loss |
| BUN | Nitrogenous waste from protein catabolism | Rises in AKI; affected by protein intake, GI bleeding, catabolic states |
| BUN:creatinine ratio | Differentiates prerenal vs intrinsic | >20:1 = prerenal; 10–15:1 = intrinsic (ATN); <10:1 may suggest liver disease or malnutrition |
| FENa | % of filtered sodium excreted; tubular function indicator | <1% = prerenal; >2% = intrinsic (ATN); 1–2% = indeterminate. Unreliable with diuretics – use FEUrea instead (<35% = prerenal) |
| Urine sodium | Tubular sodium handling | <20 mEq/L = prerenal; >40 mEq/L = ATN |
| Urinalysis + microscopy | Urine protein, blood, casts | Muddy brown granular casts = ATN; RBC casts = glomerulonephritis; WBC casts = AIN/pyelonephritis; hyaline casts = prerenal |
| Potassium | Electrolyte homeostasis | Rises in AKI; >6.0 mEq/L with EKG changes = emergency |
| ABG | Acid-base status | Metabolic acidosis (pH <7.35, low HCO3) – expect pH <7.1 as dialysis threshold |
| CBC | Hemoglobin, WBC, platelets | Normal Hgb in AKI (differentiates from CKD); low platelets may suggest HUS/TTP or DIC |
| CK (creatine kinase) | Muscle breakdown marker | Markedly elevated (>5,000–10,000 U/L) in rhabdomyolysis; urine myoglobin may be positive |
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). Contraindicated with a single kidney, uncorrected coagulopathy, or severe hypertension. 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. Furosemide does not change the course of AKI or reduce the need for dialysis, but it facilitates fluid management and may prevent the need for emergent dialysis in mild-moderate overload.
Contrast-induced AKI: prevention protocol
Contrast-induced AKI typically peaks 48–72 hours post-contrast and resolves within 5–7 days in most patients. Prevention:
- IV isotonic saline: 1 mL/kg/h for 6–12 hours before and after contrast administration
- Hold nephrotoxins before the procedure: NSAIDs, aminoglycosides
- Hold metformin 48 hours after contrast (risk of lactic acidosis if AKI develops)
- Minimize contrast volume; use iso-osmolar agents in high-risk patients
Rhabdomyolysis AKI: aggressive hydration
Myoglobin released from damaged muscle is directly nephrotoxic, causing pigment nephropathy and tubular obstruction. Management:
- Aggressive IV fluid resuscitation: 250–500 mL/hr isotonic saline
- Urine output goal: 200–300 mL/hr (to flush myoglobin)
- 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. The AEIOU indications apply regardless of creatinine level – dialysis is a clinical decision, not a lab threshold decision.
- A – Acidosis: pH <7.1 refractory to bicarbonate therapy
- 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.
Hyperkalemia management sequence:
- Calcium gluconate IV – cardiac membrane stabilization, onset within minutes; does NOT lower potassium
- Insulin (regular) + dextrose IV – shifts K+ intracellularly, lowers serum K+ by 0.5–1.5 mEq/L within 20–30 minutes
- Sodium bicarbonate IV – shifts K+ intracellularly (especially effective in metabolic acidosis)
- Sodium polystyrene sulfonate (Kayexalate) or patiromer – GI potassium removal over hours
- 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) – monitor trough levels; dose adjustments required 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 – hold for 48 hours post-exposure in high-risk patients; monitor creatinine at 48–72 hours
- Metformin – hold when creatinine rises or IV contrast given (lactic acidosis risk)
- 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 also causes skin dryness and pruritus from phosphate crystal deposition – use emollient lotions and avoid scratching education.
