Pre-Case Assessment: Test Your Baseline Knowledge
Answer these questions before reviewing the case to assess your starting knowledge
1
According to KDIGO 2024 guidelines, which of the following BEST defines Stage 2 AKI?
A) Creatinine increase ≥0.3 mg/dL within 48 hours
B) Creatinine increase to 2.0-2.9× baseline within 7 days
C) Urine output <0.3 mL/kg/hr for 24 hours
D) Requirement for renal replacement therapy
Correct Answer: B
Learning Point: Stage 2 AKI is defined by creatinine increase to 2.0-2.9× baseline. This is critical for determining monitoring intensity and need for nephrology consultation.
📚 Reference: KDIGO Staging Section
Learning Point: Stage 2 AKI is defined by creatinine increase to 2.0-2.9× baseline. This is critical for determining monitoring intensity and need for nephrology consultation.
📚 Reference: KDIGO Staging Section
2
In the evaluation of AKI, which laboratory finding MOST reliably differentiates prerenal from intrinsic AKI?
A) BUN:Creatinine ratio >20:1
B) Fresh urine microscopy findings
C) Fractional excretion of sodium (FENa)
D) Urine osmolality >500 mOsm/kg
Correct Answer: B
Learning Point: Fresh urine microscopy (<2 hours) is the most reliable differentiator. Hyaline casts suggest prerenal, while muddy brown casts indicate ATN.
📚 Reference: Urinalysis Interpretation
Learning Point: Fresh urine microscopy (<2 hours) is the most reliable differentiator. Hyaline casts suggest prerenal, while muddy brown casts indicate ATN.
📚 Reference: Urinalysis Interpretation
3
Which combination of factors creates the highest risk for AKI in elderly patients?
A) ACE inhibitor + thiazide diuretic
B) ACE inhibitor + NSAID + volume depletion
C) Diabetes + hypertension + age >80
D) Beta-blocker + calcium channel blocker
Correct Answer: B
Learning Point: The "triple threat" of ACE inhibitor + NSAID + volume depletion creates synergistic risk for AKI. This combination impairs autoregulation at both afferent and efferent arterioles.
📚 Reference: Drug-Induced AKI Module
Learning Point: The "triple threat" of ACE inhibitor + NSAID + volume depletion creates synergistic risk for AKI. This combination impairs autoregulation at both afferent and efferent arterioles.
📚 Reference: Drug-Induced AKI Module
Case Presentation
Patient: 82-year-old woman
Chief Complaint: Weakness, confusion, and decreased urine output for 3 days
History: 5-day history of profuse watery diarrhea following gastroenteritis. Poor oral intake. Lives alone, found by neighbor appearing confused and weak.
Past Medical History: Hypertension, type 2 diabetes, osteoarthritis
Home Medications: Lisinopril 10mg daily, metformin 1000mg BID, ibuprofen 600mg TID PRN pain
🤔 Initial Clinical Reasoning Questions
4
Based on the initial presentation, what is your PRIMARY working diagnosis?
A) Acute tubular necrosis from dehydration
B) Prerenal AKI from volume depletion and nephrotoxins
C) Acute interstitial nephritis from NSAIDs
D) Urinary tract obstruction
Correct Answer: B
Clinical Reasoning: The combination of volume depletion (diarrhea, poor intake), ACE inhibitor use, and high-dose NSAIDs creates a classic setup for prerenal AKI. The timeline and clinical context strongly support this diagnosis.
Clinical Reasoning: The combination of volume depletion (diarrhea, poor intake), ACE inhibitor use, and high-dose NSAIDs creates a classic setup for prerenal AKI. The timeline and clinical context strongly support this diagnosis.
5
Which medication poses the HIGHEST nephrotoxic risk in this clinical scenario?
