Liver function test (Add mnemonic if possible)

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liver function tests LFT mnemonic complete guide

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Liver Function Tests (LFTs)

Mnemonic: "ABCDEFGHI" - a popular way to remember all LFT components:
LetterTest
AAlbumin / A:G ratio / Ammonia / Alpha-1 antitrypsin
BBilirubin (Total / Direct / Indirect) / Bile pigments / Bile salts
CCholesterol / Coagulation (PT, INR)
DDe Ritis ratio (AST:ALT)
EEnzymes (ALT, AST, ALP, GGT)
FFibrinogen / Flocculation tests
GGGT (Gamma-glutamyltransferase)
HHepatitis markers (HBsAg, anti-HCV)
IINR / Immunoglobulins

Overview

The term "liver function tests" is actually a misnomer - many of the tests do not assess liver function per se, but instead identify the source and pattern of liver damage. A standard LFT panel typically includes: bilirubin, ALT, AST, ALP, GGT, albumin, total protein, and PT/INR.

Tests Grouped by Category

1. Tests of Liver Injury (Enzymes)

ALT (Alanine Aminotransferase)

  • More specific for liver disease than AST
  • AST is elevated in cardiac/skeletal muscle injury; ALT is not
  • Markedly elevated in acute viral hepatitis (elevated days before jaundice appears)
  • Primary use: sensitive indicator of hepatocellular damage

AST (Aspartate Aminotransferase)

  • Less specific (also elevated in heart, skeletal muscle)
  • AST > ALT suggests:
    • Alcoholic liver disease (AST:ALT ratio typically >2:1 - the De Ritis ratio)
    • Early hepatic injury
    • Cirrhosis (mild elevations)
    • Non-hepatic muscle injury
  • Both AST and ALT >10x upper reference limit (URL) = acute hepatitis; lower values = chronic hepatitis

ALP (Alkaline Phosphatase)

  • Elevated in obstructive (cholestatic) jaundice
  • Also elevated in bone disease (not liver-specific alone - confirm with GGT)
  • If ALP elevated in isolation, rule out non-hepatic sources (bone, placenta, intestine)
  • ALP >2x URL with AST <3x URL = cholestatic pattern

GGT (Gamma-Glutamyltransferase)

  • Rises in parallel with ALP in cholestasis
  • Used to confirm that elevated ALP is of hepatic origin (not bone)
  • Elevated by alcohol and enzyme-inducing drugs
  • Prognostic indicator for cardiovascular and all-cause mortality; rising GGT associated with type 2 diabetes and metabolic syndrome

2. Tests of Hepatic Synthetic Function

Albumin

  • Low in chronic liver disease (cirrhosis, chronic hepatitis)
  • Half-life ~20 days, so does not reflect acute changes quickly
  • Decreased albumin = indicator of chronicity and severity
  • Can also be low in malnutrition, nephrotic syndrome, inflammation (not liver-specific)
  • Serial measurements monitor disease progression

Prothrombin Time (PT) / INR

  • Liver synthesizes clotting factors I, II, V, VII, IX, X
  • Prolonged PT in acute liver failure (impaired synthesis)
  • Key differentiator: if PT corrects after vitamin K injection (10 mg SC/IM, measure after 24h) - suggests cholestasis (malabsorption of fat-soluble vitamin K), not hepatocellular failure
  • Indicator of severity of liver disease

3. Tests of Bilirubin Metabolism

Serum Bilirubin (Total, Direct, Indirect)

  • Conjugated (direct) bilirubin elevated in: obstructive jaundice, cholestasis, hepatocellular disease
  • Unconjugated (indirect) bilirubin elevated in: hemolysis, Gilbert syndrome, Crigler-Najjar
  • In hepatocellular disease: both conjugated and unconjugated rise (failure of uptake, conjugation, and excretion)
  • In obstructive jaundice: mainly conjugated rises
Quick rule: Conjugated = Can't get out (obstruction) Unconjugated = Can't get in/conjugated (hemolysis, enzyme deficiency)

4. Other Tests

TestSignificance
Total ProteinLow in cirrhosis, chronic liver disease
AmmoniaElevated in hepatic encephalopathy (impaired urea cycle)
Serum CholesterolElevated in cholestasis; low in severe hepatocellular failure
Alpha-1 AntitrypsinDeficiency causes cirrhosis and emphysema
LDHNon-specific; elevated in hepatitis and many other conditions

