๐Ÿซ˜ Acute Kidney Injury (AKI)

KDIGO 2024 Guidelines - Comprehensive Assessment & Management

๐Ÿ”„ AKI-AKD-CKD Continuum

AKI to CKD Continuum showing progression from acute injury through acute kidney disease to chronic kidney disease

Modern understanding recognizes kidney disease as a continuum rather than discrete categories, with acute kidney disease (AKD) serving as the bridge between acute injury and chronic disease.

๐Ÿšจ Emergency AKI Recognition Protocol

Time-sensitive evaluation for rapid clinical decision-making

1 IMMEDIATE ASSESSMENT: Vital signs, volume status, bladder scan, 12-lead ECG
โ€ข Check for hyperkalemia (peaked T waves) โ€ข Assess hemodynamic stability โ€ข Rule out obstruction first
2 STAT LABORATORIES: BMP, CBC, urinalysis with microscopy, ECG if hyperkalemia
โ€ข Repeat K+ if >5.5 mEq/L โ€ข Rule out hemolysis โ€ข Check magnesium and phosphorus
3 FOLEY CATHETER: If bladder scan >150mL or unexplained AKI
โ€ข May resolve AKI completely โ€ข Check post-void residual โ€ข Monitor urine output closely
4 URINE MICROSCOPY: Fresh specimen within 2 hours of collection
โ€ข Differentiate prerenal vs intrarenal vs postrenal โ€ข Look for casts, crystals, cells

๐Ÿ“Š KDIGO AKI Staging (2024 Guidelines)

Staging based on serum creatinine and urine output criteria

Stage Serum Creatinine Urine Output Clinical Implications
Stage 1 1.5-1.9ร— baseline
OR โ‰ฅ0.3 mg/dL increase		 <0.5 mL/kg/h
for 6-12 hours		 Early recognition
Identify etiology
Stage 2 2.0-2.9ร— baseline <0.5 mL/kg/h
for โ‰ฅ12 hours		 Increased monitoring
Nephrology consult
Stage 3 โ‰ฅ3.0ร— baseline
OR โ‰ฅ4.0 mg/dL
OR dialysis		 <0.3 mL/kg/h
for โ‰ฅ24 hours
OR anuria โ‰ฅ12 hours		 Consider RRT
ICU monitoring

๐Ÿง Critical Concept: Why eGFR is Invalid in AKI

Fundamental Principle: eGFR calculations are only valid when serum creatinine is at steady state

๐Ÿ”ด AKI: Rising Creatinine = Invalid eGFR

  • Creatinine Status: Rapidly rising (non-steady state)
  • eGFR Validity: โŒ INVALID - significantly overestimates true GFR
  • Clinical Reality: True GFR may be near zero while eGFR still appears "normal"
  • Time to Steady State: 3-5 days after GFR change
  • Clinical Use: Monitor creatinine trends, not absolute eGFR values

๐ŸŸข CKD: Stable Creatinine = Valid eGFR

  • Creatinine Status: Stable over months (steady state)
  • eGFR Validity: โœ… VALID - accurately reflects true GFR
  • Clinical Reality: eGFR closely approximates measured GFR
  • Time Course: Gradual changes over months to years
  • Clinical Use: Staging, monitoring, medication dosing

๐Ÿงฌ The Total Nephrectomy Teaching Example

Scenario: Patient undergoes total nephrectomy (both kidneys removed)

โšก Immediate Reality (Time = 0)

  • True GFR: 0 mL/min (no kidneys!)
  • Serum Creatinine: Still normal (1.0 mg/dL)
  • Calculated eGFR: ~90 mL/min (completely wrong!)
  • Clinical Status: Patient is anuric, requires emergency dialysis

๐Ÿ•ฐ๏ธ Day 1 Post-Op

  • True GFR: Still 0 mL/min (unchanged)
  • Serum Creatinine: 2.0 mg/dL (rising)
  • Calculated eGFR: ~38 mL/min (still way off!)
  • Clinical Status: Same - still requires dialysis

