# Clinical Cases: Acute Kidney Injury in Critical Illness

## Case 1: Sepsis-Associated AKI with Hyperkalemia

### Clinical Image
![ECG showing characteristic changes of hyperkalemia](case_01_image.jpg)
*Source: [Wikimedia Commons - ECG in Hyperkalemia](https://commons.wikimedia.org/wiki/File:ECG_in_hyperkalemia.svg) - CC BY-SA 3.0*

### Case Presentation
A 58-year-old man with type 2 diabetes mellitus is admitted to the ICU with septic shock secondary to a diabetic foot infection. His baseline creatinine is 1.2 mg/dL. On ICU day 2, despite adequate fluid resuscitation and vasopressor support achieving MAP greater than 65 mmHg, his creatinine rises to 3.8 mg/dL with urine output declining to 15 mL/hour (0.2 mL/kg/hr). Urinalysis shows muddy brown casts consistent with acute tubular necrosis. He meets KDIGO Stage 3 AKI criteria (creatinine greater than 3 times baseline). Review of his medications reveals recent aminoglycoside (gentamicin) and vancomycin exposure; vancomycin trough was 24 mcg/mL (supratherapeutic). Both nephrotoxins are discontinued and alternatives substituted. On day 3, morning labs reveal potassium of 6.8 mEq/L. ECG shows peaked T waves and widened QRS complexes (QRS 140 ms, baseline 90 ms). He receives immediate treatment: calcium gluconate 1g IV for cardiac membrane stabilization, regular insulin 10 units IV with D50 50 mL for intracellular potassium shift, and sodium polystyrene sulfonate 30g orally for potassium elimination. Repeat potassium 2 hours later is 5.9 mEq/L with improved ECG. Given his oliguric AKI with refractory hyperkalemia and developing metabolic acidosis (pH 7.22, bicarbonate 14 mEq/L), the decision is made to initiate continuous renal replacement therapy (CRRT). A dialysis catheter is placed in the right internal jugular vein, and CVVHDF is initiated with regional citrate anticoagulation. Over the following week, his sepsis resolves, and his kidney function gradually recovers. CRRT is discontinued on day 8, and he is discharged with creatinine of 1.8 mg/dL with plan for nephrology follow-up.

### Key Learning Points
- KDIGO AKI staging: Stage 1 (Cr 1.5-1.9x baseline or increase greater than 0.3 mg/dL), Stage 2 (Cr 2-2.9x baseline), Stage 3 (Cr greater than 3x baseline or greater than 4 mg/dL or RRT initiation)
- Hyperkalemia with ECG changes (peaked T waves, widened QRS, loss of P waves) is a medical emergency requiring immediate treatment: calcium for cardioprotection, insulin/glucose for shifting, binders for elimination
- Indications for RRT in AKI are summarized by AEIOU: Acidosis (refractory), Electrolytes (hyperkalemia with ECG changes), Intoxication, Overload (volume), Uremia (encephalopathy, pericarditis)
- Nephrotoxin exposure (aminoglycosides, vancomycin, contrast, NSAIDs) is a leading cause of AKI in the ICU; daily medication review and drug level monitoring are essential

---

## Case 2: Contrast-Induced AKI and CRRT Management

### Clinical Image
![CRRT machine and dialysis setup](case_02_image.jpg)
*Source: [Wikimedia Commons - Hemodialysis](https://commons.wikimedia.org/wiki/Category:Hemodialysis) - CC BY-SA 4.0*