A) Lisinopril (ACE inhibitor)
B) Ibuprofen (NSAID)
C) Metformin
D) All medications pose equal risk
Correct Answer: B
Learning Point: While ACE inhibitors contribute to risk, NSAIDs are the primary culprit in volume-depleted states. NSAIDs block prostaglandin E2, which is essential for afferent arteriolar dilation when volume depleted.
📚 Reference: NSAID-Induced AKI
Learning Point: While ACE inhibitors contribute to risk, NSAIDs are the primary culprit in volume-depleted states. NSAIDs block prostaglandin E2, which is essential for afferent arteriolar dilation when volume depleted.
📚 Reference: NSAID-Induced AKI
Physical Examination
Vital Signs
- Blood Pressure: 95/60 mmHg (baseline 145/85)
- Heart Rate: 110 bpm
- Temperature: 37.8°C (100.0°F)
- Weight: 62 kg (down 4 kg from baseline)
Physical Findings
- General: Appears tired, mild confusion
- HEENT: Dry mucous membranes, decreased skin turgor
- Cardiovascular: Tachycardic, no murmurs
- Extremities: No peripheral edema
🩺 Physical Examination Analysis
6
The blood pressure drop from 145/85 to 95/60 mmHg in this patient most likely indicates:
A) Improved blood pressure control from medications
B) Significant intravascular volume depletion
C) Sepsis from gastroenteritis
D) Myocardial infarction
Correct Answer: B
Clinical Correlation: A 50-point systolic drop from baseline, combined with tachycardia and clinical signs of dehydration, indicates significant volume depletion. This supports the prerenal AKI diagnosis.
Clinical Correlation: A 50-point systolic drop from baseline, combined with tachycardia and clinical signs of dehydration, indicates significant volume depletion. This supports the prerenal AKI diagnosis.
7
This patient presents with tachycardia (HR 110) and hypotension (BP 95/60). What is the BEST initial fluid choice for resuscitation and why?
A) Lactated Ringers - lower chloride content reduces nephrotoxicity risk
B) Normal saline - standard isotonic fluid for volume expansion
C) Half-normal saline (0.45% NaCl) - gentler fluid replacement
D) D5NS with 40 mEq KCl - addresses both volume and electrolyte needs
Correct Answer: A
Clinical Rationale: Lactated Ringers (LR) is preferred over Normal Saline for volume resuscitation in AKI. LR contains 109 mEq/L chloride vs 154 mEq/L in NS. High chloride loads from NS can cause hyperchloremic metabolic acidosis and may worsen kidney function through afferent arteriolar vasoconstriction. Multiple studies suggest LR is less nephrotoxic than NS in critically ill patients.
Other options: Half-normal saline is hypotonic and inappropriate for hemodynamic instability. D5NS with KCl is contraindicated with hyperkalemia (K+ 5.2 mEq/L). Oral salt pills are inappropriate for acute hypotension.
Clinical Rationale: Lactated Ringers (LR) is preferred over Normal Saline for volume resuscitation in AKI. LR contains 109 mEq/L chloride vs 154 mEq/L in NS. High chloride loads from NS can cause hyperchloremic metabolic acidosis and may worsen kidney function through afferent arteriolar vasoconstriction. Multiple studies suggest LR is less nephrotoxic than NS in critically ill patients.
Other options: Half-normal saline is hypotonic and inappropriate for hemodynamic instability. D5NS with KCl is contraindicated with hyperkalemia (K+ 5.2 mEq/L). Oral salt pills are inappropriate for acute hypotension.
