Acute Kidney Injury (AKI): Causes, Stages, Urine Indices & Evidence-Based Management

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Below is your **complete, concise-but-exhaustive clinical reference** for **Acute Kidney Injury (AKI)** following your preferred structure (definition → pathophysiology → causes → clinical features → investigations incl. urine indices → KDIGO staging → differential diagnoses → full management incl. drug details → monitoring → counselling). --- # **Acute Kidney Injury (AKI): Causes, Stages, Urine Indices & Evidence-Based Management** --- ## **1. Definition** **Acute Kidney Injury (AKI)** = **abrupt decline in renal function** over **hours to days**, resulting in **rise in serum creatinine**, **fall in urine output**, or both. KDIGO criteria: 1. ↑ Serum creatinine by **≥0.3 mg/dL within 48 hours**, OR 2. ↑ Creatinine to **≥1.5× baseline within 7 days**, OR 3. **Urine output <0.5 mL/kg/hr for ≥6 hours**. --- ## **2. Pathophysiology** AKI occurs due to one or more mechanisms: ### **1) Renal hypoperfusion (Prerenal)** ↓ Renal blood flow → ↑ RAAS → afferent vasoconstriction → reduced GFR. ### **2) Intrinsic renal injury** * **ATN (Acute Tubular Necrosis)**: Ischemia or nephrotoxins → tubular epithelial necrosis → backleak of filtrate → ↓ GFR. * **AIN (Acute Interstitial Nephritis)**: Immune-mediated interstitial inflammation, usually drugs. * **Glomerular injury**: Immune complex or podocyte injury → ↓ filtration surface area. ### **3) Postrenal obstruction** ↑ Intraluminal pressure → ↓ GFR → hydronephrosis → ischemic tubular injury if prolonged. --- ## **3. Causes (Prerenal–Intrinsic–Postrenal)** ### **A. Prerenal AKI** * **Volume loss:** hemorrhage, vomiting, diarrhea, burns. * **Third spacing:** pancreatitis, sepsis. * **Reduced effective volume:** HF, cirrhosis, nephrotic syndrome. * **Drugs:** NSAIDs (afferent constriction), ACEi/ARBs (efferent dilation). ### **B. Intrinsic AKI** **1. ATN** * **Ischemic:** sepsis, prolonged hypotension, major surgery. * **Nephrotoxic drugs:** aminoglycosides, amphotericin B, cisplatin, contrast. * **Pigment injury:** rhabdomyolysis (myoglobin), hemolysis (Hb). **2. AIN** * Drugs (most common): PPIs, penicillins, cephalosporins, sulfonamides, NSAIDs. * Infection: CMV, EBV, strep. * Autoimmune: Sjögren, SLE. **3. Glomerulonephritis** * RPGN, IgA nephropathy, post-infectious GN, lupus Nephritis. ### **C. Postrenal AKI** * BPH, prostate cancer, ureteric stones, cervical cancer, retroperitoneal fibrosis, anticholinergic drugs → retention. --- ## **4. Clinical Features** * Oliguria/anuria * Volume overload: edema, hypertension * Uremic symptoms: nausea, confusion, pericarditis * Hyperkalemia manifestations: weakness, arrhythmias * In AIN → fever, rash, arthralgia, eosinophilia * In GN → hematuria, RBC casts, hypertension --- ## **5. Investigations & Urine Indices** ### **A. Basic Investigations** * **Serum creatinine, BUN** * **Electrolytes:** K⁺, Na⁺, HCO₃⁻ * **Urinalysis:** protein, blood, casts * **ABG** for metabolic acidosis * **Renal ultrasound** to rule out obstruction --- ### **B. Urine Indices (Key for Prerenal vs ATN)** | Parameter | Prerenal AKI | ATN | | ---------------------------- | ------------ | -------------------------- | | **Urine Na⁺** | <20 mEq/L | >40 mEq/L | | **FENa** | <1% | >2% | | **FEUrea** (if on diuretics) | <35% | >50% | | **Urine Osmolality** | >500 mOsm | <350 mOsm | | **Urine sediment** | Bland | Muddy brown granular casts | **Formulas:** * **FENa (%) =** (UNa × SCr ×100) / (SNa × UCr) * **FEUrea (%) =** (UUrea × SCr ×100) / (SUrea × UCr) --- ## **6. KDIGO Staging** | Stage | Serum Creatinine | Urine Output | | ----- | ------------------------------------------- | ----------------------------------- | | **1** | ↑ Cr 1.5–1.9× baseline OR ↑ ≥0.3 mg/dL | <0.5 mL/kg/hr for 6–12 h | | **2** | ↑ Cr 2–2.9× baseline | <0.5 mL/kg/hr ≥12 h | | **3** | ↑ Cr ≥3× baseline OR ≥4 mg/dL OR RRT needed | <0.3 