Interpretation Patterns

PatternKey FindingLikely Cause
HepatocellularAST/ALT >> ALPViral hepatitis, alcoholic hepatitis, drug-induced
CholestaticALP/GGT >> AST/ALTBile duct obstruction, PBC, PSC
MixedBoth elevatedDrug-induced, early/resolving hepatitis
Synthetic failureLow albumin, prolonged PTCirrhosis, acute liver failure

Diagnostic Algorithm

Algorithm for using abnormal LFTs to classify liver disease
Reading the algorithm:
  • AST >3x URL + ALP <2x URL → Hepatocellular disease
    • Normal albumin → Acute hepatitis
    • Low albumin → Chronic hepatitis
  • AST <3x URL + ALP >2x URL → Cholestatic disease
    • Then use ultrasound/cholangiography to differentiate intrahepatic vs. extrahepatic cholestasis

Quick Memory Aid: LFT Pattern Mnemonics

Hepatocellular injury - "A Liver Attack":
  • ALT and AST rise markedly (>10x = acute hepatitis)
Cholestasis - "ALP and GGT Go Up":
  • Think "Blocked Bile" - ALP and GGT rise when bile can't flow
De Ritis Ratio (AST:ALT):
  • >2:1 = Alcoholic liver disease
  • <1:1 = Viral hepatitis or NAFLD
Synthetic function - "PACT":
  • PT prolonged
  • Albumin low
  • Coagulation factors impaired
  • Think chronic disease or severe acute failure

Reference Ranges (approximate)

TestNormal Range
ALT7-56 U/L
AST10-40 U/L
ALP44-147 U/L
GGT9-48 U/L
Total Bilirubin0.2-1.2 mg/dL
Direct Bilirubin0.0-0.3 mg/dL
Albumin3.5-5.0 g/dL
Total Protein6.3-8.2 g/dL
PT11-13.5 seconds

Sources: Tietz Textbook of Laboratory Medicine, 7th Ed.; Harper's Illustrated Biochemistry, 32nd Ed.; Sleisenger and Fordtran's Gastrointestinal and Liver Disease

How do I interpret abnormal LFT patterns in specific diseases (hepatitis, cirrhosis, cholestasis)?

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Interpreting Abnormal LFT Patterns in Specific Diseases


The Two Core Patterns - Master This First

The most important first step in any abnormal LFT is determining whether the pattern is hepatocellular or cholestatic. This single distinction directs the entire workup.
FeatureHepatocellularCholestatic
Dominant riseALT, AST (>ALP)ALP, GGT (>ALT, AST)
Key thresholdAST >3× URL, ALP <2× URLAST <3× URL, ALP >2× URL
BilirubinBoth conjugated + unconjugated raisedMainly conjugated raised
Albumin/PTSeverely impaired in acute failureMay be normal initially
Think ofHepatitis, drug toxicity, ischemiaObstruction, PBC, PSC, drugs

Disease-by-Disease LFT Interpretation


1. Acute Viral Hepatitis (A, B, C, D, E)

Hallmark: Dramatic ALT/AST elevation - typically >500 U/L, often >10-25× upper limit of normal (ULN)
TestFinding
ALTMarkedly elevated (≥ AST); rises days before jaundice
ASTElevated, but ALT ≥ AST
ALPMildly elevated or normal
BilirubinElevated (both fractions) once jaundice appears
AlbuminNormal (acute = no time to deplete)
PT/INRNormal unless severe/fulminant
Key rule: ALT ≥ AST in viral hepatitis. Values >25× ULN are almost exclusively seen in acute hepatocellular disease.
Caution on Hep C: ALT fluctuates in chronic HCV and can be normal even when AST is elevated - do not miss it.