๐Ÿ“ˆ Day 2 Post-Op

  • True GFR: Still 0 mL/min (unchanged)
  • Serum Creatinine: 3.5 mg/dL (continuing to rise)
  • Calculated eGFR: ~20 mL/min (getting closer but still wrong)
  • Clinical Status: Same - still requires dialysis

๐Ÿ“Š Day 3 Post-Op

  • True GFR: Still 0 mL/min (unchanged)
  • Serum Creatinine: 5.0 mg/dL (continuing upward)
  • Calculated eGFR: ~13 mL/min (improving but still overestimating)
  • Clinical Status: Same - still requires dialysis

๐ŸŽฏ Steady State (Days 4-5)

  • True GFR: Still 0 mL/min (unchanged)
  • Serum Creatinine: Plateaus (8-12 mg/dL)
  • Calculated eGFR: ~5-7 mL/min (finally approaching reality)
  • Clinical Status: Same - chronic dialysis needed

๐Ÿ’ก Key Teaching Points

  • GFR changed instantly (0 mL/min immediately after surgery)
  • Creatinine rises gradually over 3-5 days to reach new steady state
  • eGFR "catches up" slowly and significantly lags behind true GFR changes
  • Clinical decisions must be based on the clinical scenario, not misleading eGFR values
  • In AKI, trend and absolute creatinine values matter more than calculated eGFR

๐ŸŽฏ Clinical Applications in AKI Management

โŒ Don't Rely On:

  • eGFR values during rising creatinine
  • "Normal" eGFR in early AKI
  • eGFR for medication dosing in AKI
  • eGFR for dialysis timing decisions

โœ… Instead Focus On:

  • Absolute creatinine values and trends
  • KDIGO staging criteria
  • Clinical signs: urine output, volume status
  • Time course and rate of creatinine rise

๐Ÿ‘ฅ Patient Education:

  • Explain why eGFR seems "better" than reality
  • Focus on kidney function recovery, not numbers
  • Emphasize clinical improvement markers
  • Avoid false reassurance from "improving" eGFR

โš ๏ธ Common Clinical Errors to Avoid

  • "The eGFR is still 45, so the kidneys are working okay" - Wrong! In AKI, this could represent severe kidney injury
  • Using eGFR for medication dosing in AKI - Can lead to significant overdosing
  • Reassuring patients based on "stable" eGFR - While creatinine is still rising
  • Delaying nephrology consultation - Because eGFR "doesn't look that bad"
  • Comparing AKI eGFR to CKD staging - Fundamentally different clinical contexts

๐Ÿ” Systematic Diagnostic Approach

๐Ÿ”ฌ Urine Microscopy: The Key Differentiator

Fresh urine microscopy within 2 hours provides critical diagnostic information

๐Ÿ’ง Prerenal AKI

Microscopy Findings:
  • Hyaline casts (Tamm-Horsfall protein)
  • Rare renal tubular epithelial cells
  • Concentrated appearance
  • Minimal cellular elements
Laboratory: FENa <1%, UOsm >500, BUN:Cr >20:1

๐Ÿ”ฅ Intrarenal AKI

Microscopy Findings:
  • ATN: Muddy brown granular casts
  • Renal tubular epithelial cells
  • GN: RBC casts, dysmorphic RBCs
  • AIN: WBC casts, eosinophils
Laboratory: FENa >2%, UOsm ~300, isosthenuria

๐Ÿšฐ Postrenal AKI

Microscopy Findings:
  • Variable findings based on cause
  • RBCs if stones or malignancy
  • WBCs if concurrent infection
  • Crystals (uric acid, calcium oxalate)
Imaging: Urgent ultrasound, CT if indicated

๐Ÿšจ ANURIA: Nephrological Emergency

Definition: Urine output <100 mL per 24 hours

โšก Immediate Life-Threatening Causes

๐Ÿซ€ Vascular:
  • Bilateral renal artery occlusion
  • Bilateral renal vein thrombosis
  • Acute cortical necrosis
๐Ÿšฐ Obstructive:
  • Bilateral ureteral obstruction
  • Complete urethral obstruction
  • Retroperitoneal fibrosis
Emergency Management: Immediate nephrology consultation within hours, urgent imaging (CT angiography if vascular suspected), emergency decompression if obstructive, prepare for urgent dialysis

๐Ÿ’Š Furosemide Stress Test (FST): Revolutionary Risk Stratification

๐Ÿงฌ Mechanism & Clinical Utility

FST leverages furosemide's unique pharmacokinetics - relies on tubular secretion rather than glomerular filtration, making diuretic response a functional marker of tubular integrity.

