📚 Nephrology — L3: Approach To Acute Kidney Injury (Aki)

📚 Lecture Overview

This lecture covers the comprehensive medical approach to Acute Kidney Injury (AKI), outlining its diagnostic criteria, epidemiological impact, and underlying pathophysiological mechanisms. It provides clinical frameworks to differentiate AKI subtypes (prerenal, intrinsic, and postrenal) and distinguishes AKI from chronic kidney disease (CKD). Finally, it details essential management strategies, complications, specific etiologies like rhabdomyolysis and contrast-induced nephropathy, and urgent indications for renal replacement therapy.

🎯 Key Concepts & Definitions

• Acute Kidney Injury (AKI): A rapid decline in kidney function defined by KDIGO criteria as a serum creatinine increase $≥ 0.3$ mg/dL within 48 hours, $≥ 1.5$ times baseline within 7 days, or urine output $< 0.5$ mL/kg/h for 6 hours.
• Prerenal AKI: A functional form of kidney injury caused by reduced renal perfusion and hypovolemia where the renal parenchyma remains structurally intact.
• Intrinsic AKI: Direct structural damage to the renal parenchyma involving the glomeruli, tubules (as in Acute Tubular Necrosis), interstitium, or blood vessels.
• Postrenal AKI: Kidney injury resulting from acute bilateral or unilateral urinary tract obstruction.
• Acute Tubular Necrosis (ATN): The most common intrinsic form of AKI resulting from prolonged ischemic or nephrotoxic parenchymal injury characterized by tubular cell death.
• Renal Replacement Therapy (RRT): Supportive artificial replacement of kidney function, usually via intermittent hemodialysis or continuous RRT, used for refractory complications.

📖 Main Content

1. Definition, Epidemiology & Pathogenesis

• AKI affects 1 in 5 adults and 1 in 3 children during hospital stays, with high prevalence among critically ill patients.
• KDIGO Diagnostic Criteria:
• Serum creatinine increase $≥ 0.3$ mg/dL in 48 hours
• Serum creatinine increase $≥ 1.5×$ baseline in 7 days
• Urine output $< 0.5$ mL/kg/h for 6 hours
• Subtypes of AKI:
• Prerenal: Reduced kidney perfusion (responsive to volume correction).
• Intrinsic: Injury to glomerulus, tubule, or vessels (e.g., ATN, acute tubulointerstitial nephritis).
• Postrenal: Urinary tract obstruction.
• Pathophysiology shifts from adaptive renal autoregulation to GFR drop and parenchymal injury if hypoperfusion persists.

2. Diagnostic Approach

• The diagnostic aim answers three questions: Is it AKI? What is the cause? How severe is it?
• Differentiation from CKD:
• Look for CKD signs: uremic facies, scratch marks, half and half nails, bone tenderness, and small kidneys on ultrasound.
• Identifying Causes:
• Use history, exam, urinalysis, urinary microscopy (for renal tubular epithelial cells and granular casts), and ultrasound.
• Renal biopsy indications: unexplained AKI, active urine sediment, or significant proteinuria/hematuria.
• Pitfalls in Staging: Serum creatinine lags behind acute changes and depends on muscle mass; urine output is often unmeasured outside the ICU.

3. Management & Specific Etiologies

• Management is primarily supportive: optimize volume, avoid nephrotoxins, treat complications, and address the root cause.
• Hemodynamic Support:
• Use crystalloids over colloids; prefer balanced sodium solutions over normal saline (avoids hyperchloremic acidosis).
• Avoid hydroxyethyl starches as they cause AKI.
• Administer vasopressors if hypotension persists post-volume resuscitation.
• Special Etiologies:
• Rhabdomyolysis: Skeletal muscle breakdown releasing myoglobin, causing cola-colored urine, positive blood on dipstick without RBCs, and elevated creatine kinase. Managed via aggressive fluids and dialysis.
• Tumor Lysis Syndrome: Characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia.
• Contrast-Induced Nephropathy: Occurs within 24-48 hours of IV contrast; high risk in CKD, diabetes, and dehydration.

4. Indications for Renal Replacement Therapy (RRT)

• Urgent Dialysis Indications (AEIOU):
• Refractory electrolyte imbalances (e.g., severe hyperkalemia)
• Severe metabolic acidosis
• Volume overload leading to pulmonary edema
• Uremic complications (encephalopathy, pericarditis, bleeding, persistent vomiting)
• Removal of toxic alcohols (methanol, ethylene glycol) or salicylates/lithium.

📊 Visual Learning

💡 Important Points to Remember

• KDIGO Creatinine criteria: Increase $≥ 0.3$ mg/dL in 48h OR $≥ 1.5×$ baseline in 7 days.
• KDIGO Urine Output criteria: $< 0.5$ mL/kg/h for 6 hours.
• Prerenal vs ATN: Prerenal is volume-responsive and functional; ATN involves established parenchymal cell injury.
• Dipstick vs Microscopy trap: Rhabdomyolysis shows positive blood on dipstick due to myoglobin, but zero RBCs on microscopy.
• Fluid choice: Use crystalloids (balanced solutions) over normal saline and colloids (avoid hydroxyethyl starches).
• CKD differentiation: Small kidneys on ultrasound, uremic signs (half-and-half nails, uremic facies), and anemia point toward chronic disease, not acute injury.
• Tumor lysis labs: Hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia.
• Contrast nephropathy: Occurs within 24–48 hours post-exposure; prevent with hydration in high-risk groups.
• Dialysis triggers: Severe refractory hyperkalemia, pulmonary edema, uremic encephalopathy, and severe metabolic acidosis.
• Prognosis: Uncomplicated AKI has a good prognosis, whereas septic AKI carries the highest mortality and risk of progression to CKD.

⚠️ Common Exam Questions

• The "Dipstick vs. Microscopy" Trick: Examiners love to present a patient with tea-colored urine and a positive blood dipstick, listing hematuria as an option. The correct answer relies on checking microscopy: if red blood cells are absent, suspect myoglobinuria (rhabdomyolysis) or hemoglobinuria rather than glomerular bleeding.
• Fluid Selection Traps: Questions frequently test fluid choices by offering normal saline or colloids like hydroxyethyl starch in septic or ischemic AKI. Remember that balanced solutions are preferred over normal saline (which causes hyperchloremic acidosis), and starches are strictly contraindicated.
• AKI vs CKD Differentiation: MCQs will describe a patient with high creatinine and small kidneys on ultrasound, asking for the diagnosis. Students often pick AKI, forgetting that small kidneys are a hallmark of chronic disease.

📦 Quick Review Checklist

I can define AKI and list the KDIGO criteria
I understand the physiological progression from prerenal hypoperfusion to ATN
I can differentiate between prerenal, intrinsic, and postrenal AKI
I know how to distinguish AKI from CKD using clinical signs and imaging
I can recognize the laboratory findings of rhabdomyolysis and tumor lysis syndrome
I know the indications for urgent renal replacement therapy (RRT)
I can outline initial management steps including fluid selection and nephrotoxin avoidance