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Quick Reference
  • Normal Range: 10:1 to 20:1
  • Prerenal Azotemia: >20:1 (dehydration, CHF, GI bleeding)
  • Intrinsic Renal: 10:1 to 15:1 (ATN, glomerulonephritis)
  • Primary Use: Differentiate prerenal vs intrinsic vs postrenal azotemia
  • Sample Type: Serum (venous blood) - calculated from BUN and creatinine
  • GI Bleeding: Ratio often >30:1 (digested blood increases BUN)
  • Key Point: Helps guide fluid management; prerenal responds to IVF, intrinsic does not

What is the BUN:Creatinine Ratio?

The BUN:Creatinine (BUN:Cr) ratio is a calculated value that compares the concentration of blood urea nitrogen to serum creatinine.

  • What it compares: BUN level ÷ Creatinine level
  • Both are: Waste products filtered by the kidneys
  • Key difference: They respond differently to changes in kidney perfusion
  • Clinical value: Helps differentiate causes of elevated kidney values (azotemia)
Calculation: BUN:Cr Ratio = BUN (mg/dL) ÷ Creatinine (mg/dL)

Why Is This Ratio Useful?

While both BUN and creatinine rise in kidney dysfunction, they behave differently depending on the cause of azotemia:

  • BUN: Affected by renal perfusion, volume status, protein intake, GI bleeding, and tubular reabsorption
  • Creatinine: More stable, primarily determined by GFR and muscle mass

How the ratio changes:

  • Prerenal state (low perfusion): BUN is preferentially reabsorbed in proximal tubule → BUN rises more than creatinine → ratio increases (>20:1)
  • Intrinsic kidney disease: Both rise proportionally → ratio stays normal (10-20:1)
Ratio Interpretation
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BUN:Cr Ratio Interpretation Common Causes Mechanism
>20:1 Prerenal Azotemia Dehydration, Heart failure, GI bleeding, High protein intake, Sepsis/shock Increased BUN reabsorption due to decreased renal perfusion
10:1 to 15:1 Intrinsic Renal Azotemia Acute tubular necrosis (ATN), Glomerulonephritis, Interstitial nephritis Tubular dysfunction prevents BUN reabsorption; both rise proportionally
10:1-20:1 (Normal) Postrenal (Obstructive) Bilateral ureteral obstruction, Bladder outlet obstruction Both BUN and creatinine rise proportionally until prolonged obstruction causes tubular damage
<10:1 Low BUN or High Creatinine States Liver disease, Malnutrition, SIADH, Rhabdomyolysis Decreased urea synthesis or increased creatinine production
Clinical Scenarios

1. Prerenal Azotemia (Ratio >20:1)

Mechanism

Decreased renal perfusion activates the renin-angiotensin-aldosterone system (RAAS), leading to increased sodium and water reabsorption in the proximal tubule. BUN is passively reabsorbed along with sodium, causing BUN to rise disproportionately to creatinine.

Common Causes

  • Volume depletion: Dehydration, hemorrhage, excessive diuresis, third-spacing
  • Decreased cardiac output: Congestive heart failure, cardiogenic shock
  • Systemic vasodilation: Sepsis, anaphylaxis, liver disease
  • Renal vasoconstriction: NSAIDs, ACE inhibitors, hepatorenal syndrome
  • Increased protein load: GI bleeding, high protein diet, corticosteroid use

Additional Features

  • Urine sodium: Usually <20 mEq/L (kidneys trying to conserve sodium)
  • FeNA (Fractional Excretion of Sodium): <1%
  • Urine osmolality: >500 mOsm/kg (concentrated urine)
  • Responds to volume resuscitation (creatinine improves within 24-48 hours)

2. Intrinsic Renal Azotemia (Ratio 10:1-15:1)

Mechanism

Direct kidney parenchymal damage (especially tubular injury) impairs the kidney's ability to reabsorb BUN. Both BUN and creatinine rise proportionally, keeping the ratio in the normal-to-low range.

Common Causes

  • Acute tubular necrosis (ATN): Ischemic (prolonged prerenal state), nephrotoxic (aminoglycosides, contrast, rhabdomyolysis)
  • Glomerulonephritis: Post-infectious, lupus nephritis, IgA nephropathy
  • Acute interstitial nephritis: Drug-induced (NSAIDs, PPIs, antibiotics)
  • Vascular: Renal artery/vein thrombosis, vasculitis, HUS/TTP

Additional Features (ATN)

  • Urine sodium: Usually >40 mEq/L (tubules can't reabsorb sodium)
  • FeNA: >2%
  • Urine osmolality: <350 mOsm/kg (isosthenuric)
  • Urine sediment: Muddy brown casts, renal tubular epithelial cells
  • Does NOT rapidly respond to fluids

3. Postrenal Azotemia (Variable Ratio)

Mechanism

Urinary tract obstruction causes back-pressure on the kidneys. Initially, the ratio is normal (10:1-20:1) as both BUN and creatinine rise proportionally. If obstruction is prolonged, secondary tubular damage may occur, lowering the ratio.