๐Ÿ“‹ FST Protocol

  • Dose: 1.0 mg/kg IV (naive) or 1.5 mg/kg (prior exposure)
  • Requirements: Evidence of ATN + adequate resuscitation
  • Timing: Measure urine output over 2 hours
  • Interpretation: >200 mL = responsive, <200 mL = non-responsive

๐ŸŽฏ Clinical Performance

  • Sensitivity: 87% for stage 3 AKI progression
  • Specificity: 84% for avoiding unnecessary interventions
  • AUC: 0.87 (superior to biomarkers)
  • CRRT Prediction: 96% accuracy for dialysis need
Clinical Pearl: FST non-responders have 2.4ร— higher likelihood of requiring CRRT. The test can be performed outside ICU settings and helps prevent futile fluid resuscitation while enabling early identification of patients requiring advanced interventions.

๐Ÿ”ฅ Intrinsic Renal Disease: Comprehensive Overview

โšก Rapidly Progressive Glomerulonephritis (RPGN)

NEPHROLOGIC EMERGENCY: Rapid kidney function deterioration with extensive crescent formation

๐Ÿšจ Clinical Recognition Triad

๐Ÿ“ˆ Rapidly Rising Creatinine
  • Days to weeks progression
  • May double in <7 days
  • Often >50% reduction in eGFR
๐Ÿ”ฌ Active Urinary Sediment
  • RBC casts (pathognomonic)
  • Dysmorphic RBCs
  • Proteinuria >1g/day
โฐ Clinical Urgency
  • Nephrology consult <24h
  • Urgent kidney biopsy
  • Delay = permanent damage

๐Ÿงฌ RPGN Categories by Immunofluorescence

  • Anti-GBM Disease: Linear IgG staining
  • Immune Complex: Granular pattern (lupus, post-infectious)
  • Pauci-Immune: ANCA-associated vasculitis

๐Ÿงช Essential Laboratory Workup

  • ANCA: c-ANCA (PR3), p-ANCA (MPO)
  • Anti-GBM antibodies: Goodpasture's
  • Complement: C3, C4, CH50
  • ANA, anti-dsDNA: Lupus nephritis
โšก Emergency Management: High-dose corticosteroids (methylprednisolone 500-1000mg IV daily ร— 3 days) + plasmapheresis if anti-GBM positive + urgent nephrology consultation for biopsy and long-term immunosuppression planning

๐Ÿ”ฅ Acute Interstitial Nephritis (AIN)

Immune-mediated inflammation of the tubulointerstitium with varied clinical presentations

๐ŸŽฏ Classic Triad (Only 10% of Cases!)

Myth: Fever + Rash + Eosinophilia is rarely seen together. Most cases are subtle!

๐Ÿ’Š Common Drug Causes

  • PPIs: Most common cause (omeprazole, pantoprazole)
  • NSAIDs: Both prescription and OTC
  • Antibiotics: ฮฒ-lactams, sulfonamides, quinolones
  • Diuretics: Thiazides, loop diuretics
  • Immune checkpoint inhibitors: PD-1/PD-L1 inhibitors

๐Ÿ”ฌ Diagnostic Features

  • Urine: WBC casts, sterile pyuria
  • โš ๏ธ Urine eosinophils: NOT diagnostic (poor sensitivity/specificity)
  • Timeline: Days to weeks after drug exposure
  • FENa: Often >1% (tubular dysfunction)

๐Ÿ’ก Management Approach

  • Drug withdrawal: First-line therapy
  • Corticosteroids: If no improvement in 3-7 days
  • Dose: Prednisone 1 mg/kg/day ร— 2-4 weeks
  • Biopsy: If diagnosis uncertain