Laboratory Data
Initial Laboratory Values
| Parameter | Value | Normal Range | Clinical Significance |
|---|---|---|---|
| Serum Creatinine | 2.8 mg/dL | 0.6-1.2 mg/dL | Baseline 1.1 mg/dL (3 months ago) |
| BUN | 84 mg/dL | 8-20 mg/dL | BUN:Cr ratio = 30 (suggestive of prerenal) |
| Sodium | 148 mEq/L | 136-145 mEq/L | Hypernatremia from volume depletion |
| Potassium | 5.2 mEq/L | 3.5-5.0 mEq/L | Mild hyperkalemia from decreased GFR |
| Chloride | 118 mEq/L | 98-107 mEq/L | Hypochloremia from diarrheal losses |
| CO2 | 18 mEq/L | 22-28 mEq/L | Metabolic acidosis from diarrhea |
📊 Laboratory Analysis Questions
8
Calculate the KDIGO AKI stage for this patient:
Baseline creatinine: 1.1 mg/dL, Current creatinine: 2.8 mg/dL
A) Stage 1 AKI
B) Stage 2 AKI
C) Stage 3 AKI
D) No AKI present
Correct Answer: B
Calculation: 2.8 ÷ 1.1 = 2.5× baseline creatinine increase. This meets criteria for Stage 2 AKI (2.0-2.9× baseline).
📚 Reference: Interactive KDIGO Calculator
Calculation: 2.8 ÷ 1.1 = 2.5× baseline creatinine increase. This meets criteria for Stage 2 AKI (2.0-2.9× baseline).
📚 Reference: Interactive KDIGO Calculator
9
The BUN:Creatinine ratio of 30:1 in this patient is elevated. Which factors can cause an elevated BUN:Cr ratio independent of prerenal azotemia?
A) Only prerenal azotemia causes BUN:Cr >20:1
B) GI bleeding, high protein intake, steroids, and tissue catabolism
C) Acute tubular necrosis typically causes high BUN:Cr ratios
D) Glomerulonephritis is the most common cause
Correct Answer: B
Clinical Pearl: While BUN:Cr >20:1 suggests prerenal azotemia, multiple other factors can elevate this ratio:
• GI bleeding: Blood proteins are digested → increased urea production
• High protein intake: Increased amino acid metabolism → more urea
• Corticosteroids: Enhance protein catabolism and urea synthesis
• Tissue catabolism: Fever, infection, trauma, burns increase protein breakdown
• Dehydration: Concentrates BUN more than creatinine
• Tetracyclines: Anti-anabolic effects increase BUN
Key Teaching: Always interpret BUN:Cr ratio in clinical context. In this case, the combination of volume depletion history + elevated ratio supports prerenal azotemia, but other causes must be considered in different clinical scenarios.
Clinical Pearl: While BUN:Cr >20:1 suggests prerenal azotemia, multiple other factors can elevate this ratio:
• GI bleeding: Blood proteins are digested → increased urea production
• High protein intake: Increased amino acid metabolism → more urea
• Corticosteroids: Enhance protein catabolism and urea synthesis
• Tissue catabolism: Fever, infection, trauma, burns increase protein breakdown
• Dehydration: Concentrates BUN more than creatinine
• Tetracyclines: Anti-anabolic effects increase BUN
Key Teaching: Always interpret BUN:Cr ratio in clinical context. In this case, the combination of volume depletion history + elevated ratio supports prerenal azotemia, but other causes must be considered in different clinical scenarios.
10
The combination of hypernatremia (148 mEq/L) and hypochloremia (118 mEq/L) in this patient indicates:
A) Laboratory error
B) Hypotonic fluid losses from diarrhea
C) Diabetes insipidus
D) Syndrome of inappropriate ADH secretion
Correct Answer: B
Learning Point: Diarrheal fluid has lower sodium and higher chloride than plasma. Loss of hypotonic fluid leads to hypernatremia, while chloride losses exceed sodium losses, causing hypochloremia.
📚 Reference: Sodium Disorders Module
Learning Point: Diarrheal fluid has lower sodium and higher chloride than plasma. Loss of hypotonic fluid leads to hypernatremia, while chloride losses exceed sodium losses, causing hypochloremia.
