Guide — Renal
Acute Kidney Injury (AKI)
AKI is a sudden, reversible decline in kidney function occurring over hours to days. Early recognition and intervention can prevent progression to chronic kidney disease or dialysis dependence.
12 min read · Renal
Educational use only. This content is intended for nursing students and exam preparation. Clinical decisions require licensed professional judgment and institutional protocols. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
AKI Definition
AKI (formerly called acute renal failure) is defined by any of the following KDIGO criteria:
- ✦Serum creatinine rise ≥0.3 mg/dL within 48 hours
- ✦Serum creatinine rise ≥1.5× baseline within 7 days
- ✦Urine output <0.5 mL/kg/hr for ≥6 consecutive hours
AKI is potentially reversible when identified and treated promptly. It ranges from mild (stage 1) to severe (stage 3, formerly AKIN stage 3) and can require temporary or permanent renal replacement therapy.
Prerenal Causes
Prerenal AKI results from decreased renal perfusion without structural kidney damage. It is the most common type and most reversible if treated early.
| Category | Examples |
|---|---|
| Volume depletion | Dehydration, hemorrhage, severe vomiting/diarrhea, burns, diuretic overuse |
| Decreased cardiac output | Heart failure, cardiogenic shock, massive PE, cardiac tamponade |
| Vasodilation / third-spacing | Septic shock, anaphylaxis, cirrhosis with ascites, nephrotic syndrome |
| Renal vasoconstriction | NSAIDs (inhibit prostaglandin-mediated afferent dilation), ACE inhibitors/ARBs in bilateral RAS, contrast agents |
Key lab clue: BUN:Creatinine ratio >20:1 (kidneys hold onto urea to conserve volume). FENa <1% (sodium is being retained).
Intrarenal (Intrinsic) Causes
Intrarenal AKI involves direct structural damage to the nephrons. Acute tubular necrosis (ATN) is the most common intrinsic cause.
| Type | Causes |
|---|---|
| Acute tubular necrosis (ATN) | Prolonged ischemia (untreated prerenal), nephrotoxins (aminoglycosides, contrast, myoglobin from rhabdomyolysis, hemoglobin) |
| Acute glomerulonephritis | Immune-complex diseases, post-streptococcal GN, IgA nephropathy, lupus nephritis, vasculitis |
| Acute interstitial nephritis (AIN) | Drug hypersensitivity (NSAIDs, penicillins, PPIs, sulfonamides), infections, autoimmune diseases |
| Vascular | Renal artery/vein thrombosis, malignant hypertension, HUS/TTP, scleroderma renal crisis |
Key lab clue: FENa >2% (tubules cannot reabsorb sodium). Granular or muddy-brown casts on UA indicate ATN. BUN:Cr ratio often normal (~10:1).
Postrenal Causes
Postrenal AKI results from obstruction to urine outflow below the kidney level. Rapidly reversible if obstruction is relieved.
- ✦BPH (benign prostatic hypertrophy) — most common cause in elderly men
- ✦Kidney stones (bilateral or single functioning kidney)
- ✦Bladder outlet obstruction — neurogenic bladder, stricture
- ✦Pelvic tumors compressing ureters (cervical, colorectal, bladder cancer)
- ✦Retroperitoneal fibrosis
- ✦Inadvertent ureteral ligation during pelvic surgery
Suspect postrenal: elderly male + sudden oliguria/anuria. Bladder scan or renal ultrasound confirms hydronephrosis. Relief of obstruction = diuresis (post-obstructive diuresis — monitor for fluid/electrolyte loss).