๐Ÿงฌ Acute Tubular Necrosis: Intrinsic Toxins

Endogenous nephrotoxins causing direct tubular injury through various mechanisms

๐Ÿ’ช Rhabdomyolysis

  • Mechanism: Myoglobin direct toxicity + tubular obstruction
  • Triggers: Trauma, drugs, prolonged immobilization, exercise
  • Labs: CK >1000 U/L (often >5000), myoglobinuria
  • Treatment: Aggressive fluid resuscitation, alkalinization
  • Goal UOP: 200-300 mL/hr initially
  • Key Point: CK for detection, myoglobin causes actual injury

๐Ÿฉธ Hemolysis

  • Mechanism: Free hemoglobin tubular toxicity
  • Causes: Transfusion reactions, mechanical hemolysis
  • Labs: โ†“Haptoglobin, โ†‘LDH, hemoglobinuria
  • Clinical: Dark red/brown urine
  • Management: Treat underlying cause, maintain UOP

๐Ÿงช Light Chain Nephropathy

  • Setting: Multiple myeloma, plasma cell disorders
  • Mechanism: Light chain precipitation in tubules
  • Microscopy: Large, fractured casts with angular edges
  • Diagnosis: Serum/urine immunofixation, free light chains
  • Treatment: Chemotherapy, plasmapheresis in severe cases

โšก Rhabdomyolysis Emergency Protocol

๐Ÿšฐ Fluid Resuscitation
  • Normal saline 1-2 L/hr initially
  • Goal UOP: 200-300 mL/hr
  • Monitor for volume overload
๐Ÿงช Alkalinization (Controversial)
  • Sodium bicarbonate in selected cases
  • Goal urine pH >6.5
  • Avoid if volume overloaded

๐Ÿ’Š Antibiotic-Associated Kidney Injury: Comprehensive Guide

Antibiotics represent one of the most common causes of drug-induced kidney injury in clinical practice

Antibiotic Class Primary Mechanism Typical Onset (Days) Pattern of Injury Incidence Rate
Aminoglycosides Direct tubular toxicity 7-10 Acute tubular necrosis 10-25%
Glycopeptides (Vancomycin) Oxidative stress, inflammasome activation 5-10 Acute tubular necrosis 5-35%
Beta-Lactams Hypersensitivity reaction 10-14 Acute interstitial nephritis 1-3%
Polymyxins Membrane damage 5-7 Acute tubular necrosis 20-60%
Fluoroquinolones Hypersensitivity reaction 7-14 Acute interstitial nephritis <1%
Sulfonamides (Crystalluria) Crystal formation 1-3 Crystal nephropathy 1-5%
Tetracyclines Direct tubular toxicity 3-7 Fanconi syndrome <1% (modern agents)
Macrolides Hypersensitivity, drug interactions 7-14 Acute interstitial nephritis <1%
Amphotericin B Membrane damage 5-7 Acute tubular necrosis 30-80%

๐Ÿงฌ Aminoglycosides: Structure-Toxicity Relationship

Key Concept: Nephrotoxicity directly correlates with positive charge and number of amino groups

Aminoglycoside Relative Nephrotoxicity Number of Amino Groups Positive Charges Clinical Notes
Neomycin Highest (5/5) 6 +6 Topical use only due to toxicity
Gentamicin High (4/5) 5 +5 Most commonly used, high efficacy
Tobramycin Moderate to High (3/5) 5 +5 Preferred for Pseudomonas
Kanamycin Moderate (3/5) 4 +4 Limited use due to resistance
Amikacin Moderate (2/5) 4 +4 Reserved for resistant organisms
Netilmicin Low to Moderate (2/5) 3 +3 Less nephrotoxic alternative
Streptomycin Lowest (1/5) 2 +2 Primarily ototoxic, less nephrotoxic

๐Ÿ”ฌ Mechanism of Charge-Related Toxicity

1. Enhanced Membrane Binding

Higher positive charge โ†’ stronger binding to negatively charged phospholipids in proximal tubular cells

