Acute renal failure

- kidneys retain sodium to preserve volume

• Pre-renal uraemia: < 20 mmol/L
• Acute tubular necrosis: > 30 mmol/L

• Pre-renal uraemia: < 1%
• Acute tubular necrosis: > 1%

*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100

• Pre-renal uraemia: < 35%
• Acute tubular necrosis: > 35%

**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100

• Pre-renal uraemia: >1.5 
• Acute tubular necrosis: <1.1
• (đảo giấu ><)

• Pre-renal uraemia: >10:1
• Acute tubular necrosis: <8:1

• Pre-renal uraemia: >1020
• Acute tubular necrosis: <1010

• Pre-renal uraemia: bland sediment
• Acute tubular necrosis: brown granular casts

• Pre-renal uraemia: Yes
• Acute tubular necrosis: No

• * Fall in renal blood flow (Pre renal azotemia):
• - The kidney conserves sodium in true volume depletion 
• - This adaptation is appropriate because the effective arterial blood volume is reduced. 

• * Damage to the renal tubules from a toxin or ischemia (Acute tubular necrosis)
• - The renal injury characteristic of ATN limits the normal capacity of the renal tubules to conserve fluid and electrolytes.
• - This limited ability to reabsorb sodium is caused by cell necrosis and possibly by translocation of the Na+-K+ ATPase from the basolateral (or blood) side of intact renal tubular cells to the luminal side

• - Renal arteries: Stenosis
• - Glomeruli: Glomerulonephritis
• - Tubules: Acute tubular necrosis
• - Interstitium: Drugs
• - Obstruct the flow of urine from the kidney