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: avoid bananas, oranges, tomatoes, potatoes, salt substitutes
- Phosphorus restriction: limit dairy, nuts, cola drinks, processed meats; administer phosphate binders (calcium carbonate, sevelamer) with meals
- Sodium restriction: <2 g/day to reduce fluid retention
- Protein: moderate intake to prevent catabolism without excessive BUN production; nutrition consult for guidance in ICU patients
AKI vs CKD: key distinctions
| Feature | AKI | CKD |
|---|---|---|
| Onset | Hours to days | Months to years |
| Reversibility | Often reversible if caught early | Irreversible – progressive decline |
| Kidney size (ultrasound) | Normal or enlarged | Small, shrunken bilaterally |
| Anemia | Absent (unless concurrent illness) | Present – decreased erythropoietin production; normocytic normochromic |
| Renal osteodystrophy | Absent | Present with longstanding disease – PTH elevation, bone pain |
| Creatinine trend | Rapid rise from known or estimated baseline | Chronically elevated; slow progressive rise over years |
| Prior history | Usually none (or known precipitant) | Documented history – diabetes, hypertension, proteinuria |
| Dialysis | Temporary if needed; may be weaned as function recovers | Permanent once ESRD (GFR <15 mL/min) |
| Nails | Usually normal | Half-and-half nails (Lindsay's nails) – white proximal, brown/red distal |
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 confirms myoglobinuria. Potassium of 6.2 mEq/L requires an immediate EKG and hyperkalemia management (calcium gluconate first for cardiac stabilization). 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. Teach the patient that metformin is withheld 48 hours after contrast. Most cases resolve within 5–7 days 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?
- 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.
- Insulin with D50W – shifts potassium intracellularly within 20–30 minutes; lowers serum K+ by 0.5–1.5 mEq/L.
- Sodium bicarbonate – shifts potassium intracellularly by correcting acidosis; adjunct to insulin.
- 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 (KDIGO Stage 3 criterion is <50 mL over 12 hours or complete anuria)
- 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 20–30 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.
| Intervention | Rationale |
|---|---|
| Measure and record urine output hourly using an indwelling Foley catheter with urometer in all AKI patients | Hourly measurement is the only reliable method for detecting the KDIGO Stage 1 urine output threshold of <0.5 mL/kg/hr. Spot checks miss the 6-hour accumulation criterion. In a 70 kg patient, the alarm threshold is output <35 mL/hr sustained over 6 hours – calculate per patient weight at admission. |
| Weigh patient daily at the same time, using the same scale, in the same clothing; record and compare to prior day | 1 kg of weight gain = 1 L of retained fluid. Daily weight detects subclinical fluid accumulation before pulmonary crackles or peripheral edema become clinically apparent. During the ATN diuretic phase (urine output 3–6 L/day), weight loss >1 kg/day signals hypovolemia – an equally dangerous shift from the oliguric phase. |
| Differentiate AKI type using BUN:creatinine ratio, FENa, and urine specific gravity findings and report to provider | Pre-renal AKI (BUN:Cr >20:1, FENa <1%, specific gravity >1.020) requires fluid resuscitation; intrinsic AKI (BUN:Cr 10–15:1, FENa >2%, specific gravity <1.010 with muddy brown casts) requires fluid restriction and nephrotoxin removal. Applying the correct intervention to the wrong type worsens outcomes – fluids given to oliguric ATN cause pulmonary edema. |
| Administer IV isotonic crystalloid (0.9% NS or lactated Ringer’s) as ordered for prerenal AKI; restrict fluids to prior day output + 500 mL insensible losses for established ATN | Prerenal AKI responds to perfusion restoration within 24–72 hours if tubules are intact. Established ATN does not respond to fluids – fluid restriction prevents further volume accumulation that the anuric or oliguric kidneys cannot excrete. The 500 mL insensible allowance accounts for respiratory and insensible skin losses. |