2. Alcoholic Hepatitis

Hallmark: Moderate enzyme elevation with a distinctive AST:ALT ratio
TestFinding
ASTElevated, but rarely >300 U/L
ALTLower than AST
AST:ALT ratio≥2:1 (De Ritis ratio reversal) - in severe cases up to 4:1
GGTOften markedly elevated (elevated in 70% of chronic alcoholics; correlates with alcohol intake)
BilirubinElevated
PTMay be prolonged
Mnemonic: "Two Shots to One" - AST is TWO times ALT in alcoholic hepatitis.
Why AST>ALT in alcohol? Alcohol depletes pyridoxal phosphate (vitamin B6) - ALT requires more B6 to be active than AST does. Also, alcohol directly damages mitochondria, releasing mitochondrial AST.
Distinguishing from viral hepatitis:
  • Alcoholic: AST:ALT ≥2:1, AST rarely >300 U/L
  • Viral: ALT ≥ AST, transaminases often >500-1000 U/L

3. Non-Alcoholic Fatty Liver Disease (NAFLD) / NASH

TestFinding
ALTMildly-moderately elevated (usually <5× ULN)
ASTMay be normal or mildly elevated; ALT>AST initially
ALP/GGTMildly elevated
Albumin/PTNormal unless cirrhosis has developed
Key point: NAFLD is one of the most common causes of incidentally elevated liver enzymes in the Western world. Do NOT diagnose NAFLD on enzymes alone - suspect it when metabolic risk factors (obesity, T2DM, hypertension, dyslipidemia) are present.
When AST > ALT in NAFLD: Suggests progression to cirrhosis (ratio inverts as fibrosis develops).

4. Drug-Induced Liver Injury (DILI)

Two patterns exist:
TypeLFT PatternExamples
HepatocellularALT/AST >5× ULN dominantParacetamol, isoniazid, statins
CholestaticALP >2× ULN dominantChlorpromazine, erythromycin estolate, anabolic steroids, OCP
MixedBoth elevatedMany drugs
  • Predictable (dose-dependent): Classic example = paracetamol overdose. Causes extreme transaminase rise (>2000 U/L). Extreme elevation of LDH alongside extreme AST/ALT signals massive hepatic necrosis.
  • Idiosyncratic: Not dose-dependent; minority of patients. Examples: isoniazid, halothane.
Hy's Law: If both ALT >3× ULN AND bilirubin >2× ULN in DILI - high risk of acute liver failure (mortality ~10%).

5. Cirrhosis (End-Stage Liver Disease)

Counterintuitive finding: Transaminases may be normal or only mildly elevated in cirrhosis because few functional hepatocytes remain to release enzymes.
TestFindingSignificance
ALT/ASTNormal or mildly elevatedFew hepatocytes left to lyse
AST:ALT ratio>1 (reversal)Fibrosis causes this flip
ALP/GGTElevated (biliary involvement)
AlbuminLowBest marker of chronicity/severity
PT/INRProlongedSynthetic failure
BilirubinElevatedReflects severity
PlateletsLow (hypersplenism)Portal hypertension
AmmoniaElevatedHepatic encephalopathy
Mnemonic for cirrhosis: "LAPP" - Low albumin, AST>ALT, Prolonged PT, Platelets low
Child-Pugh Score uses LFTs to grade severity:
  • Bilirubin, Albumin, PT, plus Ascites and Encephalopathy
  • Score A (5-6) = compensated; Score C (10-15) = decompensated

6. Obstructive (Extrahepatic) Cholestasis

(e.g., gallstones, pancreatic cancer, bile duct stricture)
TestFinding
ALPMarkedly elevated (often >3-4× ULN)
GGTElevated in parallel with ALP
Conjugated bilirubinMarkedly elevated ("Can't get out")
ALT/ASTMildly elevated or normal
AlbuminNormal early
PTMay be prolonged - corrects with vitamin K (malabsorption of fat-soluble vitamins)
PT correction with Vitamin K = cholestasis, not hepatocellular failure. This is the key clinical differentiator.
Next step: Ultrasound - dilated bile ducts confirm extrahepatic obstruction; then CT/MRCP.

7. Intrahepatic Cholestasis

(e.g., Primary Biliary Cholangitis - PBC, Primary Sclerosing Cholangitis - PSC, drug-induced)
TestFinding
ALPMarkedly elevated
GGTElevated
BilirubinElevated (conjugated)
ALT/ASTMildly elevated
Anti-mitochondrial Ab (AMA)Positive in PBC (>90% sensitivity)
IgMElevated in PBC
ANCA, ANAMay be positive in PSC/AIH
  • PBC: Middle-aged woman, itching, fatigue, elevated ALP + AMA positive.
  • PSC: Young man with IBD, elevated ALP + beaded appearance on MRCP.

