09.1 Acute kidney injury

Acute Kidney Injury (AKI)

• AKI is a sudden decrease in kidney function over hours or days, leading to inability to regulate fluids, electrolytes, and acid-base balance.
• It can progress to chronic kidney disease (CKD) if not resolved within 3 months.
• Diagnosis is based on a rapid rise in serum creatinine and reduced urine output (oliguria).
• Early detection improves outcomes.

Learning Objectives

• Objective 1: Define AKI and its diagnostic criteria.
• Objective 2: Differentiate between pre-renal, renal, and post-renal AKI causes.
• Objective 3: Explain the pathophysiological mechanisms in AKI development.
• Objective 4: Identify risk factors for AKI and prevention strategies.
• Objective 5: Evaluate methods for clinical assessment and management of AKI.

Key Concepts

• AKI: Sudden decline in kidney function disrupting fluid-electrolyte balance.
• Oliguria: Reduced urine output, often a sign of AKI.
• Prerenal AKI: Reduced renal perfusion without structural damage; reversible with restored perfusion.
• Renal AKI: Kidney structural damage affecting tubules, glomeruli, interstitium, or vasculature.
• Postrenal AKI: Urine outflow obstruction leading to increased pressure and reduced glomerular filtration rate (GFR).

Clinical Applications

• Case Study: 70-year-old with heart failure, starting NSAIDs, experiences oliguria and elevated creatinine.
• Diagnostic Approach: Assess for volume depletion, nephrotoxic drugs, obstruction symptoms. Include monitoring fluid status, checking creatinine/urea/electrolytes, and renal ultrasound.
• Treatment Options: Fluid resuscitation (prerenal), removing nephrotoxins (renal), and treating obstruction (postrenal).
• Complications/Management: Monitor for hyperkalemia, metabolic acidosis, and possible need for renal replacement therapy if medical management fails.

Pathophysiology

• Prerenal AKI: Hypovolemia, reduced cardiac output, or systemic vasodilation reduce renal perfusion.
• Renal AKI: Direct damage to kidney structures, often due to ischemia or nephrotoxins; proximal tubule and thick ascending loop of Henle are vulnerable to ischemia.
• Postrenal AKI: Obstruction of urinary outflow increases tubular pressure, reducing GFR and potentially causing irreversible damage if untreated.

Pharmacology

• Nephrotoxic Drugs: NSAIDs (constrict afferent arterioles), ACE inhibitors/ARBs (dilate efferent arterioles), aminoglycosides, and radiocontrast agents directly damage tubules or vessels.

Differential Diagnosis

• Prerenal: History of dehydration, hypovolemia, heart failure.
• Renal: History of drug exposure, systemic illness, or nephrotoxins.
• Postrenal: Indicates urinary obstruction, such as flank pain or anuria.

Investigations

• Serum Creatinine: Key diagnostic marker for AKI.
• Urine Output: Monitor for oliguria (less than 0.5 mL/kg/hour for more than 6 hours).
• Urinalysis: Prerenal: Normal sediment; Renal: Muddy brown casts or tubular epithelial cells; Postrenal: Red/white blood cells or crystals.
• Imaging: Renal ultrasound to identify postrenal obstruction.