2. Increased Cellular Uptake

More charges โ†’ greater megalin-mediated endocytosis โ†’ higher intracellular accumulation

3. Enhanced Lysosomal Retention

Highly charged molecules accumulate more in lysosomes โ†’ greater disruption of cellular function

4. Mitochondrial Interference

Greater positive charge โ†’ stronger binding to mitochondrial ribosomes โ†’ more energy disruption

โš–๏ธ Vancomycin vs Aminoglycosides: Comparative Nephrotoxicity

Aspect Vancomycin Aminoglycosides Clinical Notes
Overall AKI incidence 5-35% 10-25% Varies by definition and population
Severe AKI requiring RRT 1-5% 2-7% Higher with prolonged therapy
Time to AKI onset 5-10 days 7-14 days Vancomycin often earlier
Persistent kidney dysfunction 5-15% 10-20% Higher with advanced age
Concomitant use (both drugs) 35-45% Synergistic toxicity
Primary mechanism NLRP3 inflammasome, oxidative stress Lysosomal disruption, mitochondrial damage Different subcellular targets
Prevention strategy AUC-guided dosing Extended-interval dosing Both reduce toxicity significantly

๐ŸŽฏ Key Clinical Decision Points

  • Vancomycin + Piperacillin-Tazobactam: 35-45% AKI risk (NNH = 8-10 patients)
  • Vancomycin + Aminoglycosides: 25-40% AKI risk (avoid when possible)
  • AUC-guided vancomycin dosing: 33-45% reduction in AKI risk
  • Extended-interval aminoglycosides: 30-50% reduction in nephrotoxicity

โš ๏ธ High-Risk Antibiotic Combinations

Synergistic nephrotoxicity from commonly used antibiotic combinations

๐Ÿ”ฅ Vancomycin + Piperacillin-Tazobactam

  • AKI Risk: 21-40% (vs 8-13% vancomycin alone)
  • Mechanism: Synergistic NLRP3 inflammasome activation
  • Risk Factors: Age >65, CKD, diabetes, high doses
  • Prevention: AUC-guided vancomycin + extended-infusion pip-tazo
  • Alternatives: Vancomycin + cefepime or meropenem

โšก Vancomycin + Aminoglycosides

  • AKI Risk: 25-40% (historic high-risk combination)
  • Mechanism: Complementary nephrotoxic pathways
  • Risk Factors: Higher doses, extended duration, pre-existing CKD
  • Management: Avoid combination when possible
  • Monitoring: Daily creatinine, enhanced biomarker surveillance

๐Ÿ’€ Polymyxins + Vancomycin

  • AKI Risk: 40-60% (extremely high-risk combination)
  • Mechanism: Synergistic membrane damage + oxidative stress
  • Indication: Extensively drug-resistant organisms only
  • Management: Nephroprotective strategies, daily monitoring
  • Alternatives: Consider newer agents when available

๐Ÿšจ Triple Combination Therapy

  • AKI Risk: 45-70% (vancomycin + aminoglycoside + beta-lactam)
  • Mechanism: Multiple complementary nephrotoxic pathways
  • Risk Factors: Nearly universal in high-risk patients
  • Management: Avoid when possible, daily monitoring, early de-escalation
  • Rule: Each additional nephrotoxin increases AKI odds by ~60%

๐Ÿญ Environmental & Heavy Metal Toxicity

โš—๏ธ Ethylene Glycol

  • Source: Antifreeze ingestion
  • Mechanism: Toxic metabolites (oxalic acid)
  • Timeline: 6-12 hours post-ingestion
  • Treatment: Fomepizole, hemodialysis
  • Lab findings: Anion gap metabolic acidosis

๐Ÿ”ถ Heavy Metals

  • Mercury: Proximal tubular necrosis
  • Lead: Chronic tubulointerstitial disease
  • Cadmium: Proximal tubular dysfunction
  • Treatment: Chelation therapy (DMSA, EDTA)
  • Monitoring: 24-hour urine metals