Common Causes

  • Bilateral ureteral obstruction: Stones, retroperitoneal fibrosis, pelvic malignancy
  • Bladder outlet obstruction: BPH, neurogenic bladder, blood clots
  • Urethral obstruction: Stricture, catheter obstruction
  • Single functioning kidney: Any unilateral obstruction

Diagnosis

  • Renal ultrasound: Hydronephrosis (may be absent in early obstruction or retroperitoneal fibrosis)
  • Post-void residual (PVR): Elevated in bladder outlet obstruction
  • CT scan: Definitive for stone disease and masses
Special Considerations

Conditions That Increase BUN Disproportionately

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Condition Mechanism Clinical Context
GI Bleeding Blood digested in GI tract increases protein/urea load Can raise BUN 20-40 mg/dL; ratio often >30:1
High Protein Diet Increased protein metabolism → increased urea production TPN, bodybuilders, very high meat intake
Corticosteroids Increased protein catabolism Prednisone, dexamethasone therapy
Tetracycline (old formulations) Anti-anabolic effect Rare with modern tetracyclines
Fever/Sepsis Increased catabolism + prerenal component Multifactorial

Conditions That Decrease BUN Disproportionately

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Condition Mechanism Clinical Context
Liver Disease Decreased urea synthesis from ammonia Cirrhosis, acute liver failure
Malnutrition Low protein intake → low urea production Cachexia, anorexia, veganism
SIADH Dilutional hyponatremia dilutes BUN BUN often <10 mg/dL
Pregnancy Increased GFR + hemodilution Normal BUN in pregnancy: 5-12 mg/dL

Conditions That Increase Creatinine Disproportionately

  • Rhabdomyolysis: Massive release of creatinine from muscle breakdown
  • Trimethoprim/Cimetidine: Block tubular secretion of creatinine (not true kidney injury)
  • High muscle mass: Bodybuilders, athletes have higher baseline creatinine
  • Creatine supplementation: Metabolized to creatinine
Limitations of BUN:Cr Ratio

Important Limitations

  • Not diagnostic alone: The ratio suggests a category of azotemia but doesn't establish a diagnosis. Always consider clinical context.
  • Overlap between categories: A ratio of 18:1 could be normal, late prerenal, or early ATN.
  • Mixed pictures: A patient with chronic prerenal state who develops ATN may have an unpredictable ratio.
  • Chronic kidney disease: Ratio is less reliable in CKD; use primarily in acute settings.
  • Non-renal factors dominate: GI bleeding, liver disease, or malnutrition can make ratio misleading.

When the Ratio Can Be Misleading

  • Patient on dialysis: Both BUN and creatinine are artificially lowered
  • ATN superimposed on CHF: May have elevated ratio despite intrinsic kidney damage
  • Severe malnutrition: Low BUN production may mask prerenal state
  • Chronic diuretic use: Can maintain elevated ratio even with normal kidney function
  • ACE inhibitor/ARB use: Can cause functional rise in creatinine without true AKI

Use Additional Tools

The BUN:Cr ratio should be interpreted alongside:

  • Urine studies: FeNA, urine sodium, urine osmolality
  • Urine microscopy: Casts, cells, crystals
  • Volume status: Physical exam, hemodynamics
  • Response to fluids: Does creatinine improve with IVF?
  • Imaging: Renal ultrasound to rule out obstruction
Clinical Pearls
"The ratio tells you WHERE the problem is, not WHAT the problem is": Use ratio to categorize azotemia (prerenal vs renal vs postrenal), then determine the specific etiology with clinical context and additional tests.
BUN:Cr >20:1 in the ED: Think dehydration first. Most common cause of elevated ratio is simple volume depletion.
GI bleed triad: BUN:Cr ratio >30:1 + melena/hematemesis + orthostatic vital signs. The protein load from digested blood significantly elevates BUN. Don't miss the bleed!
CHF patients often have ratio >20:1: Chronic prerenal state from poor cardiac output. Baseline elevated ratio is common - compare to patient's prior values.
Ratio <10:1 in trauma = think rhabdomyolysis: Massive creatinine release from muscle injury lowers the ratio. Check CK!
"Normal ratio" doesn't mean "normal kidneys": A 15:1 ratio is normal, but if both BUN (60 mg/dL) and creatinine (4.0 mg/dL) are elevated, there's significant kidney dysfunction. Look at absolute values!
Prerenal can become intrinsic: Prolonged prerenal azotemia (hypoperfusion) leads to ATN. Early intervention with fluids prevents progression. Time matters!
Post-ATN diuretic phase: As ATN recovers, polyuria occurs and BUN drops faster than creatinine, temporarily lowering ratio. This is a good sign!
Use trends, not single values: A ratio rising from 15:1 to 25:1 suggests developing prerenal state, even if creatinine hasn't changed yet.
Ratio helps guide fluid management: High ratio (>20:1) + low urine sodium (<20 mEq/L) = give more fluids. Normal ratio + high urine sodium = fluids unlikely to help.
References
  1. Kratz, A., Ferraro, M., Sluss, P. M., & Lewandrowski, K. B. (2004). Laboratory reference values. New England Journal of Medicine, 351, 1548-1564.
  2. Lee, M. (Ed.). (2009). Basic skills in interpreting laboratory data. Ashp.
  3. Farinde, A. (2021). Lab values, normal adult: Laboratory reference ranges in healthy adults. Medscape.
  4. Nickson, C. (n.d.). Critical Care Compendium. Life in the Fast Lane • LITFL.
  5. Farkas, Josh MD. (2015). Table of Contents - EMCrit Project. EMCrit Project.
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