| Administer IV furosemide (Lasix) as ordered in oliguric AKI with fluid overload; monitor urine output response within 2 hours | Loop diuretics increase urine output and facilitate fluid balance management in ATN but do not alter the course of AKI or reduce dialysis requirement (KDIGO, 2012). If urine output does not increase within 2 hours of a furosemide dose, the tubules may be too damaged to respond – this finding should be communicated to nephrology as a dialysis indicator. |
| Assess urine color and characteristics at each void or bag change; report tea-colored or brown urine, turbidity, or foam | Tea-colored or brown urine in AKI suggests myoglobinuria (rhabdomyolysis) or hemoglobinuria – pigment nephropathy requiring aggressive fluid flushing to target urine output 200–300 mL/hr. Foamy urine reflects significant proteinuria indicating glomerular damage. Turbid urine suggests superimposed infection. Each pattern directs a distinct management pathway. |
| Identify and hold all nephrotoxic medications at each medication reconciliation review: NSAIDs, ACEi/ARBs (in hypoperfusion states), aminoglycosides, IV contrast, metformin, amphotericin B | NSAIDs inhibit prostaglandin-mediated afferent arteriolar dilation – the compensatory mechanism that maintains GFR in low-perfusion states. ACEi/ARBs reduce efferent arteriolar tone, lowering GFR when perfusion pressure is already marginal. Aminoglycosides accumulate in proximal tubule cells and are directly nephrotoxic. Holding these agents removes ongoing injurious stimuli and allows tubular recovery. |
| Monitor for the ATN diuretic phase transition: rising urine output (>400 mL/day) after an oliguric period, with dilute urine (specific gravity <1.010) | The diuretic phase signals tubular recovery but carries its own risks – dehydration and hypokalemia as the recovering tubules cannot yet concentrate urine. Shift nursing priorities from fluid restriction to adequate fluid and electrolyte replacement. Document the transition clearly in the medical record as a phase change requiring order reassessment. |
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.
| Intervention | Rationale |
|---|---|
| Auscultate lung fields at every assessment; report new crackles or decreased air entry at lung bases immediately | Pulmonary crackles signal fluid in the alveoli – the earliest clinical indicator of fluid moving from the vascular to the pulmonary interstitial space. In oliguric AKI the kidneys cannot compensate for excess volume; pulmonary edema can progress rapidly. A new SpO2 drop to <94% with crackles is a respiratory emergency. |
| Assess for JVD with the patient at 45 degrees; grade peripheral edema from 1+ (slight, <2 mm depth) to 4+ (deep, >8 mm non-pitting, associated with skin breakdown risk) | JVD confirms central venous pressure elevation – the right heart is backing up fluid that the kidneys are not removing. Graded peripheral edema provides an objective serial measurement for monitoring fluid accumulation trends. Progression from 2+ to 3+ or 4+ over a shift indicates inadequate fluid control. |
| Implement prescribed fluid restriction (prior day output + 500 mL for insensible losses); distribute allowance across the 24-hour period (e.g., 400 mL over meals, remainder for medications and sips) | Fluid restriction in oliguric AKI must be calculated against actual output – not a fixed number. A patient with 200 mL of urine output plus 500 mL insensible loss receives 700 mL total. Distributing the allowance across the day prevents patient thirst from being concentrated into one large drink that immediately overloads the restrictive goal. |
| Restrict dietary sodium to <2 g/day in coordination with dietitian; provide low-sodium meal trays | Sodium drives water retention. In AKI, the impaired kidneys cannot excrete excess sodium, so each gram above the restriction exacerbates fluid overload. Low-sodium trays, paired with patient education about hidden sodium in processed foods and condiments, are evidence-based for AKI fluid management. |
| Position the patient with the head of bed elevated 30–45 degrees if dyspnea is present; maintain semi-Fowler’s or Fowler’s position | Gravity redistributes pulmonary fluid to dependent lung zones, reducing work of breathing. Supine positioning in fluid-overloaded AKI patients promotes fluid shift into the pulmonary vasculature. Semi-Fowler’s position is a standard comfort measure that reduces respiratory effort until diuresis achieves fluid balance. |