📚 Reference: Sodium Disorders Module
Urinalysis Results
Dipstick Results
- Specific Gravity: 1.030 (high)
- Protein: Trace
- Blood: Negative
- Leukocyte Esterase: Negative
- Nitrites: Negative
Microscopy
- RBCs: 0-2/hpf
- WBCs: 0-5/hpf
- Casts: Occasional hyaline casts
- Crystals: None
- Bacteria: None
🔬 Urinalysis Interpretation Questions
11
The finding of "occasional hyaline casts" in this patient's urine microscopy is:
A) Pathological and suggests acute tubular necrosis
B) Normal finding that supports prerenal AKI
C) Indicative of glomerulonephritis
D) Sign of urinary tract infection
Correct Answer: B
Learning Point: Hyaline casts are composed of Tamm-Horsfall protein and can be normal or seen in prerenal states. They distinguish from muddy brown granular casts seen in ATN.
📚 Reference: Microscopic Examination
Learning Point: Hyaline casts are composed of Tamm-Horsfall protein and can be normal or seen in prerenal states. They distinguish from muddy brown granular casts seen in ATN.
📚 Reference: Microscopic Examination
12
The specific gravity of 1.030 in this urinalysis indicates:
A) Intact urinary concentrating ability
B) Acute tubular damage
C) Chronic kidney disease
D) Diabetes insipidus
Correct Answer: A
Learning Point: High specific gravity (>1.020) indicates intact concentrating ability, supporting prerenal AKI. In ATN, specific gravity is typically around 1.010-1.012 (isosthenuria).
Learning Point: High specific gravity (>1.020) indicates intact concentrating ability, supporting prerenal AKI. In ATN, specific gravity is typically around 1.010-1.012 (isosthenuria).
Interactive Diagnostic Timeline
Work through the diagnostic process step-by-step by clicking on each time point
🚨 Emergency Department Arrival (Time 0)
Patient presents confused, hypotensive, and tachycardic. What are your immediate priorities?
Immediate Priorities:
- ABC Assessment: Ensure airway, breathing, circulation
- IV access: Large bore IV for fluid resuscitation
- STAT labs: BMP, CBC, urinalysis with microscopy
- ECG: Check for hyperkalemia (K+ 5.2 mEq/L)
- Bladder scan: Rule out urinary retention/obstruction
Clinical Pearl: In elderly patients with AKI, always check for obstruction first - it's the most rapidly reversible cause.
📊 Laboratory Results Available (Time 30 minutes)
Labs show creatinine 2.8 mg/dL (baseline 1.1), BUN 84, K+ 5.2. What's your next step?
Next Steps Based on Labs:
- Confirm AKI: 2.5× baseline increase = Stage 2 AKI
- Assess prerenal pattern: BUN:Cr ratio 30:1 suggests prerenal
- Monitor K+: 5.2 mEq/L - recheck in 4-6 hours, avoid potassium
- Order fresh urinalysis: Essential for differentiation
- Calculate FENa: Will help confirm prerenal vs intrinsic
⚠️ Key Learning: Don't just look at creatinine - the pattern of abnormalities tells the story!
🔬 Fresh Urinalysis Results (Time 60 minutes)
Urinalysis shows specific gravity 1.030, occasional hyaline casts, no muddy brown casts. What does this tell you?
Urinalysis Interpretation:
- Specific gravity 1.030: Intact concentrating ability → supports prerenal
- Hyaline casts only: Normal finding in prerenal states
- Absence of muddy brown casts: Rules against ATN
- No RBC casts: Rules against glomerulonephritis
- No WBC casts: Rules against acute interstitial nephritis
Conclusion: Urinalysis strongly supports prerenal AKI diagnosis.
📚 Reference: Urinalysis Interpretation Guide
💉 FENa Calculation (Time 90 minutes)
Additional urine studies: Urine Na+ 15 mEq/L, Urine Cr 45 mg/dL. Calculate and interpret FENa.