๐Ÿ„ Natural Toxins

  • Mushroom poisoning: Amanita species
  • Snake venom: Hemolysis, direct nephrotoxicity
  • Aristolochic acid: Chinese herbs (chronic)
  • Treatment: Supportive care, specific antidotes
  • Prevention: Education, avoid herbal remedies

๐Ÿ’Ž Crystalopathy: Crystal-Induced Tubular Obstruction & AKI

Pathophysiology: Intratubular crystal precipitation causing mechanical obstruction, direct tubular toxicity, and acute kidney injury

๐Ÿ”ฌ Common Crystalopathy Mechanisms

๐Ÿ“ˆ Supersaturation:
  • Exceed solubility limits in tubular fluid
  • Concentration-dependent precipitation
  • pH-dependent solubility (uric acid, cystine)
  • Temperature effects on crystal formation
๐Ÿšฐ Tubular Obstruction:
  • Mechanical blockage of tubular lumens
  • Increased intratubular pressure
  • Reduced effective filtration
  • Secondary tubular cell injury
๐Ÿ’ฅ Direct Toxicity:
  • Crystal-induced inflammation
  • Complement activation
  • Reactive oxygen species generation
  • Tubular epithelial cell death

๐Ÿšจ Tumor Lysis Syndrome (TLS): Life-Threatening Uric Acid Crystalopathy

Most dangerous crystalopathy - requires immediate recognition and intervention within hours

โšก Critical Recognition Triad

๐Ÿงฌ High-Risk Malignancy
  • Burkitt lymphoma (highest risk)
  • High-grade NHL with bulky disease
  • ALL/AML with high WBC count
  • Recent chemotherapy initiation
๐Ÿงช "Big Four" Lab Abnormalities
  • Hyperuricemia (>8 mg/dL)
  • Hyperkalemia (>6.0 mEq/L)
  • Hyperphosphatemia (>4.5 mg/dL)
  • Hypocalcemia (<7.0 mg/dL)
โฐ Critical Timeline
  • Peak risk: 12-72 hours post-chemo
  • Hyperkalemia most immediately lethal
  • Can progress to AKI requiring RRT
  • Prevention superior to treatment

๐Ÿ’Š Emergency Management Priorities

๐Ÿšจ Immediate (0-1 hour):
  • Cardiac monitoring for hyperkalemia
  • STAT electrolytes, uric acid, phosphorus
  • G6PD testing if rasburicase planned
  • Assess volume status
โšก Urgent (1-6 hours):
  • Hyperkalemia treatment if K+ >6.5 mEq/L
  • Rasburicase 0.2 mg/kg IV if indicated
  • Aggressive hydration if not volume overloaded
  • Nephrology consultation
๐Ÿ“Š Ongoing (6+ hours):
  • Serial electrolytes Q6-8h
  • Monitor for AKI development
  • Prepare for RRT if refractory
  • Avoid calcium if PO4 >6.5 mg/dL

๐ŸŽฏ TLS Key Clinical Pearls

๐Ÿงฌ Risk Stratification:
  • Burkitt lymphoma: Highest risk malignancy
  • High-grade NHL: Risk increases with tumor burden
  • ALL/AML: WBC >50,000 or bulky disease
  • Timing: Peak risk 12-72 hours post-chemo
๐Ÿฉธ Rasburicase Pearls:
  • Mechanism: Converts uric acid โ†’ allantoin (water-soluble)
  • Contraindications: G6PD deficiency (hemolysis risk)
  • Efficacy: Uric acid normalizes within 4 hours
  • Monitoring: Uric acid levels q6h
โš ๏ธ Critical Mistakes to Avoid:
  • Calcium administration: Risk of Ca-PO4 precipitation
  • Inadequate hydration: Must achieve high UOP
  • Delayed recognition: Monitor high-risk patients proactively
  • Urine alkalinization: Not recommended (may worsen Ca-PO4)
๐Ÿ“Š Laboratory Monitoring:
  • Baseline: BMP, uric acid, phosphorus, LDH
  • Frequency: Q6-8h x 72 hours minimum
  • AKI monitoring: Daily creatinine, urine output
  • Response: Uric acid should decline within 24h