8. Ischemic Hepatitis ("Shock Liver")

Hallmark: Explosive transaminase rise
TestFinding
AST/ALTExtreme elevation >2000-10,000 U/L (can mimic paracetamol overdose)
LDHAlso extremely elevated
BilirubinRises later
PTProlonged
Occurs with acute hypoperfusion (cardiogenic shock, septic shock, massive PE). Transaminases rise within 1-3 days then fall rapidly when perfusion is restored.
LDH + ALP both elevated = think malignant hepatic infiltration (metastases, lymphoma). LDH rises disproportionately.

9. Wilson Disease

TestFinding
AST:ALTElevated, often AST > ALT
ALPParadoxically LOW or normal (unique!)
BilirubinElevated (Coombs-negative haemolytic anemia)
CeruloplasminLow
Low ALP in a young patient with hepatitis = think Wilson disease. This is a classic exam clue.

Summary Table: LFT Patterns at a Glance

DiseaseALT/ASTALP/GGTBiliAlbuminPTKey Clue
Acute viral hepatitis↑↑↑ (ALT≥AST)Normal/↑NormalNormalALT>500 U/L
Alcoholic hepatitis↑↑ (AST≥2×ALT)↑ GGTAST:ALT ≥2:1, AST<300
NAFLD/NASH↑ (ALT>AST)↑ mildNormal/↑NormalNormalMetabolic risk factors
CirrhosisNormal/↑ mild (AST>ALT)↓↓↑↑Low albumin + reversed ratio
Extrahepatic obstructionNormal/↑ mild↑↑↑↑ conjNormal↑ (corrects with vit K)Dilated ducts on US
PBC/PSC↑ mild↑↑↑↑ conj↓ late↑ lateAMA+ (PBC), IBD (PSC)
Ischemic hepatitis↑↑↑↑↑↑LDH also extreme; rapid fall
Wilson disease↑↑ (AST>ALT)↓ or normalYoung patient, low ceruloplasmin
Liver metastases↑ mild↑↑↑LDH + ALP both ↑↑

Quick Interpretation Algorithm

Abnormal LFTs
     |
     ├── ALT/AST >> ALP?  → HEPATOCELLULAR
     │        |
     │        ├── ALT ≥ AST + >500 U/L  → Viral / toxic hepatitis
     │        ├── AST:ALT ≥2:1, AST <300 → Alcoholic hepatitis
     │        ├── AST:ALT >1, low albumin → Cirrhosis
     │        ├── Extreme >2000 U/L      → Ischemic or paracetamol
     │        └── AST>ALT + LOW ALP      → Wilson disease
     │
     └── ALP/GGT >> ALT/AST? → CHOLESTATIC
              |
              ├── PT corrects with Vit K  → Extrahepatic obstruction
              │        └── US → dilated ducts → stone/stricture/tumour
              └── Normal ducts on imaging → Intrahepatic cholestasis
                       ├── AMA+           → PBC
                       ├── IBD history    → PSC
                       └── Drug history   → Drug-induced cholestasis

Sources: Harrison's Principles of Internal Medicine, 22nd Ed.; Miller's Anesthesia, 10th Ed.; Quick Compendium of Clinical Pathology, 5th Ed.; Tietz Textbook of Laboratory Medicine, 7th Ed.

Generate a diagnostic flowchart poster (ALP vs AST for rapid diagnosis)

