# Clinical Cases: Acute Kidney Injury ## Case 1: Prerenal AKI from Volume Depletion ### Patient Presentation A 78-year-old male with heart failure and hypertension presents to the emergency department with weakness and decreased oral intake for 5 days following a gastrointestinal illness. He continued taking his furosemide throughout his illness. ### History of Present Illness - Diarrhea and vomiting for 5 days (now resolved) - Decreased appetite and fluid intake - Progressive weakness and lightheadedness - Continued all medications including furosemide 40 mg twice daily - Also takes lisinopril 20 mg daily ### Physical Examination - Blood pressure: 88/52 mmHg (baseline 130/80) - Heart rate: 108 bpm - Orthostatic: Unable to stand due to dizziness - Dry mucous membranes, poor skin turgor - Flat neck veins - Clear lungs, no peripheral edema ### Workup **Laboratory Studies:** - Baseline creatinine (1 month ago): 1.2 mg/dL - Current creatinine: 3.8 mg/dL - BUN: 68 mg/dL - BUN:Creatinine ratio: 18:1 - Sodium: 134 mEq/L - Potassium: 5.4 mEq/L - Urine sodium: 6 mEq/L - FENa: 0.3% - Urine osmolality: 620 mOsm/kg - Urinalysis: Specific gravity 1.028, no blood, no protein, hyaline casts only ### Diagnosis **Prerenal Acute Kidney Injury from Volume Depletion** ### Discussion This case illustrates classic prerenal AKI: - **KDIGO Criteria**: Creatinine rose from 1.2 to 3.8 mg/dL, representing more than 3x baseline within 7 days, meeting criteria for Stage 3 AKI. - **Intact Tubular Function**: The lecture describes how prerenal AKI reflects decreased perfusion with preserved tubular function. The kidney responds appropriately by maximally conserving sodium (FENa <1%, urine Na <20 mEq/L) and concentrating urine (osmolality >500 mOsm/kg). - **BUN:Creatinine Ratio**: The elevated ratio (>20:1) reflects enhanced urea reabsorption in the hypovolemic state. - **Contributing Factors**: Continued diuretics during volume losses, plus ACE inhibitor removing compensatory efferent arteriolar constriction, created a "triple whammy" effect as described in the lecture. - **Bland Sediment**: Hyaline casts only, without muddy brown casts or cellular elements, supports prerenal rather than intrinsic injury. ### Treatment - Hold furosemide and lisinopril - IV normal saline 1 liter bolus, then 150 mL/hour - Monitor urine output (goal >0.5 mL/kg/hour) - Creatinine improved to 1.6 mg/dL after 48 hours of hydration - Cautiously restart medications after recovery ### Clinical Pearl In prerenal AKI, laboratory indices reflect appropriate kidney responses to hypoperfusion: FENa <1%, urine sodium <20 mEq/L, concentrated urine, and BUN:Cr ratio >20:1. The rapid improvement after volume restoration confirms the diagnosis. If FENa remains low despite ATN (as with contrast or pigment nephropathy), consider using FEUrea (<35% suggests prerenal). --- ## Case 2: Acute Tubular Necrosis from Aminoglycosides ### Patient Presentation A 58-year-old male with endocarditis on IV gentamicin and ampicillin for 12 days presents with decreasing urine output. He was admitted with Enterococcus faecalis mitral valve endocarditis. ### History of Present Illness - Enterococcal endocarditis diagnosed 2 weeks ago - Started on ampicillin and gentamicin - Progressive decrease in urine output over past 3 days - No hypotensive episodes documented - No other nephrotoxic medications ### Physical Examination - Blood pressure: 128/76 mmHg - Heart rate: 82 bpm - Temperature: 37.2°C (afebrile) - Mild lower extremity edema - III/VI systolic murmur at apex - Lungs with bibasilar crackles ### Workup **Laboratory Studies:** - Baseline creatinine (admission): 1.0 mg/dL - Day 7 creatinine: 1.3 mg/dL - Day 12 creatinine: 2.8 mg/dL - BUN: 42 mg/dL - BUN:Creatinine ratio: 15:1 - Gentamicin trough: 2.8 mcg/mL (elevated, target <1) - Urine sodium: 52 mEq/L - FENa: 3.2% - Urine osmolality: 320 mOsm/kg - Urinalysis: Muddy brown granular casts, renal tubular epithelial cells ### Diagnosis **Aminoglycoside-Induced Acute Tubular Necrosis** ### Discussion This case demonstrates nephrotoxic ATN: - **Aminoglycoside Nephrotoxicity**: The lecture describes how aminoglycosides accumulate in proximal tubular cells over days of therapy. Toxicity is dose- and duration-dependent, typically manifesting after 5-7 days. - **Non-Oliguric Pattern**: Aminoglycoside ATN often presents with non-oliguric AKI and concentrating defect, as mentioned in the lecture. - **Laboratory Indices**: Unlike prerenal AKI, ATN shows impaired tubular function: FENa >2%, urine sodium >40 mEq/L, inability to concentrate urine (<350 mOsm/kg), and near-normal BUN:Cr ratio. - **Muddy Brown Casts**: The lecture identifies these as characteristic of ATN, representing degenerating tubular cells. - **Elevated Trough Levels**: Poor drug clearance led to