โš ๏ธ TLS Prevention Strategies

๐Ÿ“Š Pre-Treatment Assessment:
  • Tumor burden assessment (CT, PET scan)
  • Baseline electrolytes, uric acid, LDH
  • G6PD testing if rasburicase anticipated
  • Renal function and volume status
๐Ÿ’ช Prophylactic Measures:
  • Allopurinol 300mg daily x 1-2 days pre-chemo
  • Aggressive hydration (3-4 L/day if tolerated)
  • Rasburicase prophylaxis in very high-risk patients
  • Consider modified chemotherapy regimen
๐Ÿ•ฐ๏ธ Monitoring Protocol:
  • Electrolytes Q6h x 72 hours minimum
  • Daily weights and strict I/O monitoring
  • Continuous cardiac monitoring if K+ >6.0
  • Early nephrology involvement for high-risk cases

๐Ÿ’Ž Other Important Crystallopathies in AKI

Additional crystal-induced kidney injury patterns requiring specific recognition and management

๐ŸŽฏ Uric Acid Crystalopathy (Non-TLS)

  • Causes: Gout flares, dehydration, acidic urine (pH <5.5)
  • Mechanism: Uric acid precipitation in acidic tubular fluid
  • Recognition: Yellow-brown needle-shaped crystals
  • Treatment: Alkalinization (target pH 6.5-7.0), hydration
  • Prevention: Allopurinol for chronic hyperuricemia

๐Ÿงก Calcium Oxalate Crystalopathy

  • Causes: Ethylene glycol poisoning, high-dose vitamin C
  • Mechanism: Oxalate overproduction or ingestion
  • Recognition: Envelope-shaped crystals, anion gap acidosis
  • Treatment: Fomepizole (ethylene glycol), hemodialysis
  • Timeline: AKI develops 6-12 hours post-ingestion

๐Ÿ’Š Drug-Induced Crystallopathy

  • Acyclovir: Rapid IV infusion, dehydration
  • Sulfonamides: Crystalluria in acidic urine
  • Methotrexate: High-dose therapy, delayed excretion
  • Indinavir: HIV protease inhibitor crystallopathy
  • Prevention: Adequate hydration, appropriate infusion rates

โšก Calcium Phosphate Precipitation

  • Triggers: Rapid calcium administration + high phosphate
  • Risk factors: CKD, phosphate retention, alkalotic urine
  • Recognition: Sudden AKI after calcium/phosphate administration
  • Prevention: Avoid calcium if phosphate >6.5 mg/dL
  • Clinical context: Common complication in TLS management

๐Ÿ”ด Cystine Crystalopathy

  • Cause: Cystinuria (genetic defect in amino acid transport)
  • Recognition: Hexagonal crystals, family history
  • Management: Alkalinization (pH >7.0), high fluid intake
  • Medications: Tiopronin, penicillamine for stone prevention
  • Complication: Recurrent nephrolithiasis and AKI

๐Ÿ”ฌ 2,8-Dihydroxyadenine Crystalopathy

  • Cause: Adenine phosphoribosyltransferase (APRT) deficiency
  • Recognition: Mimics uric acid stones, genetic testing
  • Treatment: Allopurinol (blocks adenine metabolism)
  • Importance: Often misdiagnosed as uric acid crystalopathy
  • Outcome: Excellent response to allopurinol if recognized

๐ŸŽฏ General Crystallopathy Management Principles

๐Ÿ’ง Hydration Strategies:
  • Target UOP 2-3 mL/kg/hr when possible
  • Monitor for volume overload in CKD patients
  • Consider loop diuretics if fluid retention
  • Maintain euvolemia while maximizing clearance
๐Ÿงช pH Management:
  • Uric acid: Alkalinize urine pH >6.5
  • Cystine: Alkalinize urine pH >7.0
  • Calcium phosphate: Avoid alkalinization
  • Monitor: Urine pH q6h during treatment
๐Ÿ”„ Prevention Strategies:
  • Identify high-risk patients early
  • Prophylactic hydration for procedures
  • Appropriate drug dosing and infusion rates
  • Monitor for drug interactions affecting clearance
โฑ๏ธ Monitoring Parameters:
  • Serial creatinine and urine output
  • Urine microscopy for crystal identification
  • Electrolyte panel q6-8h in acute phase
  • Specific markers (uric acid, oxalate) as indicated

