A 52-year-old man with hypertension and chronic kidney disease (baseline creatinine 1.8 mg/dL) is admitted with acute coronary syndrome. He receives aspirin, atorvastatin, and an ACE inhibitor. On day 2, he undergoes coronary angiography with iodinated contrast (150 mL). By day 4, his serum creatinine has risen to 3.4 mg/dL. Urine dipstick shows 2+ proteinuria and muddy brown casts. Urine sodium is 65 mEq/L and FENa is 3.2%. Urine osmolality is 320 mOsm/kg. What is the most likely diagnosis?

Explanation

## Clinical Diagnosis: Contrast-Induced Acute Tubular Necrosis (CI-ATN) ### Key Diagnostic Features **Key Point:** This patient has classic contrast-induced nephropathy (CIN) progressing to acute tubular necrosis (ATN), triggered by iodinated contrast in the setting of CKD and ACE inhibitor use. ### Diagnostic Criteria for CI-ATN | Feature | Finding | Interpretation | |---------|---------|----------------| | **Temporal relationship** | Creatinine rise 48–72 hrs post-contrast | Typical timing for CIN | | **Risk factors** | CKD (baseline Cr 1.8), ACE-I, contrast volume 150 mL | High-risk profile | | **FENa** | 3.2% (> 2%) | Indicates tubular dysfunction | | **Urine sodium** | 65 mEq/L (> 40) | Tubules cannot reabsorb Na^+^ | | **Urine osmolality** | 320 mOsm/kg (< 350) | Dilute urine; tubular concentrating ability lost | | **Urine sediment** | Muddy brown casts | Pathognomonic for ATN (pigmented casts from myoglobin or hemoglobin) | | **Proteinuria** | 2+ | Consistent with tubular injury | ### Pathophysiology of Contrast-Induced Nephropathy 1. **Direct tubular toxicity** — iodinated contrast is hyperosmolar (600–2000 mOsm/kg) 2. **Renal medullary ischemia** — contrast causes vasoconstriction → reduced oxygen delivery 3. **Oxidative stress** — generation of reactive oxygen species 4. **Tubular obstruction** — precipitation of contrast in tubular fluid 5. **Result:** Acute tubular necrosis with loss of tubular function ### Risk Stratification for CIN **High-Yield:** Risk factors for CIN include: - **Chronic kidney disease** (eGFR < 60) - **Diabetes mellitus** - **Volume depletion** - **Concomitant nephrotoxins** (NSAIDs, ACE-I/ARB in certain settings) - **High contrast volume** (> 100 mL) - **Age > 70 years** This patient has **≥ 3 major risk factors** (CKD, ACE-I, contrast volume 150 mL). ### Prevention and Management ```mermaid flowchart TD A[High-risk patient<br/>requiring contrast]:::outcome --> B[Assess eGFR]:::decision B -->|eGFR < 30| C[Avoid contrast if possible<br/>Consider alternative imaging]:::urgent B -->|eGFR 30-60| D[Minimize contrast volume<br/>Hold metformin 48 hrs]:::action D --> E[IV isotonic saline<br/>0.5-1 mL/kg/hr × 12 hrs pre & post]:::action B -->|eGFR > 60| F[Standard precautions]:::action E --> G[Hold ACE-I/ARB<br/>24-48 hrs post-contrast]:::action F --> G G --> H[Monitor Cr at 48-72 hrs]:::action ``` **Clinical Pearl:** Holding ACE inhibitors for 24–48 hours post-contrast reduces the risk of CIN in high-risk patients, because ACE-I impairs autoregulation of glomerular filtration in the setting of renal hypoperfusion. **Mnemonic: CI-ATN Risk Factors — CONTRAST** - **C**hronic kidney disease - **O**lder age (> 70) - **N**ephrotoxins (NSAIDs, ACE-I) - **T**ype 2 diabetes - **R**enal artery stenosis - **A**cute decompensation (volume depletion) - **S**evere proteinuria - **T**iming (high-volume contrast)