Chart — Renal
AKI Types Comparison Chart
Prerenal vs intrarenal (ATN/glomerulonephritis) vs postrenal acute kidney injury — mechanism, causes, urine labs (FENa, BUN:Cr ratio, urine sodium, specific gravity, casts), response to fluids, treatment, nursing priorities, and NCLEX memory aids.
Chart · Renal
Educational use only. AKI classification requires clinical correlation with history, physical exam, and labs. FENa interpretation is altered by diuretics — use FEUrea in that setting. 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.
Prerenal AKI
Problem BEFORE kidneys
Low perfusion → intact kidney trying to compensate
Intrarenal AKI
Problem INSIDE the kidneys
Structural damage to tubules, glomeruli, interstitium
Postrenal AKI
Problem AFTER kidneys
Obstruction to urine outflow → back-pressure
| Feature | Prerenal AKI | Intrarenal AKI | Postrenal AKI |
|---|---|---|---|
| Mechanism | Reduced renal perfusion → kidneys not receiving enough blood flow. Kidney structure is INTACT. | Direct damage to kidney parenchyma (tubules, glomeruli, interstitium, or vessels). Structural injury present. | Obstruction to urine flow distal to kidney → back-pressure → tubular injury if prolonged. |
| Common Causes | Dehydration, hemorrhage, heart failure (low CO), sepsis (vasodilation), burns, cirrhosis (hepatorenal syndrome), overdiuresis, NSAIDs + ACE/ARB combination | ATN (most common): ischemia (prolonged prerenal) or nephrotoxins (aminoglycosides, contrast, cisplatin, myoglobinuria from rhabdomyolysis). Glomerulonephritis, interstitial nephritis (NSAID, penicillin, PPIs), vasculitis. | BPH (most common in elderly men), ureteral stones, urethral stricture, cervical cancer, prostate cancer, blood clots in ureters, neurogenic bladder, tumors extrinsic compression, bilateral ureteral obstruction (must be bilateral to cause AKI unless single kidney) |
| Urine Output | Oliguria (< 0.5 mL/kg/hr) — kidneys aggressively retain water and sodium; concentrated urine produced in small volume | Variable: oliguria (< 0.5 mL/kg/hr) in ATN is common; may have non-oliguric ATN (volume maintained but rising creatinine) | Variable: may have anuria (complete obstruction), oliguria, or even polyuria (post-obstructive diuresis after relief of obstruction) |
| BUN:Creatinine Ratio | ELEVATED > 20:1 — BUN rises disproportionately because increased urea reabsorption occurs when ADH promotes water reabsorption | Normal 10:1 to 15:1 — tubular damage impairs BUN reabsorption, proportionate rise in both BUN and Cr | Variable — often elevated > 20:1 early (urea back-diffuses across obstructed tubules); may normalize as AKI progresses |
| Urine Sodium (UNa) | LOW — < 20 mEq/L (kidneys avidly reabsorb sodium to restore intravascular volume — intact tubular function) | HIGH — > 40 mEq/L (tubular cells damaged → cannot reabsorb sodium; sodium spills into urine) | Variable — early can be high (tubular dysfunction from back-pressure) or variable |
| Fractional Excretion of Sodium (FENa) | < 1% — kidneys efficiently reabsorbing sodium (intact tubular function conserving sodium to restore perfusion). Formula: (UNa × PCr) / (PNa × UCr) × 100 | > 2% — tubular damage impairs sodium reabsorption. ATN classically: FENa 2–4%. Note: contrast nephropathy and myoglobinuria may have FENa < 1% despite intrarenal AKI. | Variable — unreliable in postrenal. May be high (> 2%) as obstruction progresses. |
| Urine Specific Gravity | HIGH — > 1.020 (concentrated urine; intact tubular concentration ability preserving water) | LOW/FIXED — 1.010 isosthenuria (tubular cells can neither concentrate nor dilute; fixed at same osmolality as plasma) | Variable — early may be concentrated; late may be fixed isosthenuria |
| Urine Casts | Hyaline casts only (concentrated urine — normal finding in small numbers). No cellular casts. | MUDDY BROWN GRANULAR CASTS (hallmark of ATN — sloughed tubular epithelial cells). RBC casts = glomerulonephritis. WBC casts = interstitial nephritis. | No pathognomonic casts. May have RBCs (stone injury), WBCs (if infected), or hyaline casts. |
