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Dr S. Ratnayake
BUN
UOP (<400ml/24hrs)
Causes
Prerenal
Postrenal
Obstruction
Renal
Acute tubular necrosis
Clinical features
Investigations
Commonest cause of ARF (50% of all cases) Clinical significance Reversible injury Early and proper management Complete recovery
2 types Ischemic ATN Nephrotoxic ATN In both types the changes are due to Tubular damage Persistent and severe disturbance in blood flow
Tubules are highly susceptible to ischemia and toxic damage due to High metabolic rate and high oxygen consumption rate Toxins are absorbed by tubular epithelium
Ischemia
Fluid leakage
Epithelial dysfunction
Tubular injury
Vasoconstriction
Irreversible injury
Necrosis Apoptosis
Tubuloglomerular feedback
Distal tubular Na
Oliguria
PCT - Straight portion Loop of Henle Thick ascending limb Multiple points with skip areas Loss of PT brush border Sloughing of epithelial cells Swelling and vacuolation
Flattened tubular epithelium Casts - DCT and collecting ducts With recovery - Regenerative changes with mitotic figures Interstitium Oedema Inflammatory cells Vessels Vasa recta Dilated with neutrophils Glomeruli No significant change
Commonly affect PCT Nonspecific changes or Specific changes in the tubular epithelium
Carbon tetrachloride - Lipid in cells Ethylene glycol - Hydropic degeneration Mercuric chloride Large acidophilic inclusions Desquamate and calcify
Clinical features
3 phases Initiation Maintenance Recovery
Initiation Due to transient blood loss Last about 36 hrs Slight reduction UOP with elevated BUN
Prognosis
Depends on the initiating event and damage to other organs With modern therapy - 95% recovery