### Case Presentation
A 70-year-old woman with chronic kidney disease stage 3b (baseline creatinine 2.4 mg/dL, eGFR 38) and coronary artery disease undergoes cardiac catheterization for unstable angina. Despite pre-procedure hydration with normal saline and use of low-osmolar contrast (150 mL total), her creatinine rises from 2.4 to 4.1 mg/dL on post-procedure day 2. Urine output decreases to 300 mL over 24 hours. Renal ultrasound shows no hydronephrosis. She is diagnosed with contrast-induced AKI (Stage 2 KDIGO). Her medications are reviewed: lisinopril and metformin are held. Nephrotoxins are avoided. Despite conservative management, by day 4 her creatinine peaks at 5.8 mg/dL, she develops pulmonary edema refractory to IV furosemide (no response to 160 mg IV), and her potassium rises to 5.6 mEq/L. Given volume overload unresponsive to diuretics and progressive AKI with oliguria, CRRT is initiated. A 13.5 French dialysis catheter is placed in the right femoral vein (internal jugular avoided due to her severe pulmonary edema requiring upright positioning). CVVHDF is started with citrate anticoagulation, effluent rate of 25 mL/kg/hour, and initial fluid removal goal of 100 mL/hour. Labs are monitored every 6 hours including ionized calcium (for citrate anticoagulation management). Over 48 hours, 4 liters of net fluid are removed, her respiratory status improves, and she no longer requires supplemental oxygen. After 5 days of CRRT, her urine output improves to 50 mL/hour, and CRRT is discontinued. She is discharged 10 days after catheterization with creatinine 3.2 mg/dL and follow-up with nephrology scheduled.

### Key Learning Points
- Contrast-induced AKI typically occurs 24-72 hours post-exposure; risk factors include pre-existing CKD, diabetes, volume depletion, high contrast volumes, and concurrent nephrotoxins
- Prevention strategies include pre-procedure hydration (isotonic saline), using minimal contrast volume, and avoiding concurrent nephrotoxins; evidence for N-acetylcysteine is limited
- CRRT is preferred over intermittent hemodialysis in hemodynamically unstable patients as it provides slower, more physiologic fluid and solute removal
- CRRT dosing targets effluent rate of 20-25 mL/kg/hour; regional citrate anticoagulation is preferred as it reduces bleeding risk while maintaining circuit patency

---

## Case 3: Rhabdomyolysis-Induced AKI

### Clinical Image
![Diagram showing kidney physiology and tubular function](case_03_image.jpg)
*Source: [Wikimedia Commons - Kidney](https://commons.wikimedia.org/wiki/Category:Kidney_diseases) - CC BY-SA 3.0*

### Case Presentation
A 32-year-old man is found unresponsive in his apartment after a suspected drug overdose. He was likely down for over 24 hours based on his last contact with family. On arrival, vital signs show heart rate 115 bpm, blood pressure 92/58 mmHg, respiratory rate 22/min, and temperature 38.1C. He is obtunded with GCS 8 and is intubated for airway protection. Physical examination reveals firm, swollen thighs and buttocks from prolonged immobilization on hard surfaces. Initial labs show: potassium 7.2 mEq/L, creatinine 4.8 mg/dL (baseline unknown, likely normal given age), CK greater than 40,000 U/L (markedly elevated), myoglobin 28,000 ng/mL, urine dipstick positive for blood but microscopy shows no RBCs (indicating myoglobinuria). ECG shows peaked T waves and QRS widening. He is diagnosed with rhabdomyolysis-induced AKI with severe hyperkalemia. Emergency treatment for hyperkalemia is initiated (calcium gluconate, insulin/glucose, albuterol). Aggressive IV fluid resuscitation with normal saline is started at 400 mL/hour targeting urine output of 200-300 mL/hour to dilute myoglobin and prevent tubular precipitation. A Foley catheter is placed for precise urine output monitoring. Despite initial fluid resuscitation, he remains oliguric at 20 mL/hour after 4 liters of fluid, and his potassium remains 6.4 mEq/L. Given refractory hyperkalemia with ECG changes and oliguric AKI unresponsive to fluids, emergent hemodialysis is initiated. He requires dialysis for 4 sessions over 8 days, after which his kidney function recovers (creatinine 1.4 mg/dL at discharge). CK trends down appropriately with aggressive hydration.

### Key Learning Points
- Rhabdomyolysis causes AKI through myoglobin-induced tubular toxicity, renal vasoconstriction, and tubular obstruction; CK greater than 5,000-10,000 U/L carries significant AKI risk
- Myoglobinuria causes positive urine dipstick for blood without RBCs on microscopy (dipstick detects heme in both hemoglobin and myoglobin)
- Treatment of rhabdomyolysis focuses on aggressive IV crystalloid resuscitation targeting urine output 200-300 mL/hour to dilute myoglobin; bicarbonate for urine alkalinization is controversial
- Indications for RRT in rhabdomyolysis are the same as other AKI: refractory hyperkalemia, acidosis, volume overload, or uremic symptoms