accumulation, worsening the injury. ### Treatment - Discontinue gentamicin immediately - Switch to daptomycin monotherapy for enterococcal endocarditis - Supportive care with fluid management - Avoid additional nephrotoxins - Infectious disease and cardiology consultation - Monitor for recovery (typically 1-3 weeks) ### Clinical Pearl Aminoglycoside nephrotoxicity develops gradually over 5-7 days as the drug accumulates in proximal tubule cells. Monitor creatinine and drug levels closely. Non-oliguric AKI is typical, which may delay recognition. Once ATN is established, drug clearance decreases and levels rise further, creating a vicious cycle. --- ## Case 3: Acute Interstitial Nephritis from Proton Pump Inhibitor ### Patient Presentation A 54-year-old female presents with fatigue and mild flank discomfort. Laboratory studies ordered for pre-operative evaluation (elective knee replacement) revealed unexpected renal dysfunction. ### History of Present Illness - Routine pre-operative labs showed elevated creatinine - Mild bilateral flank discomfort for 2 weeks - No dysuria or gross hematuria - Started omeprazole 20 mg daily 3 months ago for GERD - No recent antibiotic use - No fever or rash reported ### Physical Examination - Blood pressure: 138/84 mmHg - Heart rate: 76 bpm - Temperature: 37.0°C - No rash - Mild bilateral costovertebral angle tenderness - No peripheral edema ### Workup **Laboratory Studies:** - Creatinine 1 year ago: 0.9 mg/dL - Current creatinine: 2.4 mg/dL - BUN: 34 mg/dL - WBC: 8,200/mcL with 6% eosinophils (480/mcL) - Urinalysis: 2+ protein, 25 WBC/hpf, no bacteria, occasional WBC casts - Urine eosinophils: Present (though low sensitivity) - Urine culture: Negative **Renal Biopsy:** - Interstitial edema with lymphocytic infiltrate and scattered eosinophils - Tubulitis present - No granulomas - Glomeruli normal ### Diagnosis **Proton Pump Inhibitor-Induced Acute Interstitial Nephritis** ### Discussion This case illustrates drug-induced AIN: - **PPI-Associated AIN**: The lecture notes that PPIs have emerged as an increasingly recognized cause of AIN, often with insidious onset weeks to months after starting therapy (unlike the 1-3 week onset typical of beta-lactams). - **Classic Triad Absent**: The lecture emphasizes that the complete triad of fever, rash, and eosinophilia occurs in <10% of cases. This patient had only mild eosinophilia. - **Sterile Pyuria with WBC Casts**: These findings support interstitial inflammation rather than infection. WBC casts are characteristic of AIN, as noted in the lecture. - **Idiosyncratic Reaction**: AIN is not dose-dependent; it represents a type IV hypersensitivity reaction where the drug acts as a hapten. - **Biopsy Findings**: Interstitial edema, lymphocytic infiltrate, tubulitis, and eosinophils confirm the diagnosis. ### Treatment - Discontinue omeprazole - Switch to H2 blocker (famotidine) for GERD - Observe for improvement over 1 week - If no improvement, start prednisone 1 mg/kg/day for 2-4 weeks with taper - Elective surgery postponed until renal function improves - Creatinine improved to 1.3 mg/dL at 3 weeks ### Clinical Pearl PPI-induced AIN has a longer latency period (weeks to months) compared to classic antibiotic-induced AIN. The absence of fever and rash is common, making clinical suspicion essential. Withdrawal of the offending agent is the cornerstone of treatment; steroids may accelerate recovery if improvement does not occur within 1 week. --- ## Image Reference For visual reference of AKI concepts, see: - Radiopaedia: [Acute tubular necrosis](https://radiopaedia.org/articles/acute-tubular-necrosis) - Histology and clinical information - Wikimedia Commons: [Kidney histology](https://commons.wikimedia.org/wiki/Category:Histology_of_kidney) - Normal and pathologic tubular structures - Radiopaedia: [Acute interstitial nephritis](https://radiopaedia.org/articles/acute-interstitial-nephritis) - Biopsy findings --- ## Learning Points 1. **FENa Distinguishes Prerenal from ATN**: FENa <1% with concentrated urine suggests prerenal AKI with intact tubular function; FENa >2% with isosthenuria suggests ATN. 2. **Urinary Sediment is Diagnostic**: Bland sediment (hyaline casts only) supports prerenal; muddy brown casts indicate ATN; WBC casts suggest AIN or pyelonephritis. 3. **Drug-Induced AIN Classic Triad is Rare**: Fever, rash, and eosinophilia together occur in <10% of cases. Maintain suspicion based on timing and clinical context. 4. **PPIs Have Delayed Onset AIN**: Unlike beta-lactams (1-3 weeks), PPI-induced AIN may develop months after starting therapy. 5. **AEIOU for Dialysis Indications**: Acidosis (refractory), Electrolytes (hyperkalemia), Intoxication (dialyzable toxins), Overload (volume), Uremia (symptomatic) - memorize these indications for emergency dialysis.