FENa Calculation:
Formula: FENa = (UNa × SCr) / (SNa × UCr) × 100
Calculation: (15 × 2.8) / (148 × 45) × 100 = 42/6660 × 100 = 0.6%
Interpretation:
- FENa <1%: Suggests prerenal AKI
- FENa >2%: Suggests intrinsic AKI (ATN)
- FENa 1-2%: Intermediate/indeterminate
⚠️ Important Caveat: FENa can be <1% in some cases of ATN (contrast, sepsis, burns). Clinical context is crucial!
📚 Interactive Tool: FENa Calculator with Clinical Caveats
Treatment Decision Making
13
Given the diagnosis of prerenal AKI, what is the MOST important initial treatment intervention?
A) Immediate hemodialysis
B) Cautious IV fluid resuscitation
C) High-dose loop diuretics
D) Vasopressor support
Correct Answer: B
Treatment Rationale: Prerenal AKI responds to volume repletion. In elderly patients, start with 250-500mL boluses with frequent reassessment to avoid volume overload.
Treatment Rationale: Prerenal AKI responds to volume repletion. In elderly patients, start with 250-500mL boluses with frequent reassessment to avoid volume overload.
14
Which medications should be immediately discontinued in this patient?
A) Metformin only
B) Lisinopril only
C) Lisinopril and ibuprofen
D) All medications should be held
Correct Answer: D
Comprehensive Medication Management in AKI:
• Lisinopril (ACE inhibitor): Hold - impairs efferent arteriolar autoregulation, can worsen GFR in volume-depleted states
• Ibuprofen (NSAID): Hold - blocks prostaglandin-mediated afferent arteriolar dilation, highly nephrotoxic in volume depletion
• Metformin: Hold - contraindicated when creatinine >1.5 mg/dL (men) or >1.4 mg/dL (women) due to lactic acidosis risk. Current creatinine 2.8 mg/dL makes this dangerous
Key Teaching: In AKI, comprehensive medication review is essential. All potentially nephrotoxic medications should be held, and renally eliminated drugs need dose adjustment. Metformin accumulation with decreased clearance can cause fatal lactic acidosis.
📚 Reference: Complete AKI Drug Management Guide
Comprehensive Medication Management in AKI:
• Lisinopril (ACE inhibitor): Hold - impairs efferent arteriolar autoregulation, can worsen GFR in volume-depleted states
• Ibuprofen (NSAID): Hold - blocks prostaglandin-mediated afferent arteriolar dilation, highly nephrotoxic in volume depletion
• Metformin: Hold - contraindicated when creatinine >1.5 mg/dL (men) or >1.4 mg/dL (women) due to lactic acidosis risk. Current creatinine 2.8 mg/dL makes this dangerous
Key Teaching: In AKI, comprehensive medication review is essential. All potentially nephrotoxic medications should be held, and renally eliminated drugs need dose adjustment. Metformin accumulation with decreased clearance can cause fatal lactic acidosis.
📚 Reference: Complete AKI Drug Management Guide
15
What is the target urine output for this 62 kg patient during initial resuscitation?
A) >15 mL/hr
B) >31 mL/hr (0.5 mL/kg/hr)
C) >62 mL/hr (1.0 mL/kg/hr)
D) >124 mL/hr (2.0 mL/kg/hr)
Correct Answer: B
Calculation: Target urine output = 0.5 mL/kg/hr × 62 kg = 31 mL/hr minimum. This is the threshold below which oliguria is defined in AKI staging.
Calculation: Target urine output = 0.5 mL/kg/hr × 62 kg = 31 mL/hr minimum. This is the threshold below which oliguria is defined in AKI staging.
Clinical Course & Teaching Points
Hospital Day 1-6 Summary:
- Day 1-2: Total 2.5L normal saline over 24 hours, nephrotoxins discontinued
- Day 2: Creatinine peaked at 3.1 mg/dL, urine output improved to 1.2 mL/kg/hr
- Day 3-5: Progressive improvement, mental status cleared
- Day 6 Discharge: Creatinine 1.4 mg/dL (approaching baseline)
🎯 Final Assessment Questions
16
The fact that creatinine continued to rise to 3.1 mg/dL on Day 2 despite adequate resuscitation indicates:
A) Treatment failure
B) Expected lag time in creatinine response
C) Development of acute tubular necrosis
D) Need for immediate dialysis
Correct Answer: B
Learning Point: Creatinine may continue to rise for 24-48 hours after adequate resuscitation in prerenal AKI due to the time needed for improved GFR to reflect in serum creatinine levels. Monitor urine output as an earlier indicator of response.
