7.1bi Intrarenal acute kidney injury (acute renal failure) - causes, symptoms & pathology - video 2

• Characterized by deterioration in kidney function.
• Manifested by an increase in serum creatinine level with or without reduced urine output.

Kidney Function and Structure

• Anatomy
  • Kidneys: left and right.
  • Renal artery supplies blood to kidneys.
  • Nephrons: functional units of kidneys.
  • Glomerulus: filters blood into nephron tubules.
• Processes in Nephrons
  • Filtration: Occurs in the glomerulus.
  • Reabsorption and Secretion: Nephron tubules process filtrate.
  • Excretion: Final product is urine.

Acute Kidney Injury Overview

• Rapid decrease in glomerular filtration rate.
• Results in abnormal fluid and electrolyte balance.
• Leads to azotemia (increased wastes like nitrogen and creatinine).

Clinical Diagnosis

• Diagnosed by an abrupt increase in serum creatinine.
• Creatinine is freely filtered and is not reabsorbed by nephrons.

Factors Affecting Glomerular Filtration

• Hydrostatic Pressure: Blood pressure.
• Colloid Osmotic Pressure: Opposing pressure to filtration.
• Fluid Pressure: Opposing pressure to filtration.

Causes of AKI

1. Pre-Renal Causes
   • Decreased perfusion to kidneys.
   • Hypovolemia, reduced cardiac output, reduced circulatory volume.
   • Impaired renal autoregulation (e.g., NSAIDs, ACE inhibitors).
   • Reversible but can lead to ischemia if prolonged.
2. Post-Renal Causes
   • Obstruction along urinary tract.
   • Causes include renal stones, prostate enlargement, cancers.
   • Can lead to increased serum creatinine.
3. Intra-Renal Causes
   • Glomerular Nephritis: Inflammation of glomerulus.
   • Tubular Disease: Includes acute tubular necrosis from prolonged ischemia.
   • Interstitial Disease: Inflammation of interstitial tissue.
   • Vascular Disease: Includes vasculitis, microangiopathic hemolytic anemia.

Pathophysiology of Intra-Renal AKI

• Tubular injury leads to epithelial casts formation.
• Inflammatory response results in leukocyte activation.
• Vasoconstriction exacerbates ischemia, vulnerable to nephrotoxins.

Investigations for AKI

• Blood Tests: Full blood count, electrolytes, urea, creatinine.
• Urine Tests: Urinalysis, urine microscopy, culture and sensitivity, urine casts.
• Imaging: Renal ultrasound, bladder scan, CT for obstructions.

Management of AKI

• Pre-Renal AKI: Fluid management (fluids if hypovolemic, diuretics if overloaded).
• Nephrotoxins: Avoidance is crucial.
• Underlying Causes: Treat infections, remove stones, relieve obstructions.
• Complications: Manage electrolyte imbalances, possible dialysis.

Indications for Dialysis

• AEIOU Criteria
  • A: Acidosis (refractory).
  • E: Electrolyte imbalance (severe hyperkalemia).
  • I: Intoxication (e.g., salicylate, lithium).
  • O: Overload (fluid overload).
  • U: Uremic complications (e.g., pericarditis, bleeding disorders).

Conclusion

• AKI involves complex interactions within the kidney’s filtration system.
• Early recognition and management are crucial to prevent progression and complications.

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