| Response to IV Fluids | RESOLVES with fluid challenge (if cause is volume depletion) — creatinine improves, urine output increases. Classic: give 500 mL NS bolus → UO increases. | Does NOT improve with fluids alone (structural damage present). Fluids may worsen if cause is cardiorenal or fluid overload is present. | Does NOT improve with fluids — requires relief of obstruction (catheterization, stent, nephrostomy). Post-obstructive diuresis can occur after relief. |
| Urinalysis Findings | Concentrated (high specific gravity, high osmolality). Hyaline casts. Bland sediment — no cells or cellular casts. | Muddy brown granular casts (ATN). RBC casts + proteinuria (GN). WBC casts (interstitial nephritis). Dipstick positive for blood without RBCs = myoglobinuria. | May be normal or show hematuria (stone), pyuria + bacteriuria (infected obstruction). No pathognomonic cast. |
| Treatment | Restore perfusion: IV fluid resuscitation (if volume depleted), treat underlying cause (sepsis, CHF, hemorrhage). Hold NSAIDs and ACE/ARBs. Avoid further nephrotoxins. | Remove offending agent (hold nephrotoxins, treat infection). Supportive care: fluid management, electrolyte correction, nutrition. Dialysis if severe. Treat cause of GN or interstitial nephritis. Rhabdomyolysis: aggressive IV fluids to maintain UO 200–300 mL/hr. | RELIEVE OBSTRUCTION urgently: urethral catheter (BPH, urethral obstruction), ureteral stent (ureteral stones), nephrostomy tube (external drainage). Treat underlying cause. Post-obstructive diuresis: monitor UO and electrolytes closely after relief. |
| Nursing Priority | Accurate I&O measurement. Daily weights. Assess volume status (JVP, skin turgor, mucous membranes, orthostatic BP). Fluid challenge as ordered. Hold nephrotoxins. Report oliguria (< 0.5 mL/kg/hr) immediately. | Monitor creatinine trends. Strict I&O. Daily weights. Electrolyte monitoring (hyperkalemia, metabolic acidosis). Dialysis access care (if initiated). Medication safety: adjust doses for reduced GFR. Report muddy brown casts or rising creatinine. | Immediately report anuria or sudden oliguria — obstruction must be ruled out. Check for bladder distension (bladder scanner). Catheterize if urinary retention. Monitor post-obstructive diuresis (copious urine output after relief — replace IV fluids carefully). Electrolyte monitoring after relief. |
| NCLEX Memory Aid | PRE = PROBLEM is BEFORE the kidneys. Low flow → kidneys try to save everything (low UNa, high SG, FENa < 1%). Reverse the cause → AKI reverses. | INTRA = INSIDE the kidneys. Structural damage. Muddy brown casts = ATN fingerprint. Tubules can't concentrate or reabsorb (isosthenuria, high UNa, FENa > 2%). Needs time to recover (days to weeks). | POST = PROBLEM is AFTER the kidneys. Pipes are blocked. Relieve obstruction = treatment. Anuria in elderly man = BPH until proven otherwise. Post-obstructive diuresis = watch electrolytes and replace fluids. |
FENa Quick Reference
| Formula | (Urine Na × Plasma Cr) / (Plasma Na × Urine Cr) × 100 |
| FENa < 1% | Prerenal — kidneys saving sodium |
| FENa > 2% | Intrarenal (ATN) — tubular damage |
| Diuretic use | Invalidates FENa — use FEUrea instead (FEUrea < 35% = prerenal) |
| Exception | Contrast nephropathy, rhabdomyolysis = intrarenal AKI but FENa < 1% |
KDIGO AKI Staging
| Stage | Creatinine | Urine Output |
|---|---|---|
| 1 | Rise ≥ 0.3 mg/dL in 48h OR 1.5–1.9× baseline | < 0.5 mL/kg/hr × 6–12h |
| 2 | 2.0–2.9× baseline | < 0.5 mL/kg/hr × ≥ 12h |
| 3 | ≥ 3× baseline OR ≥ 4.0 mg/dL OR dialysis initiated | < 0.3 mL/kg/hr × ≥ 24h OR anuria × 12h |
NCLEX Key Points
Prerenal: FENa < 1%, urine Na < 20, BUN:Cr > 20:1, SG > 1.020. Responds to fluid challenge. Bland urine sediment.
Intrarenal (ATN): FENa > 2%, urine Na > 40, BUN:Cr ~ 10:1, isosthenuria (SG 1.010). Muddy brown casts. Does NOT respond to fluids alone.
Postrenal: Anuria or sudden oliguria. No response to fluids. Relieve obstruction = treatment. Elderly man + anuria = think BPH. Post-obstructive diuresis after catheterization = watch electrolytes.
Prolonged prerenal = intrarenal ATN — if renal hypoperfusion lasts long enough, tubular cells die → prerenal converts to ATN. Structural damage now present.
Report sustained oliguria (< 0.5 mL/kg/hr for > 6h) immediately — may represent AKI Stage 1 regardless of creatinine.
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 →