Acute kidney injury Study Guide

📖 Core Concepts Acute Kidney Injury (AKI): Sudden loss of kidney function ≤ 7 days, shown by ↑ serum creatinine or ↓ urine output. RIFLE Staging (Risk‑Injury‑Failure‑Loss‑End‑stage): Graded by % rise in creatinine or % fall in GFR and urine output thresholds. Prerenal vs. Intrinsic vs. Postrenal: Prerenal – ↓ renal perfusion → ↓ GFR. Intrinsic – Direct damage to glomeruli, tubules, interstitium. Postrenal – Obstruction ↑ upstream pressure → ↓ filtration. Key Lab Cut‑offs: ↑ 0.3 mg/dL (≥26.5 µmol/L) creatinine in 48 h or 1.5× baseline in 7 d. Urine output < 0.5 mL kg⁻¹ h⁻¹ for ≥ 6 h. --- 📌 Must Remember Incidence: 10‑15 % of all admissions; > 50 % in ICU. Risk Factors for Post‑op AKI: Pre‑op Cr > 1.2 mg/dL, combined valve + bypass surgery, emergency case, intra‑aortic balloon pump. BUN/Creatinine Ratio: ↑ > 20 suggests prerenal, but rises slowly (up to 24 h). Dialysis Triggers: refractory hyper‑K⁺, uncontrolled acidosis, fluid overload threatening respiration, refractory volume overload after fluids. Mortality: 20 % overall, up to 50 % in ICU. Long‑term Risk: 8.8‑fold higher chance of chronic kidney disease (CKD) after AKI. --- 🔄 Key Processes Diagnosing AKI Check serum creatinine change (≥0.3 mg/dL in 48 h or ≥1.5× baseline in 7 d). Record urine output; <0.5 mL kg⁻¹ h⁻¹ for 6 h = AKI. RIFLE Staging | Stage | Creatinine ↑ | GFR ↓ | Urine Output | |-------|--------------|-------|--------------| | Risk | ≥1.5× baseline | ↓ 25 % | < 0.5 mL kg⁻¹ h⁻¹ (6 h) | | Injury | ≥2× baseline | ↓ 50 % | < 0.5 mL kg⁻¹ h⁻¹ (12 h) | | Failure | ≥3× baseline or ≥4 mg/dL | ↓ 75 % | < 0.3 mL kg⁻¹ h⁻¹ (24 h) or anuria 12 h | | Loss | Persistent renal replacement > 4 wks | — | — | | End‑stage | RRT > 3 mo | — | — | Prerenal Management Give IV crystalloids (unless fluid‑overloaded). If MAP still low → vasopressor (norepinephrine). Add inotrope (dobutamine) for cardiogenic shock. Intrinsic Management (cause‑specific) Stop nephrotoxins. Treat glomerulonephritis/vasculitis with steroids ± cyclophosphamide ± plasma exchange. Postrenal Management Relieve obstruction: catheter, nephrostomy, surgery as needed. Dialysis Initiation (see above triggers). --- 🔍 Key Comparisons Prerenal AKI vs. Intrinsic AKI Perfusion: ↓ effective renal blood flow vs. structural damage. BUN/Cr Ratio: ↑ > 20 vs. usually normal (≈10‑15). Urine Microscopy: bland sediment vs. granular casts, RBC casts. Intermittent Hemodialysis vs. Continuous RRT Schedule: 3–4 h sessions vs. 24 h continuous. Hemodynamic stability: less stable with intermittent; continuous better tolerated in ICU. Outcomes: No clear mortality difference. Nephrotoxic Agents vs. Safe Fluids NS/Crystalloid: volume expansion, no nephrotoxicity. NSAIDs, aminoglycosides, iodinated contrast: afferent arteriole constriction or tubular toxicity. --- ⚠️ Common Misunderstandings “Creatinine rise = AKI” – Small rises (≥0.3 mg/dL) matter only if within 48 h; chronic CKD can have higher baseline. BUN/Cr ratio alone diagnoses prerenal – It can be misleading; consider timing and urine studies. All hyperkalemia needs dialysis – Only refractory or life‑threatening hyper‑K⁺ (ECG changes) after medical measures. Fluid restriction always helps – In prerenal AKI, restriction worsens hypoperfusion; give fluids unless overt overload. --- 🧠 Mental Models / Intuition “Perfusion‑Damage‑Obstruction” Triangle: Quickly place AKI into one of three boxes; each has a distinct treatment pathway. “RIFLE = 1‑2‑3‑4‑5”: Remember the numbers of creatinine rise (1.5×, 2×, 3×) to match Risk‑Injury‑Failure. “Kidney as a Sieve”: Prerenal: Not enough water → sieve clogs because of low pressure. Intrinsic: Sieve material damaged → leaks (electrolytes, waste). Postrenal: Sieve outlet blocked → back‑pressure stops flow. --- 🚩 Exceptions & Edge Cases Pregnant patients: Serum creatinine normally lower; a rise of 0.3 mg/dL may be more significant. Muscle wasting or malnutrition: Low baseline creatinine; a “normal” value may hide AKI. Rapidly rising BUN without creatinine: May reflect GI bleed or catabolism, not necessarily prerenal AKI. Contrast‑induced AKI: May occur even with adequate hydration if high‑osmolar agents used. --- 📍 When to Use Which Imaging: Start with renal ultrasound for suspected obstruction; proceed to CT/MRI if ultrasound nondiagnostic. Biopsy: Indicated when AKI is unexplained, kidneys are normal‑sized, or there is concurrent nephritic syndrome/systemic disease. Vasopressor choice: Norepinephrine first‑line for septic/hypotensive AKI; add vasopressin or phenylephrine if refractory. Dialysis modality: Choose continuous RRT for hemodynamically unstable ICU patients; intermittent hemodialysis for stable patients or scheduled outpatient sessions. --- 👀 Patterns to Recognize Low urine Na⁺ (<20 mmol/L) + high BUN/Cr → Prerenal. Urine Na⁺ >40 mmol/L + granular casts → Intrinsic ATN. Sudden oliguria after catheter removal or stone passage → Postrenal. Rapid rise in K⁺ + peaked T‑waves → Hyperkalemia needing urgent cardiac protection. --- 🗂️ Exam Traps “Creatinine ↑ 0.2 mg/dL = AKI” – Threshold is ≥ 0.3 mg/dL within 48 h. Choosing dialysis for any hyperkalemia – Only if refractory or ECG changes present. Assuming NSAIDs are safe if patient is euvolemic – NSAIDs can cause afferent constriction regardless of volume status. Confusing “Risk” stage with “Mild AKI” – Remember Risk = 1.5× Cr or 25 % GFR drop and urine output <0.5 mL kg⁻¹ h⁻¹ for 6 h. Believing BUN/Cr >20 always indicates prerenal – Can be elevated in GI bleed, high protein intake, or steroid use. ---