| Administer prescribed IV loop diuretics (furosemide) on time; monitor urine output 60–120 minutes after dose | Furosemide blocks the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle, producing natriuresis and diuresis. In AKI with tubular injury, higher doses (or continuous infusion) are often required because tubular secretion of furosemide is impaired. A >50% increase in urine output within 2 hours suggests a treatment response. |
| Monitor serum sodium daily for dilutional hyponatremia (Na <135 mEq/L); restrict free water if present | In oliguric AKI, water is retained proportionally more than sodium, diluting the serum sodium concentration. Dilutional hyponatremia (not sodium depletion) is managed by restricting free water intake. Rapid sodium correction (>8–12 mEq/L per 24 hours) risks osmotic demyelination syndrome – correction must be gradual. |
| Protect edematous skin: reposition every 2 hours, apply pressure-redistributing surfaces, use barrier cream on intertriginous areas, inspect bony prominences at every turn | Edematous skin is taut, poorly perfused, and at high risk for pressure injury. Fluid in the interstitial space impairs oxygen and nutrient delivery to skin cells. Grade 3–4 pitting edema significantly elevates the Braden scale pressure injury risk score. Uremia from AKI also reduces platelet function and contributes to skin fragility. |
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 and bicarbonate ≥18 mEq/L without cardiac arrhythmia during hospitalization. Long-term goal: Patient will verbalize dietary potassium and phosphorus restrictions and identify foods to avoid prior to discharge.
| Intervention | Rationale |
|---|---|
| Monitor potassium level with each lab draw; obtain a 12-lead EKG immediately when K+ ≥5.5 mEq/L | Hyperkalemia is the most immediately life-threatening complication of AKI. At K+ 5.5 mEq/L, peaked T waves appear on EKG. At 6.0–6.5 mEq/L, PR prolongation and widening QRS appear. At >7.0 mEq/L, a sine-wave pattern precedes ventricular fibrillation. EKG changes at any potassium level are a medical emergency requiring immediate provider notification regardless of the absolute potassium value. |
| In K+ ≥6.0 mEq/L with EKG changes, administer medications in sequence as ordered: calcium gluconate IV → regular insulin + D50W IV → sodium bicarbonate IV → potassium binders or dialysis | Calcium gluconate (1–2 g IV over 5–10 minutes) raises the cardiac action potential threshold, stabilizing the membrane – onset within minutes. It does not lower serum potassium; it buys time while potassium-lowering measures work. Insulin (10 units regular) + D50W shifts K+ intracellularly within 20–30 minutes, lowering serum K+ by 0.5–1.5 mEq/L. Sodium bicarbonate corrects co-existing acidosis, shifting K+ intracellularly. Patiromer or sodium polystyrene sulfonate removes potassium via GI excretion over 4–6 hours. Dialysis provides definitive removal when refractory. |
| Hold oral and IV potassium supplementation; restrict dietary potassium to <2 g/day; avoid salt substitutes, bananas, oranges, potatoes, tomatoes, and nuts | Salt substitutes contain potassium chloride as a sodium substitute – patients may inadvertently add large quantities, triggering hyperkalemia. Dietary restriction is a non-pharmacologic intervention that reduces ongoing potassium load. Coordinate with dietitian for a low-potassium meal plan and provide written food lists. |
| Monitor serum bicarbonate and arterial blood gas (ABG) at least daily in oliguric AKI; report pH <7.2 or bicarbonate <15 mEq/L | Impaired kidneys cannot excrete H+ ions or regenerate bicarbonate. Metabolic acidosis reduces myocardial contractility, shifts the oxyhemoglobin dissociation curve rightward, and worsens hyperkalemia (acidosis drives K+ out of cells in exchange for H+). pH <7.1 refractory to bicarbonate therapy is an AEIOU indication for renal replacement therapy. |
| Administer IV sodium bicarbonate as ordered for metabolic acidosis; monitor for tetany, calcium levels, and overcorrection | Sodium bicarbonate temporarily increases serum bicarbonate and shifts K+ intracellularly. However, rapid alkalinization lowers ionized calcium (alkalosis drives calcium binding to albumin), risking hypocalcemic tetany. Monitor total and ionized calcium alongside bicarbonate replacement. Overcorrection to pH >7.5 paradoxically worsens cellular oxygenation. |
