Acute Kidney Injury (AKI):

Definition:

• Sudden, severe decline in kidney function occurring within 48 hours. Often reversible if treated. (Formerly called Acute Kidney Failure)

Features:

• • Rapid reduction in glomerular filtration rate (GFR).
  • Leads to accumulation of nitrogenous wastes (urea, creatinine, ammonia, uric acid) in the blood (azotemia).
  • Disrupts fluid and electrolyte balance.
  • Causes metabolic acidosis due to retention of acids.

Effects on the Body:

• • Toxic wastes impair cell function in organs like the heart, brain, and skeletal muscles.
  • Imbalance of pH and electrolytes significantly influences heart rhythm and muscle function.

Causes of Acute Renal Injury:

• • Severe shock or circulatory failure:
    • Sudden decreased blood flow, e.g., any form of prolonged/untreated shock such as:
      • hypovolemic shock due to burns/injuries/hemorrhaging,
      • septic shock due to serious infections,
      • cardiogenic shock due to myocardial infarction.
      • Pathogenesis:
        • Drops blood flow significantly, causing ischemia.
        • Results in necrosis of the nephron cells.
        • Inflammation and white blood cell infiltration can cause obstruction.
  • Primary Lesions:
    • Trauma or infection causing inflammation and necrosis.
  • Nephrotoxins:
    • Drugs like NSAIDs, acetaminophen, and aspirin in overdose can damage renal nephrons.
    • Results in necrosis, inflammation, and obstruction of filtrate flow, reducing urine output.
  • Obstructions: Back pressure from obstructive stones or tumors.
    • Can be caused by blood clots, kidney stones, tumors, or scarring.
    • Blockage increases pressure, damages nephrons in a backward (retrograde) manner.
  • Secondary to rhabdomyolysis: Damage to skeletal muscles results in myoglobinemia, myoglobin accumulation damages nephron tubules and leads to myoglobinuria and brown-tinged urine
  • Secondary to Post-streptococcal Glomerulonephritis (PSGN):

• • • Upper respiratory infection (“Strep Throat”) with Group A beta-hemolytic Streptococcus can trigger glomerulonephritis
    • PSGN:  damage and inflammation to glomeruli due to accumulation of antibody complexes, causing inflammation and damage.

Pathological Features:

• • Necrosis: Death of nephron cells reduces filtration capacity.
  • Inflammation: White blood cells and edema further impair nephron function.
  • Obstruction of tubules: Increases backpressure, reduces urine output (oliguria).

Symptoms & Signs:

• • Oliguria: Reduced urine output (common in critically ill).
  • Accumulation of waste products (azotemia): elevated urea and creatinine.
  • Electrolyte imbalances, acid-base disturbances:
    • Metabolic acidosis: due to impaired hydrogen ion secretion.
    • Hyperkalemia: excess potassium in blood.
  • Toxic accumulation: Systemic effects including confusion, weakness, arrhythmias, respiratory issues.

Reversibility:

• • Often recoverable if the underlying cause is promptly treated.
  • Damage can be prevented or minimized if managed early.

Summary:

Acute kidney injury (AKI) occurs suddenly due to blood flow reduction (ischemia), infection, inflammation, toxin exposure, or obstruction, leading to nephron dysfunction, nephron death and kidney failure.  Signs and symptoms relate to the rapid accumulation of wastes and electrolyte imbalance in the bloodstream.  Prompt diagnosis and management are essential to prevent permanent damage.  Recognizing the causes and early signs allows prompt treatment—such as removing offending agents and supporting kidney function—to prevent irreversible damage.  Acute and toxic kidney injuries impair fluid, electrolyte, and waste balance, threatening life if not managed urgently.