Acute Kidney Injury (AKI) Stages and Nursing Management for NCLEX: KDIGO and RIFLE Criteria

Acute kidney injury (AKI) is a sudden decline in kidney function over hours to days, defined by KDIGO criteria as: a rise in serum creatinine of ≥0.3 mg/dL within 48 hours, OR ≥1.5x baseline within 7 days, OR urine output <0.5 mL/kg/hr for 6+ hours. AKI is categorized by mechanism: pre-renal (decreased perfusion — most common, 60-70%), intrinsic (damage to nephron — 25-35%), and post-renal (obstruction — 5-10%). The nursing priorities: identify cause (history, exam, labs, imaging), restore renal perfusion if pre-renal (fluids if hypovolemic, treat underlying cause), avoid further nephrotoxic insults (medications, contrast), monitor electrolytes (especially potassium), monitor fluid balance (strict I/O), and prepare for dialysis if indicated. AKI is staged 1-3 by severity, with stage 3 having the highest mortality. About 30-50% of hospitalized AKI patients have at least partial residual loss of kidney function — preventing AKI is more effective than treating it.

Pre-renal AKI accounts for 60-70% of AKI cases. The kidneys are anatomically intact, but blood flow to them is reduced. Causes: **Hypovolemia**: hemorrhage, dehydration, severe vomiting/diarrhea, burns, third-spacing (sepsis, ascites, pancreatitis). **Decreased cardiac output**: heart failure, MI, cardiogenic shock, pulmonary embolism, tamponade. **Decreased systemic vascular resistance**: sepsis, anaphylaxis, neurogenic shock. **Renal vasoconstriction**: hepatorenal syndrome, NSAIDs (block prostaglandin-mediated afferent vasodilation), ACE inhibitors/ARBs (block angiotensin-mediated efferent vasoconstriction), contrast media. **Lab pattern in pre-renal AKI**: - BUN:Creatinine ratio >20:1 (BUN reabsorption increases with hypoperfusion) - Urine sodium <20 mEq/L (kidney conserves Na in low-perfusion state) - FENa <1% (fractional excretion of sodium) - Urine osmolality >500 mOsm/kg (concentrated urine) - Urinalysis: bland (no casts) **Treatment**: address the cause. Hypovolemia → IV fluids (crystalloids first, blood if hemorrhage). Heart failure → optimize cardiac output. Sepsis → fluids + vasopressors + antibiotics. Discontinue NSAIDs and ACE-Is/ARBs if contributing. If hypoperfusion is corrected quickly, pre-renal AKI is fully reversible. If sustained for hours-days, it can progress to intrinsic AKI (acute tubular necrosis from prolonged ischemia) — at which point it's no longer easily reversible.

Intrinsic AKI accounts for 25-35% of cases. The kidney parenchyma is damaged. Subcategories by location: **Acute tubular necrosis (ATN)**: most common intrinsic cause. Tubular cell death from: - Ischemia (prolonged pre-renal AKI, surgery, sepsis) - Nephrotoxins: aminoglycosides (gentamicin), vancomycin, contrast media, NSAIDs, chemotherapy (cisplatin), myoglobin from rhabdomyolysis, hemoglobin from hemolysis **Acute glomerulonephritis**: glomerular damage from: - Post-streptococcal GN - Lupus nephritis - IgA nephropathy - Goodpasture syndrome - ANCA-associated vasculitis **Acute interstitial nephritis (AIN)**: drug-induced (penicillins, NSAIDs, PPIs, sulfa drugs, allopurinol). Often presents with rash, fever, eosinophilia (drug allergy triad). **Lab pattern in intrinsic AKI (ATN specifically)**: - BUN:Creatinine ratio <20:1 (more like 10-15:1) - Urine sodium >40 mEq/L (damaged tubules can't reabsorb Na) - FENa >2% - Urine osmolality 300-400 (isosthenuric — can't concentrate) - Urinalysis: muddy brown/granular casts (pathognomonic for ATN), epithelial cell casts **Treatment**: supportive — there's no specific antidote for ATN. Maintain fluid balance, manage electrolytes, avoid further insults, dialysis if needed. Recovery typically takes 1-3 weeks but tubules can regenerate. Some patients have permanent residual deficit.

Post-renal AKI (5-10%) is caused by obstruction of urine flow. Less common but reversible if caught early. Causes: - Bladder outlet obstruction: BPH (most common in older men), bladder/prostate cancer, urethral stricture - Ureteral obstruction: kidney stones (must be bilateral or unilateral with one functioning kidney to cause AKI), retroperitoneal fibrosis, malignancy compression - Bladder dysfunction: neurogenic bladder, anticholinergic medications causing retention - Catheter obstruction: clots, kinking, debris **Lab pattern**: variable. Acute obstruction → reduced urine output, rising creatinine. With prolonged obstruction → tubular damage develops, lab pattern resembles intrinsic AKI. **Diagnosis**: bladder scan (post-void residual), renal ultrasound (hydronephrosis), CT if obstruction suspected. **Treatment**: relieve obstruction. - Bladder outlet obstruction → straight or indwelling catheter - Ureteral obstruction → urology consult, possible stent or nephrostomy - Catheter obstruction → flush or replace catheter Post-obstructive diuresis: after relieving obstruction, patient may produce massive amounts of urine (3-5 L/day) for several days. Monitor for electrolyte derangements (especially Na, K, Mg) and dehydration. Replace fluids and electrolytes carefully.