Generating Image

A clean medical diagnostic flowchart poster titled "LFT Rapid Diagnosis: ALP vs AST Pattern" for clinical use. The poster uses a white background with a professional medical color scheme (deep navy, crimson red, teal green, amber yellow). At the top: bold title "LFT RAPID DIAGNOSIS" with subtitle "ALP vs AST Pattern Recognition" The flowchart starts with a central box "ABNORMAL LIVER FUNCTION TESTS" in navy blue. It splits into TWO main branches with arrows: LEFT BRANCH (crimson/red): - Box: "AST > 3× URL AND ALP < 2× URL" - Label below: "HEPATOCELLULAR PATTERN" - Splits into two sub-branches: LEFT: "Normal Albumin" → green box "ACUTE HEPATITIS" with bullet points: "• Viral (ALT ≥ AST, >500 U/L)", "• Toxic/Drug-induced", "• Ischemic (>2000 U/L)" RIGHT: "Low Albumin" → orange box "CHRONIC HEPATITIS / CIRRHOSIS" with bullets: "• AST:ALT ratio >1", "• Alcoholic (AST:ALT ≥2:1)", "• NASH/NAFLD" RIGHT BRANCH (teal/green): - Box: "AST < 3× URL AND ALP > 2× URL" - Label below: "CHOLESTATIC PATTERN" - Splits into two sub-branches: LEFT: "PT corrects with Vit K" → teal box "EXTRAHEPATIC CHOLESTASIS" with bullets: "• Gallstones", "• Pancreatic cancer", "• Bile duct stricture" and note "→ Ultrasound: dilated ducts" RIGHT: "Normal ducts on imaging" → purple box "INTRAHEPATIC CHOLESTASIS" with bullets: "• PBC (AMA+)", "• PSC (IBD history)", "• Drug-induced" At the bottom: a SPECIAL CASES section in amber/yellow banner: "⚠ SPECIAL PATTERNS: Wilson Disease = LOW ALP + elevated AST in young patient | Liver Mets = LDH + ALP both markedly elevated | Shock Liver = extreme AST/ALT >2000 U/L, rapid rise and fall" Bottom footer: "De Ritis Ratio (AST:ALT): >2:1 = Alcoholic | <1 = Viral/NAFLD | >1 with low albumin = Cirrhosis" The flowchart has clean arrows, rounded rectangle boxes, clear hierarchy, bold labels, and is suitable for printing as an A3 clinical reference poster.

LFT Rapid Diagnosis: ALP vs AST Diagnostic Flowchart Poster
Here's your diagnostic flowchart poster. It covers:
  • Two core branches - Hepatocellular (AST >3× URL, ALP <2× URL) vs Cholestatic (ALP >2× URL, AST <3× URL)
  • Sub-classification using albumin level (acute vs chronic hepatocellular) and PT response to Vitamin K (extra- vs intrahepatic cholestasis)
  • Special patterns highlighted at the bottom - Wilson disease (paradoxically low ALP), liver metastases (LDH + ALP both elevated), and shock liver (extreme transaminases >2000 U/L)
  • De Ritis ratio guide as a quick footer reference
You can right-click and save the image for printing as an A3 clinical reference. Let me know if you'd like any section expanded, recolored, or reformatted!

Kidney function test (add mnemonic if possible) Identification of abnormalities

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Kidney Function Tests (KFTs)

Mnemonic: "CUBAGE" - to remember all KFT components:
LetterTest
CCreatinine (serum) / Creatinine clearance
UUrea / BUN (Blood Urea Nitrogen)
BBlood electrolytes (Na⁺, K⁺, HCO₃⁻, Cl⁻)
AAlbumin / Acid-base status (pH, bicarbonate)
GGFR (eGFR - estimated glomerular filtration rate)
EElectrolytes + Examination of urine (urinalysis, casts, protein)

Overview

KFTs assess glomerular filtration, tubular function, and urinary composition. The kidney has enormous reserve capacity - serum creatinine may not rise meaningfully until 50-75% of nephron function is already lost (see graph below).
Nonlinear relationship between GFR and serum creatinine - large drops in GFR cause only modest creatinine rise until function is severely reduced
Key concept: A 75% reduction in GFR (from 120 to 30 mL/min) corresponds to only a modest rise in serum creatinine. This is why creatinine is a late marker of kidney injury.

Tests Grouped by Category


1. Glomerular Filtration Tests

Serum Creatinine

  • End product of muscle creatine phosphate metabolism
  • Freely filtered; minimally secreted by tubules
  • Normal: Males ~0.7-1.3 mg/dL; Females ~0.5-1.1 mg/dL
  • Limitations: Confounded by muscle mass, age, sex, drugs (e.g. trimethoprim blocks tubular secretion), fluid status, and laboratory technique
  • Not renal-specific alone - must interpret with clinical context

eGFR (Estimated GFR)

  • Calculated using CKD-EPI or MDRD equations from serum creatinine, age, sex, race
  • The single best overall marker of kidney function in clinical practice
  • Normal: 100-120 mL/min/1.73 m²
GFR StageeGFR (mL/min)Interpretation
Normal>90With markers of kidney damage
Mildly reduced60-89
Mildly-moderately reduced45-59CKD G3a
Moderately-severely reduced30-44CKD G3b
Severely reduced15-29CKD G4
Kidney failure<15ESRD - consider dialysis