mL/kg/hr ≥24 h OR anuria ≥12 h | --- ## **7. Differential Diagnosis** * CKD (small kidneys, chronic anemia, long duration) * Hepatorenal syndrome * Cardiorenal syndrome * Rhabdomyolysis-induced renal failure * Acute glomerulonephritis * Drug-induced AIN --- # **8. Management: Evidence-Based & Complete** ## **General Principles** 1. **Identify & treat underlying cause** 2. **Optimize hemodynamics** 3. **Avoid nephrotoxic drugs** 4. **Correct electrolyte & acid–base issues** 5. **Consider timely dialysis** --- ## **A. Management by Type** ### **1. Prerenal AKI** * **Isotonic fluids (NS) bolus:** 10–20 mL/kg, reassess perfusion. * Treat underlying: GI losses, hemorrhage, sepsis, HF. * Stop ACEi/ARBs, NSAIDs. --- ### **2. Intrinsic AKI** #### **ATN** * Supportive care (no proven drug reverses ATN). * Maintain MAP >65 mmHg (vasopressors if septic). * Avoid nephrotoxins. * Adequate hydration. #### **AIN** * Stop offending drug. * **Corticosteroids**: * **Prednisolone 1 mg/kg/day for 2–3 weeks**, then taper 4–6 weeks. * Indication: persistent AKI after drug withdrawal. #### **Glomerulonephritis** Treatment depends on cause; commonly: * **High-dose steroids (methylpred 500–1000 mg IV ×3 days)** * **Cyclophosphamide 0.5–1 g/m² monthly** * **Plasmapheresis** for anti-GBM, ANCA severe disease. --- ### **3. Postrenal AKI** * Bladder catheterization * Treat obstruction: * BPH → tamsulosin, catheter * Stones → stent/nephrostomy * Malignancy → stent or diversion --- ## **B. Electrolyte Management** ### **Hyperkalemia (life-threatening)** * **IV Calcium gluconate 10 mL of 10%** over 10 min (stabilizes myocardium). * **Insulin + Dextrose**: Regular insulin 10 units IV + 25 g glucose. * **Salbutamol nebulization** 10–20 mg. * **Loop diuretics** if volume overloaded. * **Dialysis** if refractory. --- ### **Metabolic Acidosis** * Sodium bicarbonate only if **pH <7.1** or severe hyperkalemia. * Dialysis if severe refractory acidosis. --- ## **C. Indications for Dialysis (AEIOU)** * **A**cidosis (pH <7.1) * **E**lectrolyte imbalance (K⁺ >6.5 not responding) * **I**ngestions (methanol, ethylene glycol, lithium, salicylates) * **O**verload (pulmonary edema refractory to diuretics) * **U**remia (pericarditis, encephalopathy, seizures) --- # **9. Drugs in AKI — Complete Prescribing Notes** ### **1. Furosemide** * **Indication:** Volume overload in AKI, pulmonary edema. * **MOA:** Inhibits NKCC2 in loop of Henle → natriuresis. * **Dose:** 20–80 mg IV; escalate up to 200 mg. * **PK:** Renal excretion; reduced efficacy in low GFR. * **Adverse Effects:** Hypokalemia, hypovolemia, ototoxicity. * **Contraindications:** Sulfa allergy (relative), dehydration. * **Interactions:** Aminoglycosides ↑ ototoxicity. * **Monitoring:** Urine output, electrolytes, weight. * **Counselling:** Report hearing changes, maintain hydration. ### **2. Prednisolone (AIN)** * **Indication:** Drug-induced AIN not improving after drug withdrawal. * **MOA:** Immunosuppression via T-cell inhibition. * **Dose:** 1 mg/kg/day. * **Side Effects:** Hyperglycemia, infections, GI bleed. * **Monitor:** BP, glucose, infections. ### **3. Vasopressors (Norepinephrine)** * **Indication:** Septic shock causing AKI. * **MOA:** α1 agonist → ↑ SVR. * **Dose:** 0.05–1 µg/kg/min. * **AE:** Arrhythmias, ischemia. * **Monitoring:** MAP goal ≥65. --- # **10. Monitoring in AKI** * Daily creatinine, urine output * Electrolytes every 4–6 h in severe AKI * Fluid balance chart * Watch for pulmonary edema * Avoid contrast; if required → hydration + N-acetylcysteine (controversial) --- # **11. Patient Counselling** * Maintain hydration * Avoid NSAIDs and unnecessary OTC drugs * Early reporting of ↓ urine output, swelling, breathlessness * If on steroids: glucose control, infection risk * Adherence to follow-ups & labs --- If you want, I can also generate **NEET PG–level 20–40 MCQs**, **case-based HTML-CSS-JS quiz**, **SEO-friendly title**, or **long-tail tags** for this topic.