| Monitor serum phosphorus and administer prescribed phosphate binders (calcium carbonate, sevelamer) with each meal | GFR impairment reduces phosphorus excretion, causing hyperphosphatemia. Elevated phosphate binds serum calcium, precipitating hypocalcemia – monitor for Chvostek’s sign (facial twitch on CN VII tap) and Trousseau’s sign (carpopedal spasm with BP cuff). Phosphate binders must be taken with meals to bind dietary phosphorus in the GI tract before absorption. |
| Restrict dietary phosphorus to <800 mg/day: avoid dairy products, nuts, cola drinks, processed meats, and canned goods | Processed foods contain phosphate additives that are nearly 100% bioavailable, compared to 50–60% for naturally occurring phosphorus. Colas contain phosphoric acid. Dietary phosphorus restriction, combined with binders, reduces the phosphorus load on already impaired renal excretion. |
| Recognize the ROME mnemonic to understand AKI metabolic acidosis: Respiratory Opposite, Metabolic Equal – in metabolic acidosis, pH and bicarbonate both decrease; expect compensatory respiratory rate increase (Kussmaul respirations) | Kussmaul respirations (deep, labored breathing at rate 20–30/min) are the respiratory compensation for metabolic acidosis – the body eliminates CO2 to raise pH. Document respiratory rate and pattern at each assessment. Absence of expected respiratory compensation despite severe acidosis suggests neurologic compromise, sedation overdose, or respiratory muscle fatigue requiring intubation. |
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.
| Intervention | Rationale |
|---|---|
| Implement full CAUTI prevention bundle for all patients with indwelling Foley catheters: daily necessity assessment, periurethral meatal care with soap and water, dependent drainage at all times, secured catheter tubing to prevent traction | In AKI, the Foley catheter placed for accurate I&O monitoring simultaneously creates a direct bacterial pathway to the bladder. CAUTI is the leading nosocomial infection in hospitalized patients. Uremia from AKI further impairs neutrophil function, reducing the immune response to ascending bacteria. The CAUTI bundle reduces infection risk by 50–70% in ICU settings. |
| Assess daily whether the urinary catheter remains clinically necessary; document medical necessity (KDIGO staging, UO monitoring for RRT decision); remove as soon as strict I&O monitoring is no longer required | The risk of CAUTI rises approximately 3–7% per catheter-day. Bacteriuria occurs in 100% of patients with catheters for 30 days. Catheters placed for convenience, not clinical necessity, should be removed and replaced with a validated non-catheter output measurement method (external catheter, incontinence brief weights, or graduated-cylinder voiding for ambulatory patients). |
| Perform daily skin assessment over edematous areas: inspect skin folds, sacrum, heels, and intertriginous areas for breakdown, maceration, or ulceration | Edema impairs skin perfusion and oxygen delivery to cells. Macerated or broken skin in uremic patients becomes colonized with gram-negative organisms easily. Any skin breakdown provides an entry point for bacteremia – especially dangerous in immunosuppressed uremic patients where bacteremia can rapidly progress to sepsis. |
| Monitor IV access sites at each shift for erythema, warmth, induration, or purulent discharge; change peripheral IV sites per institutional protocol (typically every 72–96 hours) | IV access is a direct portal to the bloodstream. Uremia impairs the normal inflammatory response, meaning early signs of catheter-related bloodstream infection (CRBSI) may be muted. Central line-associated bloodstream infection (CLABSI) in AKI patients carries significantly higher mortality than in non-AKI patients due to compromised host defenses. |
| Monitor temperature every 4 hours; report any temperature ≥38.3°C (101°F) to the provider with current lab values | Uremia blunts the normal febrile response – an AKI patient may have significant infection with a temperature of only 37.8–38°C. Any fever in a uremic patient warrants a full sepsis screen (blood cultures, CBC, urinalysis, chest X-ray). Sepsis is both a cause and complication of AKI – the bidirectional relationship (sepsis → AKI → impaired immunity → worsened sepsis) must be recognized. |