Creatinine Clearance (CrCl)

  • 24-hour urine collection method
  • Formula: CrCl = (U × V) / P where U = urine creatinine, V = urine volume (mL/min), P = plasma creatinine
  • Slightly overestimates GFR (due to tubular secretion of creatinine)
  • Normal: 100-120 mL/min

2. BUN / Blood Urea Nitrogen

  • Urea is the main end product of protein catabolism (urea cycle in liver)
  • Normal: 5-20 mg/dL (1.8-7.2 mmol/L)
  • Not purely renal - confounded by:
    • Protein intake (high protein diet raises BUN)
    • Liver disease (impaired synthesis lowers BUN)
    • GI bleed, catabolic states, dehydration (raise BUN disproportionately)

BUN:Creatinine Ratio - Clinically Vital

RatioInterpretation
>20:1Prerenal azotemia (dehydration, GI bleed, heart failure)
10-20:1Normal / Intrinsic renal disease
<10:1Low protein intake, liver failure, SIADH
Mnemonic: "Twenty-to-One = Pre-Renal Run" - BUN:Cr >20 = prerenal

3. Electrolytes

ElectrolyteNormalSignificance in Renal Disease
Sodium (Na⁺)135-145 mEq/LHyponatremia in SIADH, dilutional states; altered in CKD
Potassium (K⁺)3.5-5.0 mEq/LHyperkalemia is a cardinal feature of AKI/CKD - life-threatening
Bicarbonate (HCO₃⁻)22-26 mEq/LLow in metabolic acidosis from CKD (failure to excrete H⁺)
Chloride (Cl⁻)98-106 mEq/LRaised in hyperchloremic metabolic acidosis
Phosphate2.5-4.5 mg/dLElevated in CKD (kidneys fail to excrete phosphate)
Calcium8.5-10.5 mg/dLLow in CKD (reduced vitamin D activation)
Uric Acid2.4-7.0 mg/dL (M)Elevated in gout, CKD; low in Fanconi syndrome

4. Urinalysis (Urine Examination)

Dipstick Analysis

ParameterNormalAbnormal FindingSignificance
ProteinNegative (<150 mg/day)PositiveGlomerular damage, nephrotic syndrome
Blood/HematuriaNegativePositiveGN, stones, UTI, malignancy
GlucoseNegativePositive with normal blood sugarTubular dysfunction (Fanconi syndrome)
NitritesNegativePositiveBacterial UTI
Leukocyte esteraseNegativePositivePyuria, UTI, AIN
pH4.5-8.0Alkaline in RTARenal tubular acidosis
Specific Gravity1.001-1.035Fixed at 1.010Isosthenuria = tubular damage (AKI)
KetonesNegativePositiveDKA, starvation

Urine Microscopy - Casts and What They Mean

Urinary sediments in AKI: A=epithelial cell aggregate, B=hyaline cast (prerenal), C=epithelial cast (early ATN), D=muddy brown cast (established ATN), E=erythrocyte cast (glomerulonephritis), F-G=indinavir crystals
Mnemonic for casts: "Hyaline = Fine; RBC = Glomerulonephritis; WBC = interstitial; Muddy Brown = ATN; Broad Waxy = CKD"
Cast TypeDiagnosis
Hyaline castsNormal or prerenal AKI (dehydration, mild)
RBC (red cell) castsGlomerulonephritis, vasculitis (GOLD STANDARD finding)
WBC (white cell) castsAcute interstitial nephritis (AIN), pyelonephritis
Granular "muddy brown" castsAcute tubular necrosis (ATN) - >10/LPF = 100% PPV for ATN
Fatty casts / oval fat bodiesNephrotic syndrome (heavy proteinuria)
Broad / waxy castsChronic kidney disease (dilated tubules)
Epithelial cell castsEarly ATN