Learning Point: Creatinine may continue to rise for 24-48 hours after adequate resuscitation in prerenal AKI due to the time needed for improved GFR to reflect in serum creatinine levels. Monitor urine output as an earlier indicator of response.
17
When should ACE inhibitor therapy be resumed in this patient?
A) Immediately upon discharge
B) When creatinine returns to baseline
C) 1-2 weeks after discharge with stable kidney function
D) Never - permanently contraindicated
Correct Answer: C
Management Strategy: Resume ACE inhibitor gradually once volume status is stable and kidney function has recovered. Start at low dose with close monitoring. The drug isn't permanently contraindicated but requires careful management.
Management Strategy: Resume ACE inhibitor gradually once volume status is stable and kidney function has recovered. Start at low dose with close monitoring. The drug isn't permanently contraindicated but requires careful management.
18
What is the most important long-term prevention strategy for this patient?
A) Permanent discontinuation of all antihypertensive medications
B) Patient education about NSAID avoidance and sick day management
C) Prophylactic low-dose furosemide
D) Monthly creatinine monitoring
Correct Answer: B
Prevention Focus: Education is key - avoid NSAIDs permanently, hold ACE inhibitors during illnesses with poor oral intake, maintain adequate hydration during GI illnesses, and seek early medical attention for concerning symptoms.
Prevention Focus: Education is key - avoid NSAIDs permanently, hold ACE inhibitors during illnesses with poor oral intake, maintain adequate hydration during GI illnesses, and seek early medical attention for concerning symptoms.
Learning Objectives Assessment
Evaluate your mastery of the key learning objectives from this case
🎯 Learning Objective 1: KDIGO AKI Staging
Objective: Apply KDIGO criteria to stage AKI severity and determine appropriate monitoring and management strategies.
19
A 70-year-old man has baseline creatinine 1.5 mg/dL. Today his creatinine is 4.8 mg/dL. What KDIGO stage and immediate actions are indicated?
A) Stage 2 AKI - standard monitoring
B) Stage 3 AKI - consider nephrology consult and RRT evaluation
C) Stage 1 AKI - continue current management
D) CKD progression - no acute intervention needed
Correct Answer: B
Rationale: 4.8 ÷ 1.5 = 3.2× baseline = Stage 3 AKI. Also, creatinine ≥4.0 mg/dL automatically qualifies as Stage 3. This requires urgent nephrology consultation and RRT readiness.
📚 Master This: KDIGO Interactive Calculator
Rationale: 4.8 ÷ 1.5 = 3.2× baseline = Stage 3 AKI. Also, creatinine ≥4.0 mg/dL automatically qualifies as Stage 3. This requires urgent nephrology consultation and RRT readiness.
📚 Master This: KDIGO Interactive Calculator
🎯 Learning Objective 2: Prerenal vs Intrinsic AKI Differentiation
Objective: Use clinical presentation, laboratory findings, and urinalysis to distinguish prerenal from intrinsic AKI.
20
Which combination of findings MOST strongly suggests intrinsic AKI rather than prerenal?
A) BUN:Cr 25:1, FENa 0.8%, hyaline casts
B) BUN:Cr 15:1, FENa 3.2%, muddy brown granular casts
C) Urine osmolality 600 mOsm/kg, specific gravity 1.025
D) Volume depletion, hypotension, tachycardia
Correct Answer: B
Key Teaching: Muddy brown granular casts are pathognomonic for ATN. Combined with FENa >2% and lower BUN:Cr ratio, this strongly indicates intrinsic AKI.
📚 Master This: Urinalysis Interpretation Guide
Key Teaching: Muddy brown granular casts are pathognomonic for ATN. Combined with FENa >2% and lower BUN:Cr ratio, this strongly indicates intrinsic AKI.
📚 Master This: Urinalysis Interpretation Guide
🎯 Learning Objective 3: Drug-Induced AKI Prevention
Objective: Identify high-risk medication combinations and implement prevention strategies to reduce AKI risk.
21
An 75-year-old woman with CKD (eGFR 45) is prescribed vancomycin and piperacillin-tazobactam for pneumonia. What is the estimated AKI risk and best prevention strategy?
A) Low risk (5%) - no special precautions needed
B) High risk (25-40%) - consider alternative antibiotics and AUC-guided dosing
C) Moderate risk (10-15%) - standard monitoring sufficient
D) Contraindicated combination - must avoid
Correct Answer: B
High-Risk Combination: Vancomycin + piperacillin-tazobactam has 25-40% AKI risk, especially in elderly with CKD. Consider vancomycin + cefepime or AUC-guided vancomycin dosing with extended-infusion piperacillin-tazobactam.
📚 Master This: Drug Nephrotoxicity Calculator
High-Risk Combination: Vancomycin + piperacillin-tazobactam has 25-40% AKI risk, especially in elderly with CKD. Consider vancomycin + cefepime or AUC-guided vancomycin dosing with extended-infusion piperacillin-tazobactam.
📚 Master This: Drug Nephrotoxicity Calculator
Case Reflection & Multi-Module Integration
🚨 AKI Module Integration
- KDIGO staging application in real patient
- Emergency recognition protocols
- Systematic diagnostic approach
- Prerenal AKI pathophysiology
- Furosemide stress test principles
🔬 Urinalysis Module Integration
- Microscopy prioritization over dipstick
- Fresh specimen importance (<2 hours)
- FENa calculation and limitations
- Hyaline vs granular cast differentiation
- Clinical context integration
💊 Drug Nephrotoxicity Integration
- NSAID mechanism in volume depletion
- ACE inhibitor effects on autoregulation
- "Triple threat" concept application
- Risk stratification tools
- Prevention strategies implementation
⚡ Electrolyte Module Integration
- Volume depletion assessment
- Hypernatremia from hypotonic losses
- Hypochloremia from diarrhea
- Metabolic acidosis evaluation
- Potassium monitoring in AKI
🎯 Key Integration Concepts
This case demonstrates how nephrology knowledge integrates across multiple domains. The systematic approach to AKI requires understanding kidney physiology, pharmacology, fluid and electrolyte balance, and laboratory interpretation. Real clinical excellence comes from synthesizing these different knowledge areas into coherent diagnostic and treatment strategies.
💡 Clinical Integration
How different body systems interact during illness and how medications can disrupt normal physiology
🔍 Diagnostic Integration
Using multiple data sources (history, exam, labs, urine) to build a complete clinical picture
🛡️ Prevention Integration
How understanding pathophysiology leads to effective prevention strategies for future episodes
📝 Case Summary & Clinical Pearls
This case exemplifies prerenal AKI in an elderly patient with the perfect storm of volume depletion, ACE inhibitor use, and NSAID nephrotoxicity. The systematic approach using KDIGO staging, laboratory interpretation, and evidence-based fluid resuscitation led to complete recovery.
🔑 Key Clinical Pearls from This Case:
- The "Triple Threat": ACE-I + NSAID + Volume Depletion = High AKI Risk
- Microscopy is King: Fresh urine microscopy differentiates AKI causes better than any other test
- Creatinine Lag: May continue rising 24-48 hours after successful treatment - don't panic!
- Prevention Focus: Patient education about sick day management prevents future episodes
- Cautious Resuscitation: Elderly patients need smaller, more frequent fluid boluses with close monitoring