| Maintain aseptic technique for all IV, central line, arterial line, and urinary catheter manipulations; use chlorhexidine skin preparation for venipuncture | Uremic toxins accumulate over days of AKI and progressively impair neutrophil chemotaxis, phagocytosis, and oxidative burst. Even routine contamination from non-aseptic technique that a healthy immune system would clear may result in systemic infection in a uremic patient. Chlorhexidine reduces skin surface bacterial counts by 80–95% versus alcohol alone for venipuncture. |
| Provide oral care every 4 hours with chlorhexidine mouthwash or at minimum moistened swabs; apply lip balm to prevent mucosal cracking | Uremia produces a characteristic metallic or ammonia-like taste and fosters oral mucosal changes – uric acid crystals may deposit on mucosal surfaces (uremic frost). Dry, cracked oral mucosa creates a bacterial entry point for aspiration pneumonia and systemic infection. Oral hygiene also reduces aspiration pneumonia risk in patients with altered mental status from uremic encephalopathy. |
| Instruct patient and visitors on hand hygiene technique; provide hand sanitizer at the bedside and require hand washing before and after patient contact | Uremic immune dysfunction makes normal hand-transmitted organisms dangerously pathogenic. Patient education about hand hygiene is a Joint Commission National Patient Safety Goal. Family members who understand the rationale – that the patient’s immunity is specifically reduced by kidney failure – are more compliant than those given generic instructions. |
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).
| Intervention | Rationale |
|---|---|
| Teach the MAKE-90 outcome framework: Major Adverse Kidney Events at 90 days include sustained creatinine doubling from baseline, new dependence on dialysis, or death within 90 days of the AKI episode | MAKE-90 is the standard research outcome for AKI recovery used in clinical trials and nephrology practice. Patients who understand that their recovery window is 90 days and that creatinine monitoring directly informs that assessment are more likely to attend follow-up appointments. A normal discharge creatinine does not confirm kidney recovery – 30–40% of AKI survivors develop new or worsened CKD within 12 months. |
| Explain the five nephrotoxins to hold and why: NSAIDs (remove prostaglandin-mediated GFR protection), ACEi/ARBs (reduce efferent arteriolar tone in low-perfusion states), aminoglycoside antibiotics (proximal tubule accumulation), IV contrast (tubular vasoconstriction and direct cytotoxicity), and metformin (lactic acidosis risk if AKI recurs) | Patients who understand the mechanism behind each restriction are more adherent than those given a list without explanation. NSAIDs are the highest-risk nephrotoxin in the outpatient setting – OTC ibuprofen and naproxen are purchased without awareness of AKI risk. Up to 30% of patients discharged after AKI fill an NSAID prescription within 30 days. Specific brand names (Advil, Motrin, Aleve, Toradol) improve recognition. |
| Teach contrast-induced AKI (CIAKI) precautions: before any procedure requiring IV contrast, the patient must inform the ordering provider of the prior AKI episode; prophylactic saline hydration (1 mL/kg/hr for 6–12 hours before and after contrast) reduces CIAKI risk | Patients with prior AKI have a 3–5× higher risk of contrast nephropathy with subsequent exposures. The creatinine checkpoint before contrast (eGFR <30 mL/min/1.73m² is a contraindication to iodinated contrast) prevents preventable AKI recurrence. Many patients are unaware of this risk and receive contrast at outpatient imaging centers without nephrology awareness. |
| Provide a written fluid and dietary restriction guide covering: fluid allowance calculation method, low-potassium foods, phosphorus-high foods to limit, sodium restriction goals (<2 g/day), and protein intake guidance | Verbal-only teaching is recalled at <30% at 24 hours. Written materials with concrete examples (specific branded foods to avoid or limit) improve adherence. Patients managing oliguria at home – or recovering with residual CKD – benefit from understanding how dietary choices directly affect lab values. A low-potassium food list protects against outpatient hyperkalemia in patients with residual AKI-related GFR reduction. |