5. Proteinuria Quantification

AmountCategorySignificance
<150 mg/dayNormal
150-3500 mg/dayNon-nephroticCKD, hypertensive nephropathy
>3.5 g/dayNephrotic rangeMinimal change, FSGS, membranous nephropathy, diabetic nephropathy
Spot urine protein:creatinine ratio (UPCR): a ratio of >3.5 = nephrotic range (equivalent to 24h protein >3.5 g)
Types of proteinuria (remember "GOTS"):
  • Glomerular - filtered proteins (albumin predominant; failure of filtration barrier)
  • Overflow - excess production saturates reabsorption (Bence-Jones proteins in myeloma)
  • Tubular - failed reabsorption of normally filtered small proteins
  • Secretory/tissue - inflammation (Tamm-Horsfall protein)

6. Fractional Excretion of Sodium (FENa)

Used to distinguish prerenal AKI from ATN:
$$\text{FENa} = \frac{U_{Na} / S_{Na}}{U_{Cr} / S_{Cr}} \times 100%$$
FENaInterpretation
<1%Prerenal AKI (tubules intact, avidly reabsorbing Na)
>3%ATN (tubular damage, can't reabsorb Na)
1-3%Indeterminate
Caveat: FENa <1% can occur in ATN with contrast, myoglobin, sepsis, or heart failure. If patient is on diuretics, use FEUrea <35% = prerenal instead.

Identifying Abnormalities: Disease Patterns

AKI vs CKD - First Differentiation

FeatureAKICKD
OnsetSudden (hours-days)Gradual (months-years)
Urine outputOften oliguriaNormal initially
Kidney size on USNormal or enlargedSmall, echogenic
AnaemiaAbsent earlyPresent (low EPO)
Broad waxy castsAbsentPresent
Calcium/PhosphateUsually normal initiallyHyperphosphatemia, hypocalcemia
Prior creatinineNormalChronically elevated

KDIGO Classification of AKI

StageSerum Creatinine CriteriaUrine Output
1Rise ≥0.3 mg/dL within 48h OR 1.5-1.9× baseline<0.5 mL/kg/h for 6-12h
22.0-2.9× baseline<0.5 mL/kg/h for ≥12h
3≥3× baseline OR ≥4.0 mg/dL OR dialysis<0.3 mL/kg/h for ≥24h or anuria ≥12h

Distinguishing Prerenal, Intrinsic, and Postrenal AKI

ParameterPrerenalIntrinsic (ATN)Postrenal
BUN:Cr ratio>20:110-15:1Variable
FENa<1%>3%Variable
Urine Na<20 mEq/L>40 mEq/LVariable
Urine osmolality>500 mOsm/kg~300 (isosthenuria)Variable
Urine specific gravity>1.020~1.010Variable
Urine castsHyaline (or none)Muddy brown granularNone
Response to fluidsImprovesNo improvementImproves with relief
Mnemonic: "Prerenal LOVES sodium - holds it tight (FENa <1%, UNa <20)" "ATN LOSES sodium - can't hold it (FENa >3%, UNa >40)"

Nephrotic vs Nephritic Syndrome

FeatureNephroticNephritic
Proteinuria>3.5 g/day<3.5 g/day
HaematuriaAbsent/mildPresent (RBC casts)
HypertensionMild/absentProminent
OedemaSevere (anasarca)Mild-moderate
GFRNear normal earlyReduced
Serum albuminLowNormal/mildly low
Serum cholesterolHighNormal
Urine castsFatty, oval fat bodiesRBC casts
Mnemonic - Nephrotic = "PALE": Protein (massive), Albumin (low), Lipids (high), Edema (severe) Mnemonic - Nephritic = "PHARH": Protein (mild), Haematuria, Azotemia, RBC casts, Hypertension

Reference Ranges Summary

TestNormal Value
Serum Creatinine (M/F)0.7-1.3 / 0.5-1.1 mg/dL
BUN5-20 mg/dL
BUN:Creatinine ratio10-20:1
eGFR>90 mL/min/1.73m² (normal)
Creatinine Clearance100-120 mL/min
Urine Protein<150 mg/day
Urine specific gravity1.001-1.035
Serum K⁺3.5-5.0 mEq/L
Serum Na⁺135-145 mEq/L
Serum HCO₃⁻22-26 mEq/L
FENa (prerenal)<1%
FENa (ATN)>3%

Sources: Comprehensive Clinical Nephrology, 7th Ed.; Brenner and Rector's The Kidney; Morgan and Mikhail's Clinical Anesthesiology, 7th Ed.; Barash Clinical Anesthesia, 9th Ed.; Harper's Illustrated Biochemistry, 32nd Ed.
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