Acute Kidney Injury (AKI) Lecture Notes

Introduction

• Acute Kidney Injury (AKI): An abrupt drop in urine output & an increase in serum creatinine.
• Three types of AKI:
  • Pre-renal: Due to reduced renal perfusion.
  • Intra-renal: Due to nephron injuries.
  • Post-renal: Due to urinary tract obstructions.
• AKI is a part of the clinical medicine section.

Definitions

• AKI Indicators:
  • Serum creatinine increase ≥ 0.3 mg/dL within 48 hours.
  • Serum creatinine ≥ 1.5 times baseline within 7 days.
  • Urine output ≤ 0.5 mL/kg/hr for over 6 hours (oliguria).

Types of AKI

Pre-renal AKI

• Cause: Reduced blood flow to kidneys.
• Mechanism: Reduced renal perfusion leads to decreased GFR & increased serum creatinine.
• Indicators:
  • Low effective arterial blood volume.
  • Intense renal vasoconstriction.
  • Renal artery obstruction.

Intra-renal AKI

• Cause: Damage to kidney structures (nephrons).
• Mechanism: Injury to glomeruli or tubules prevents normal filtration and secretion.
• Indicators: Nephron injury decreases GFR, increases serum creatinine, and reduces urine output.
• Types:
  • Acute Tubular Necrosis (ATN): Most common intra-renal cause, often due to ischemia or nephrotoxins.
  • Acute Interstitial Nephritis (AIN): Often medication-induced with fever, rash, and eosinophilia.
  • Glomerulonephritis: Includes ANCA vasculitis and immune complex diseases like lupus nephritis.

Post-renal AKI

• Cause: Urinary tract obstruction.
• Mechanism: Obstruction increases backflow pressure in nephrons, decreasing GFR.
• Indicators: Presence of hydronephrosis and hydroureter.

Pathophysiology

Pre-renal Pathophysiology

• Volume Reduction Causes: Hypovolemia, cardiorenal syndrome, hepatorenal syndrome.
• Renal Artery Obstruction: Atherosclerosis or fibromuscular dysplasia.
• Medicine Effects: NSAIDs and ACE inhibitors can cause vasoconstriction or dilation.

Intra-renal Pathophysiology

• ATN Causes: Ischemic or nephrotoxic insults.
• AIN Indicators: White blood cell casts & eosinophils.
• Glomerulonephritis Indicators: Hematuria, proteinuria, red blood cell casts.

Post-renal Pathophysiology

• Obstruction Sites: Proximal (renal pelvis, ureter) or distal (bladder, urethra).
• Indicators: Enlarged bladder, post-void residuals.

Complications of AKI

• Metabolic Acidosis: Due to decreased filtering of bicarbonate and secretion of protons.
• Hyperkalemia: Reduced potassium excretion, risk of AV block & ECG changes.
• Hypervolemia: Causes pulmonary edema, pleural effusion, peripheral edema.
• Uremia: High blood urea can lead to encephalopathy, pericarditis, platelet dysfunction.

Diagnosis

• AKI Confirmation: Elevated creatinine or oliguria.
• Post-renal Diagnosis: Ultrasound for hydronephrosis, bladder size assessment.
• Intra-renal vs. Pre-renal:
  • Pre-renal indicators: Low fractional excretion of sodium (FENa < 1%).
  • Intra-renal indicators: High FENa (>2%), urine microscopy for casts.
• Ferid Stress Test: Differentiate pre-renal vs. intra-renal.

Treatment

General Treatment

• Metabolic Acidosis: Sodium bicarbonate if pH < 7.2.
• Hyperkalemia: Loop diuretics, potassium binding resins.
• Hypervolemia: Loop diuretics.
• Uremia: Dialysis if severe.

Specific Treatments

• Pre-renal:
  • Hypovolemia: IV fluids.
  • Cardiorenal: Diuretics, afterload reducers, inotropes.
  • Hepatorenal: Albumin, octreotide, midodrine.
• Intra-renal:
  • ATN: Remove nephrotoxins, supportive care.
  • AIN: Discontinue offending drugs, steroids if needed.
  • Glomerulonephritis: Immunosuppressants.
• Post-renal:
  • Proximal Obstruction: Stenting or nephrostomy.
  • Distal Obstruction: Catheterization.

Conclusion

• AKI Management: Tailored based on type and cause.
• Monitoring: Critical for preventing complications and ensuring recovery.
• Resource Utilization: Use educational resources and clinical guidelines for optimal management.