Acute Kidney Injury

Acute Kidney Injury

1. Structure of uriniferous tubules

2. Function of uriniferous tubules

   • Proximal convoluted tubule
     • Early
     • Late
   • Loop of Henle
     • Thin descending
       • water reabsorption and solutes secretion --> hyperosmotic
     • Thin ascending
       • water impermeability and solute reabsorption --> hypoosmotic
     • Thick ascending
   • Distal convoluted tubule
     • Early
     • Late + collecting duct

3. Regulation of body fluid osmolarity

4. Causes of renal impairment

   • Pre-renal
   • Intrarenal
     • Tubular
       • Drugs, heavy metals, ethylene glycol, myoglobinuria, radiocontrast dye, urate
     • interstitial
       • Drug-induced hypersensitivity (e.g. NSAIDs, penicillin, and diuretics)
     • glomerular
   • Post-renal

5. Pathogenesis of Acute Tubular Necrosis

   • Injury and necrosis of tubular epithelial cells
     • Necrotic cells plug tubules; obstruction decreases GFR Brown granular casts are seen in the urine
       • Dysfunctional tubular epithelium results in decreased reabsorption of BUN (ratio < 15) (FENa>2%) (urine osm < 500 mOsm/kg)
   • ischemic
     • Proximal tubule and medullary segment of TAL are susceptible
   • Nephrotoxic
     • Proximal tubule is susceptible

6. Complications of Acute Kidney Injury

   • Hyperkalemia
   • Pulmonary edema
   • Metabolic acidosis
   • Hyperphosphatemia

7. Management of Acute Kidney Injury

   • Diuretics
     • CA inhibitors
       • Act on PCT
     • Osmotic diuretics
       • Act on PCT and thick ascending
     • Loop diuretics
       • Act on thick ascending (Na-2Cl-K transporter)
     • Thiazides
       • Early DCT
     • K sparing diuretics
       • Late DCT and collecting duct

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