| Instruct patient to seek emergency care immediately for: urine output significantly below normal for more than 6 hours, swelling that is rapidly worsening, shortness of breath or inability to lie flat, confusion or extreme fatigue, or symptoms of hyperkalemia (palpitations, muscle weakness, tingling) | Outpatient recognition of AKI recurrence or MAKE-90 endpoint criteria prevents delayed presentation. Palpitations and muscle weakness are common outpatient presentations of hyperkalemia in recovering AKI – patients who can connect these symptoms to their kidney history seek care faster. A written emergency threshold list at discharge is standard nephrology practice. |
| Discuss the importance of post-discharge creatinine follow-up: baseline creatinine should be rechecked at 7 days, 30 days, and 90 days post-discharge; a nephrology referral is recommended if baseline does not recover or new proteinuria persists | The KDIGO 2012 guidelines recommend creatinine surveillance at 3 months to identify AKI-to-CKD transition. A creatinine that has not returned to within 25% of pre-AKI baseline at 90 days meets criteria for CKD staging. Patients who understand this monitoring rationale keep appointments. Nephrology follow-up within 30 days for Stage 2–3 AKI is associated with lower 1-year mortality in observational studies. |
| For patients who required or nearly required dialysis, provide education on renal replacement therapy modalities: intermittent hemodialysis (IHD) vs continuous RRT (CRRT); explain that RRT initiated for AKI may be temporary if kidney function recovers | Fear of dialysis is a significant barrier to hospitalization consent for RRT when indicated. Patients who understand that AKI-related RRT is frequently temporary – 50–60% of AKI patients who initiate dialysis recover sufficient renal function to discontinue within weeks to months – are more willing to accept the intervention when needed. CRRT is the preferred modality for hemodynamically unstable patients because solute removal is continuous and gradual, preventing abrupt fluid shifts. |
| Provide a medication wallet card listing current kidney status, nephrotoxins to avoid, and the date of the AKI episode | Primary care providers, pharmacists, and urgent care physicians outside the hospital system may not have access to the patient’s inpatient records. A wallet card ensures that prescribers and radiologists at any facility know to check renal function before prescribing NSAIDs, aminoglycosides, or iodinated contrast, preventing iatrogenic AKI recurrence. |
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 prevents fatal arrhythmia while other agents work. Second, administer regular insulin 10 units IV with D50W to shift K+ intracellularly (onset 20–30 minutes, lowers K+ by 0.5–1.5 mEq/L). Third, IV sodium bicarbonate addresses co-existing metabolic acidosis and further shifts K+ intracellularly. Fourth, patiromer or sodium polystyrene sulfonate provides GI potassium removal over 4–6 hours. Emergency threshold is K+ ≥6.0 mEq/L with any 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 (60–70% of community cases) 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 all AKI) 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 (metabolic acidosis approaching dialysis threshold of pH <7.1); 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 doubling from baseline confirms AKI; 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.
Sources
- 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.
- Kellum JA, Lameire N, KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a synopsis of the Kidney Disease: Improving Global Outcomes 2012 clinical practice guideline. Ann Intern Med. 2013;158(11):825–830.
- 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.
- 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.
- 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
- Perazella MA, Coca SG. Three feasible strategies to minimize drug-associated acute kidney injury. Nat Rev Nephrol. 2012;8(10):598–606.
- Ronco C, Bellomo R, Kellum JA. Acute kidney injury. Lancet. 2019;394(10212):1949–1964.
- National Kidney Foundation. KDOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis. 2002;39(2 Suppl 1):S1–S266.