๐Ÿฅ Contrast-Associated AKI (CA-AKI)

Evolution from "Contrast-Induced": Recognition of multifactorial pathogenesis beyond direct contrast toxicity

โšก Risk Factors

  • Primary: CKD (eGFR <60), diabetes, volume depletion
  • Procedural: High contrast volume, intra-arterial route
  • Patient: Age >75, heart failure, multiple myeloma
  • Concurrent: Nephrotoxic medications, hypotension

๐Ÿ›ก๏ธ Prevention Strategies

  • Hydration: Isotonic saline 1-1.5 mL/kg/hr ร— 6-12h
  • Contrast: Minimize volume, use iso/low-osmolar agents
  • Medications: Hold nephrotoxins, avoid NSAIDs
  • Timing: Space procedures โ‰ฅ48-72 hours apart

๐Ÿ“Š Management Pearls

  • Timeline: AKI develops 24-72h post-exposure
  • Peak: Creatinine peaks at 3-5 days
  • Recovery: Usually complete within 1-2 weeks
  • Monitoring: Serial creatinine, urine output

๐Ÿงฎ AKI Assessment Tools

Enhanced Drug Nephrotoxicity Risk

Calculating enhanced nephrotoxicity risk...

KDIGO Staging Calculator

Calculating KDIGO stage...

Furosemide Stress Test

Calculating FST interpretation...

CA-AKI Risk Assessment

Calculating CA-AKI risk...

๐Ÿ—บ๏ธ AKI Diagnostic Flowchart

1. RECOGNIZE AKI
โ†‘Creatinine (โ‰ฅ0.3 mg/dL or 1.5ร— baseline) OR โ†“UOP (<0.5 mL/kg/hr ร— 6h)
2. ASSESS SEVERITY
KDIGO Staging + Check for life-threatening complications (hyperkalemia, acidosis, volume overload)
3. DETERMINE ETIOLOGY
History + Exam + Urine microscopy + Laboratory assessment + Imaging if indicated
4. INITIATE TREATMENT
Address underlying cause + Supportive care + Monitor for recovery vs progression
5. CONSIDER NEPHROLOGY CONSULTATION
Stage 2-3 AKI + Unclear etiology + Need for RRT + Complicated cases

๐ŸŽฏ Essential AKI Learning Points

๐Ÿšจ Emergency Recognition

  • Anuria = nephrological emergency
  • Check hyperkalemia immediately
  • Foley catheter if obstruction suspected
  • Fresh urine microscopy <2 hours

๐Ÿ”ฌ Diagnostic Essentials

  • Urine microscopy differentiates causes
  • FENa <1% suggests prerenal
  • Muddy brown casts = ATN
  • RBC casts = glomerulonephritis

๐Ÿงช Advanced Tools

  • FST predicts progression/RRT need
  • Superior to biomarkers
  • KDIGO staging guides management
  • CA-AKI is multifactorial

๐Ÿ’ก Clinical Pearls

  • AKI-AKD-CKD continuum concept
  • Prevention better than treatment
  • Early nephrology consultation
  • Monitor for recovery patterns

๐Ÿ”ฅ Intrinsic Disease

  • RPGN = nephrologic emergency
  • Classic AIN triad rarely present
  • Urine eosinophils NOT diagnostic
  • Drug withdrawal first-line for AIN

๐Ÿ’Š Drug Nephrotoxicity

  • Aminoglycosides: delayed onset (5-10 days)
  • Vancomycin: trough level dependent
  • PPIs most common cause of AIN
  • Multiple nephrotoxins = exponential risk

๐Ÿ“š For Educational Purposes Only

ยฉ 2025 Andrew Bland MD - All Rights Reserved