Clinical Manifestations
Fluid/Electrolyte Imbalances
- ✦Oliguria (<400 mL/day) or anuria
- ✦Peripheral edema, pulmonary edema
- ✦Hyperkalemia (cardiac arrhythmias)
- ✦Hyponatremia (dilutional)
- ✦Metabolic acidosis
Uremic Symptoms
- ✦Nausea, vomiting, anorexia
- ✦Altered mental status, asterixis
- ✦Pericarditis (uremic friction rub)
- ✦Pruritus (uremic frost in severe cases)
- ✦Fatigue, weakness
Cardiovascular
- ✦Hypertension (fluid overload)
- ✦Tachycardia
- ✦Dysrhythmias (hyperkalemia)
- ✦Pericardial effusion
Hematologic
- ✦Anemia (decreased EPO)
- ✦Platelet dysfunction → bleeding risk
- ✦Prolonged bleeding time
Laboratory Findings
| Lab | AKI Finding | Clinical Significance |
|---|---|---|
| Serum creatinine | Elevated (rise ≥0.3 mg/dL) | Best single marker of GFR reduction |
| BUN | Elevated | Less specific (affected by diet, bleeding, steroids) |
| BUN:Cr ratio | >20:1 (prerenal); ~10:1 (intrarenal) | Differentiates prerenal from intrarenal AKI |
| eGFR | Decreased | Derived from creatinine; quantifies degree of impairment |
| Potassium | Elevated (hyperkalemia) | Life-threatening — can cause fatal dysrhythmias |
| Bicarbonate | Decreased | Metabolic acidosis — kidneys cannot excrete H+ |
| Phosphorus | Elevated | Kidneys cannot excrete phosphate |
| Calcium | Decreased | Hyperphosphatemia binds calcium |
| Hemoglobin | Decreased | Decreased EPO production → anemia |
| Urine output | <0.5 mL/kg/hr (oliguria) | Key monitoring parameter in AKI management |
| Urinalysis | Casts, protein, hematuria depending on type | ATN: muddy-brown granular casts; GN: RBC casts; AIN: WBC casts |
| FENa | <1% (prerenal); >2% (intrarenal) | Fractional excretion of sodium — helps differentiate AKI type |
Treatment Overview
Identify and treat the underlying cause
Prerenal: fluid resuscitation (IV fluids, blood products). Postrenal: relieve obstruction (Foley catheter for BPH, ureteral stent/nephrostomy for stone/tumor). Intrarenal: stop nephrotoxic agents, treat infection, manage immune-mediated disease.
Fluid and electrolyte management
Restrict fluid if oliguric/fluid overloaded. Treat hyperkalemia aggressively: calcium gluconate (membrane stabilization), sodium bicarbonate, insulin + dextrose, Kayexalate, dialysis if refractory. Correct metabolic acidosis.
Strict intake and output monitoring
Hourly urine output (Foley catheter). Daily weights. Fluid balance totaling every 8–12 hours. Target: UO ≥0.5 mL/kg/hr. Trend creatinine and BUN daily.
Avoid nephrotoxins
Hold NSAIDs, ACE inhibitors/ARBs (in bilateral renal artery stenosis), aminoglycoside antibiotics, contrast agents. Use minimum effective doses when nephrotoxic agents unavoidable.
Renal replacement therapy (if indicated)
Indications: refractory hyperkalemia, severe metabolic acidosis (pH <7.1), fluid overload unresponsive to diuretics, uremic encephalopathy or pericarditis. Options: hemodialysis (intermittent), CRRT (continuous — preferred in hemodynamically unstable ICU patients).
Nursing Priorities
Monitor urine output hourly
Oliguria (<0.5 mL/kg/hr) or anuria requires immediate notification. Insert Foley catheter per order. Document strict I&O.
Cardiac monitoring for hyperkalemia
Peaked T waves → widened QRS → sine wave pattern = fatal arrhythmia imminent. Have emergency hyperkalemia treatment at bedside.
Daily weights and fluid balance
2.2 lb (1 kg) weight gain = approximately 1 L fluid retention. Weight gain >2 kg/day = fluid emergency.
Assess for uremic symptoms
Monitor mental status, asterixis (flapping tremor), pericardial friction rub, nausea/vomiting, bleeding tendency.
Medication safety
Renally-cleared drugs accumulate in AKI — digoxin, metformin, opioids, antibiotics. Verify dose adjustments with pharmacy. Hold metformin immediately.
Dietary restrictions
Restrict potassium, phosphorus, sodium. Protein restriction in non-dialysis AKI (reduce urea load). Coordinate with dietitian.
NCLEX Pearls
- ✦AKI is potentially REVERSIBLE — key distinction from CKD (irreversible). NCLEX loves this difference.
- ✦Three types: Prerenal (perfusion problem), Intrarenal (structural damage), Postrenal (obstruction). Treat the cause.
- ✦Hyperkalemia is the most life-threatening complication of AKI — monitor ECG, have calcium gluconate and insulin/dextrose ready.
- ✦BUN:Cr >20:1 = prerenal AKI (volume depletion). Normal ratio (~10:1) = intrinsic damage.
- ✦FENa <1% = kidneys conserving sodium (prerenal). FENa >2% = damaged tubules cannot reabsorb sodium (intrarenal).
- ✦First action for oliguria in AKI = assess fluid status, then notify provider, not automatically give fluids (patient may be fluid overloaded).
- ✦Muddy-brown casts on urinalysis = ATN (acute tubular necrosis). RBC casts = glomerulonephritis. WBC casts = pyelonephritis/AIN.
- ✦Post-obstructive diuresis after relieving obstruction: can cause massive fluid/electrolyte loss — monitor closely.
- ✦Indications for emergent dialysis: AEIOU — Acidosis, Electrolytes (hyperK), Intoxication, Overload (fluid), Uremia.
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with KDIGO Clinical Practice Guidelines · National Kidney Foundation (NKF). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →