# Clinical Cases: Acute Kidney Injury

## Case 1: Prerenal AKI

### Patient Presentation
A 78-year-old woman is brought from a nursing home with altered mental status and decreased oral intake for 3 days. Staff reports she has been febrile and had multiple episodes of diarrhea. Her medical history includes hypertension, heart failure (EF 35%), and type 2 diabetes. Medications include lisinopril, furosemide, and metformin.

### Vital Signs
- Blood Pressure: 88/52 mmHg
- Heart Rate: 108 bpm
- Respiratory Rate: 20/min
- Oxygen Saturation: 96% on room air
- Temperature: 38.4°C

### Physical Examination
- General: Lethargic, dry mucous membranes
- Cardiovascular: Tachycardic, flat JVP
- Pulmonary: Clear
- Abdomen: Soft, hyperactive bowel sounds
- Skin: Decreased turgor, dry axillae
- Neurologic: Oriented to person only

### Laboratory Results
- **Creatinine**: 3.2 mg/dL (baseline 1.1)
- **BUN**: 68 mg/dL
- **BUN/Cr ratio**: 21:1
- **Sodium**: 148 mEq/L
- **Potassium**: 5.4 mEq/L
- **Urinalysis**: SG 1.030, bland sediment, no protein
- **Urine sodium**: 8 mEq/L
- **FENa**: 0.4%
- **Lactate**: 3.8 mmol/L

### Clinical Image
![Prerenal AKI Diagram](image_01.png)
*Figure 1: Diagram illustrating the pathophysiology of prerenal AKI: decreased renal perfusion leads to reduced GFR while tubular function remains intact, resulting in low urine sodium and FENa.*

**Image Source**: Educational illustration for teaching purposes.

### Questions

1. **What are the KDIGO criteria for staging AKI?**
   - A) Based on BUN levels alone
   - B) Based on creatinine rise and/or urine output
   - C) Based on need for dialysis
   - D) Based on symptoms

2. **What laboratory findings support prerenal AKI in this patient?**
   - A) High urine sodium and high FENa
   - B) BUN/Cr ratio >20:1, low urine sodium (<20), low FENa (<1%), high urine specific gravity
   - C) Muddy brown casts
   - D) Hematuria and proteinuria

3. **What is this patient's AKI stage according to KDIGO?**
   - A) Stage 1
   - B) Stage 2
   - C) Stage 3
   - D) Not AKI

4. **What medications should be held in this patient?**

5. **What is the initial management priority?**

### Answers

1. **B) Based on creatinine rise and/or urine output**
   - Stage 1: Cr 1.5-1.9x baseline OR ≥0.3 mg/dL rise within 48h OR UOP <0.5 mL/kg/h for 6-12h
   - Stage 2: Cr 2.0-2.9x baseline OR UOP <0.5 mL/kg/h for ≥12h
   - Stage 3: Cr ≥3.0x baseline OR rise to ≥4.0 mg/dL OR UOP <0.3 mL/kg/h for ≥24h OR anuria ≥12h OR RRT initiation

2. **B) BUN/Cr ratio >20:1, low urine sodium (<20), low FENa (<1%), high urine specific gravity** - These indicate intact tubular function with appropriate sodium and water reabsorption in response to decreased perfusion. Concentrated urine (high SG) reflects ADH-mediated water retention.

3. **C) Stage 3** - Creatinine rose from 1.1 to 3.2 mg/dL, which is approximately 2.9x baseline, meeting Stage 3 criteria (≥3.0x baseline or ≥4.0 mg/dL).

4. **Medications to hold**:
   - **Lisinopril** (ACE inhibitor): Reduces efferent arteriolar tone, decreasing GFR in hypoperfused state
   - **Furosemide**: Worsens volume depletion
   - **Metformin**: Risk of lactic acidosis in AKI, contraindicated with eGFR <30
   - NSAIDs (if taking): Reduce prostaglandin-mediated afferent arteriolar dilation
   - Resume after renal function recovers

5. **Initial management**:
   - Aggressive IV fluid resuscitation (crystalloids)
   - Treat underlying cause (infection with diarrhea - consider antibiotics if bacterial)
   - Monitor urine output closely (Foley catheter)
   - Hold nephrotoxic medications
   - Repeat creatinine in 24-48 hours
   - Address hyperkalemia if it worsens
   - Expect creatinine to improve with volume repletion if prerenal

---

## Case 2: Intrinsic AKI - Acute Tubular Necrosis

### Patient Presentation
A 62-year-old man with a history of diabetes and peripheral vascular disease underwent aortic aneurysm repair 3 days ago. He had intraoperative hypotension requiring vasopressors and received IV contrast for preoperative imaging. His urine output has progressively decreased over the past 24 hours despite fluid resuscitation.

### Vital Signs
- Blood Pressure: 118/72 mmHg (on norepinephrine)
- Heart Rate: 88 bpm
- Respiratory Rate: 18/min
- Oxygen Saturation: 96% on 2L NC
- Temperature: 37.2°C
- Urine output: 180 mL in past 12 hours

### Physical Examination
- General: Sedated, intubated
- Cardiovascular: Regular rhythm, no murmurs, CVP 12 cmH2O
- Pulmonary: Bilateral crackles at bases
- Abdomen: Midline surgical incision, soft
- Extremities: Trace edema

### Laboratory Results
- **Creatinine**: 4.8 mg/dL (baseline 1.4, was 2.8 yesterday)
- **BUN**: 52 mg/dL
- **BUN/Cr ratio**: 11:1
- **Potassium**: 6.1 mEq/L
- **Bicarbonate**: 18 mEq/L
- **Urinalysis**: Muddy brown granular casts, renal tubular epithelial cells
- **Urine sodium**: 48 mEq/L
- **FENa**: 3.2%

### Clinical Image
![Muddy Brown Casts](image_02.png)
*Figure 2: Urine microscopy demonstrating muddy brown granular casts, pathognomonic for acute tubular necrosis.*

**Image Source**: Educational illustration for teaching purposes.

### Questions

1. **What urine findings are characteristic of acute tubular necrosis?**
   - A) Bland sediment with low urine sodium
   - B) Muddy brown granular casts, renal tubular epithelial cells, high urine sodium, FENa >2%
   - C) RBC casts and dysmorphic RBCs
   - D) White blood cell casts

2. **What are the likely causes of ATN in this patient?**
   - A) Glomerulonephritis
   - B) Ischemia (intraoperative hypotension) and nephrotoxin (contrast)
   - C) Obstructive uropathy
   - D) Interstitial nephritis

3. **What is the typical clinical course of ATN?**
   - A) Immediate recovery
   - B) Initiation (insult) → Extension → Maintenance (oliguria) → Recovery phases over 1-3 weeks
   - C) Permanent kidney failure
   - D) Fluctuating course

4. **What indications for renal replacement therapy (dialysis) are present or developing?**

5. **What preventive measures could have reduced the risk of contrast-induced nephropathy?**

### Answers

1. **B) Muddy brown granular casts, renal tubular epithelial cells, high urine sodium, FENa >2%** - These findings indicate tubular damage with loss of ability to reabsorb sodium. Muddy brown casts are composed of degenerating tubular cells and are pathognomonic for ATN.

2. **B) Ischemia (intraoperative hypotension) and nephrotoxin (contrast)** - This patient has multifactorial ATN from ischemic insult (prolonged hypotension during surgery) and contrast nephropathy. These are the two most common causes of ATN in hospitalized patients.

3. **B) Initiation (insult) → Extension → Maintenance (oliguria) → Recovery phases over 1-3 weeks** - ATN typically evolves through phases. Maintenance phase with oliguria lasts 1-2 weeks. Recovery with polyuria follows as tubules regenerate. Most patients recover if they survive the underlying illness.

4. **Indications for RRT (AEIOU)**:
   - **A**cidemia: Severe metabolic acidosis (pH <7.1) refractory to bicarbonate
   - **E**lectrolytes: Refractory hyperkalemia (6.1 mEq/L is concerning)
   - **I**ngestion: Toxic ingestions (not applicable here)
   - **O**verload: Volume overload refractory to diuretics
   - **U**remia: Uremic symptoms (encephalopathy, pericarditis, bleeding)
   - This patient has hyperkalemia and oliguria - may need RRT if not responsive to medical management

5. **Prevention of contrast-induced nephropathy**:
   - Pre-procedural volume expansion with IV isotonic crystalloid
   - Use of low-osmolar or iso-osmolar contrast agents
   - Minimizing contrast volume
   - Holding nephrotoxic medications (NSAIDs, ACE inhibitors) before procedure
   - Avoiding repeated contrast exposure within 48-72 hours
   - N-acetylcysteine (limited evidence, sometimes used)

---

## Case 3: Postrenal AKI - Obstructive Uropathy

### Patient Presentation
A 72-year-old man with a history of benign prostatic hyperplasia presents with 2 days of lower abdominal discomfort and inability to urinate. He reports feeling the urge to void but producing only small amounts of urine with significant straining. He has also had some nausea and decreased appetite.

### Vital Signs
- Blood Pressure: 152/88 mmHg
- Heart Rate: 82 bpm
- Respiratory Rate: 16/min
- Oxygen Saturation: 98% on room air
- Temperature: 37.0°C

### Physical Examination
- General: Mild discomfort
- Cardiovascular: Normal
- Pulmonary: Clear
- Abdomen: Distended lower abdomen, palpable bladder to umbilicus, suprapubic tenderness
- GU: Enlarged prostate on digital rectal exam (non-tender, smooth)

### Laboratory Results
- **Creatinine**: 5.2 mg/dL (baseline 1.0 from 6 months ago)
- **BUN**: 78 mg/dL
- **Potassium**: 5.8 mEq/L
- **Bicarbonate**: 19 mEq/L

### Imaging
- **Bladder scan**: Post-void residual 850 mL
- **Renal ultrasound**: Bilateral hydronephrosis, distended bladder

### Clinical Image
![Hydronephrosis Ultrasound](image_03.png)
*Figure 3: Renal ultrasound demonstrating moderate hydronephrosis with dilated renal pelvis and calyces secondary to bladder outlet obstruction.*

**Image Source**: Educational illustration for teaching purposes.

### Questions

1. **What is the first-line intervention for this patient?**
   - A) IV fluids
   - B) Hemodialysis
   - C) Urethral catheter placement
   - D) Emergent nephrostomy tubes

2. **What is post-obstructive diuresis and when does it occur?**
   - A) Decreased urine output after catheter removal
   - B) Massive diuresis (>200 mL/hr) after relief of obstruction, can lead to volume depletion
   - C) Inability to concentrate urine permanently
   - D) Rare complication of catheter placement

3. **What level of obstruction causes bilateral hydronephrosis?**
   - A) Unilateral ureteral stone
   - B) Bladder outlet or urethral obstruction
   - C) Renal pelvis obstruction
   - D) Single kidney obstruction

4. **How should post-obstructive diuresis be managed?**

5. **What are the causes of obstructive uropathy at each level?**

### Answers

1. **C) Urethral catheter placement** - The immediate priority is relieving the obstruction. Foley catheter placement will decompress the bladder and restore urine flow. This is both diagnostic and therapeutic.

2. **B) Massive diuresis (>200 mL/hr) after relief of obstruction, can lead to volume depletion** - Post-obstructive diuresis occurs after relief of bilateral obstruction or obstruction of a solitary kidney. It results from accumulated urea acting as an osmotic diuretic, impaired concentrating ability, and natriuretic peptide release.

3. **B) Bladder outlet or urethral obstruction** - Bilateral hydronephrosis indicates obstruction below the bladder (prostatic urethra, bladder neck) or at the bladder level. Unilateral obstruction (e.g., ureteral stone) causes unilateral hydronephrosis unless there is a solitary kidney.

4. **Management of post-obstructive diuresis**:
   - Monitor urine output closely (initially hourly)
   - Replace 50-75% of urine output with 0.45% saline if >200 mL/hour
   - Avoid over-replacement (can perpetuate diuresis)
   - Monitor electrolytes every 6-12 hours
   - Most cases resolve within 24-48 hours
   - Watch for hyponatremia, hypokalemia, hypomagnesemia

5. **Causes of obstructive uropathy by level**:
   - **Upper tract (kidney/ureter)**: Nephrolithiasis, malignancy (transitional cell, cervical, bladder), retroperitoneal fibrosis, ureteral stricture, blood clots
   - **Lower tract (bladder)**: Neurogenic bladder, bladder cancer, bladder stones
   - **Outlet (prostate/urethra)**: BPH (most common in older men), prostate cancer, urethral stricture, posterior urethral valves (pediatric)

---

## Learning Points

1. **AKI classification** using KDIGO criteria helps stage severity based on creatinine rise and urine output.

2. **FENa** helps differentiate prerenal (<1%) from intrinsic (>2%) AKI; however, it can be unreliable with diuretic use (use FEUrea instead).

3. **Urine sediment** provides critical diagnostic information: bland sediment (prerenal/postrenal), muddy brown casts (ATN), RBC casts (glomerulonephritis), WBC casts (pyelonephritis/interstitial nephritis).

4. **Postrenal AKI** is reversible with prompt relief of obstruction; renal ultrasound is the imaging modality of choice.

5. **Hold nephrotoxic medications** (ACE inhibitors, ARBs, NSAIDs, aminoglycosides) in AKI and reassess for resumption after recovery.