KDIGO (Kidney Disease: Improving Global Outcomes) is the current standard. Stages 1-3 by severity using creatinine OR urine output (whichever is worse): **Stage 1 (mild)**: - Creatinine: 1.5-1.9× baseline OR ≥0.3 mg/dL increase - Urine output: <0.5 mL/kg/hr for 6-12 hours **Stage 2 (moderate)**: - Creatinine: 2.0-2.9× baseline - Urine output: <0.5 mL/kg/hr for ≥12 hours **Stage 3 (severe)**: - Creatinine: ≥3× baseline OR ≥4.0 mg/dL OR initiation of renal replacement therapy - Urine output: <0.3 mL/kg/hr for ≥24 hours OR anuria for ≥12 hours Mortality scales with stage: stage 1 ~5-10%, stage 2 ~15-25%, stage 3 30-50% in hospitalized patients. **RIFLE criteria** (older, less commonly used now): - R: Risk - I: Injury - F: Failure - L: Loss (sustained AKI >4 weeks) - E: End-stage (sustained AKI >3 months) KDIGO is more commonly used in current practice, but you may see RIFLE referenced — both classify by similar parameters.

Dialysis (renal replacement therapy) is indicated when AKI causes complications that cannot be managed medically. AEIOU: **A - Acidosis** (severe, refractory metabolic acidosis with pH <7.1 not responsive to bicarbonate) **E - Electrolyte abnormalities** (most often hyperkalemia >6.5 mEq/L unresponsive to medical management — calcium gluconate stabilizes membrane, insulin/glucose shifts K intracellularly, kayexalate or new agents like patiromer remove K, but hemodialysis is fastest) **I - Ingestion / Intoxication** (toxic ingestions removable by dialysis: methanol, ethylene glycol, lithium, salicylates, theophylline) **O - Overload** (fluid overload causing pulmonary edema unresponsive to diuretics) **U - Uremia** (severe uremic symptoms: pericarditis, encephalopathy, bleeding from platelet dysfunction) Most AKI patients do NOT require dialysis — only those with refractory complications. Modes: - Intermittent hemodialysis (IHD): 3-4 hours, 3x/week, hemodynamically stable patients - Continuous renal replacement therapy (CRRT): 24/7, hemodynamically unstable patients (ICU) - Peritoneal dialysis: rare in AKI, more common in chronic disease Nursing during dialysis: monitor BP frequently (hypotension common), check vascular access patency, monitor electrolytes pre/post, assess for disequilibrium syndrome (rapid shifts can cause cerebral edema in patients with very high BUN), strict I/O.

Across all AKI types, nursing priorities: **Strict I/O monitoring**: every shift at minimum, hourly in ICU. Document all sources (urine, drains, NG, stool). Compare with weights (1 kg = 1 L). **Daily weights**: same time, same scale, same clothing. Weight gain >1 kg/day in oliguric patient = fluid retention. **Electrolyte monitoring**: especially K+. Hyperkalemia is the most acutely lethal complication of AKI. - K+ >5.5: alert provider, consider treatment - K+ >6.0: hold all K-sparing medications, treat with calcium gluconate (membrane stabilization), insulin + dextrose (shift), kayexalate or new binders (remove) - K+ >6.5 with ECG changes (peaked T waves, widened QRS, sine wave): EMERGENCY **Avoid nephrotoxins**: review all medications. Hold or dose-adjust ACE-Is/ARBs, NSAIDs, aminoglycosides, contrast, vancomycin (or use levels). Pharmacist consult for renal dose adjustments. **Fluid management**: hypovolemic → cautious fluids; euvolemic/overloaded → fluid restriction + diuretics. Loop diuretics (furosemide) preferred. Diuretic resistance common in AKI — may need higher doses or combination (loop + thiazide). **Nutrition**: AKI is hypercatabolic. Adequate protein (0.8-1.0 g/kg/day if not on dialysis; 1.0-1.5 if on dialysis), adequate calories, restrict sodium, restrict potassium and phosphorus per labs. **Skin care**: edematous patients are at high risk for breakdown. Reposition q2hr, pressure-relieving surfaces, skin assessment q shift. **Patient and family education**: explain AKI is potentially reversible, dialysis may be temporary, importance of medication review and avoidance of nephrotoxins (NSAIDs especially) post-discharge.

NurseIQ generates patient scenarios with vital signs, lab trends (Cr, BUN, K, HCO3, urine output), medications, and presenting symptoms, and asks you to: identify AKI category (pre-renal, intrinsic, post-renal), stage by KDIGO criteria, prioritize nursing interventions, recognize dialysis indications (AEIOU), and identify nephrotoxic medications to hold or modify. Useful for med-surg, ICU rotation prep, and NCLEX practice. NurseIQ is an educational tool to support nursing student learning.