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Acute tubular necrosis

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Acute tubular necrosis
SpecialtyNephrology Edit this on Wikidata

Acute tubular necrosis or (ATN) is a medical condition involving the death of tubular cells that form the tubule that transports urine to the ureters while reabsorbing 99% of the water (and highly concentrating the salts and metabolic byproducts). Tubular cells continually replace themselves and if the cause of ATN is removed then recovery is likely. ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI.[1] The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN.[2]

Classification

It may be classified as either toxic or ischemic. Toxic ATN occurs when the tubular cells are exposed to a toxic substance (nephrotoxic ATN). Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition that they are highly sensitive and susceptible to, due to their very high metabolism.[3]

Diagnosis

Acute tubular necrosis is classified as a "renal" (i.e. not pre-renal or post-renal) cause of acute kidney injury. Diagnosis is made by a FENa (fractional excretion of sodium) > 3% and presence of muddy casts in urinalysis. On histopathology, there is usually tubulorrhexis, that is, localized necrosis of the epithelial lining in renal tubules, with focal rupture or loss of basement membrane.[4] Proximal tubule cells can shed with variable viability and not be purely "necrotic".[5][6][7][8][9]40_75%

Toxic ATN

Toxic ATN can be caused by free hemoglobin or myoglobin, by medication such as antibiotics such as aminoglycoside and cytoxic drugs such as cisplatin, or by intoxication (ethylene glycol, "anti-freeze").

Histopathology: Toxic ATN is characterized by proximal tubular epithelium necrosis (no nuclei, intense eosinophilic homogeneous cytoplasm, but preserved shape) due to a toxic substance (poisons, organic solvents, drugs, heavy metals). Necrotic cells fall into the tubule lumen, obturating it, and determining acute renal failure. Basement membrane is intact[citation needed], so the tubular epithelium regeneration is possible. Glomeruli are not affected.[1]

Ischemic ATN

Ischemic ATN can be caused when the kidneys are not sufficiently perfused for a long period of time (i.e. renal artery stenosis) or during shock. Hypoperfusion can also be caused by embolism of the renal arteries. Ischemic ATN specifically causes skip lesions through the tubules.[2]

See Also

Renal Cortical Necrosis

Acute Interstitial Nephritis

Renal Papillary Necrosis

References

  1. ^ a b "Acute Tubular Necrosis (ATN)". Nephrology Channel. HealthCommunities.com. 2008. Retrieved 2008-09-23.
  2. ^ a b Goldman, Lee; Cecil, Russell L. (2008). Cecil medicine. Philadelphia, PA: Saunders Elsevier. p. 705. ISBN 0-8089-2377-3. OCLC 191854838.{{cite book}}: CS1 maint: multiple names: authors list (link)
  3. ^ Goldman, Lee; Cecil, Russell L. (2008). Cecil medicine. Philadelphia, PA: Saunders Elsevier. ISBN 0-8089-2377-3. OCLC 191854838.{{cite book}}: CS1 maint: multiple names: authors list (link)[page needed]
  4. ^ TheFreeDictionary > tubulorrhexis Citing: The American Heritage Medical Dictionary 2007
  5. ^ Glynne PA, Picot J, Evans TJ (2001). "Coexpressed nitric oxide synthase and apical beta(1) integrins influence tubule cell adhesion after cytokine-induced injury". Journal of the American Society of Nephrology. 12 (11): 2370–83. PMID 11675413. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  6. ^ Glynne PA, Evans TJ (1999). "Inflammatory cytokines induce apoptotic and necrotic cell shedding from human proximal tubular epithelial cell monolayers". Kidney International. 55 (6): 2573–97. doi:10.1046/j.1523-1755.2002.t01-1-00456.x. PMID 10354308. {{cite journal}}: Unknown parameter |month= ignored (help)
  7. ^ Racusen LC (1998). "Epithelial cell shedding in acute renal injury". Clinical and Experimental Pharmacology & Physiology. 25 (3–4): 273–5. doi:10.1111/j.1440-1681.1998.t01-3-.x. PMID 9590582.
  8. ^ Solez K, Racusen LC, Marcussen N; et al. (1993). "Morphology of ischemic acute kidney injury, normal function, and cyclosporine toxicity in cyclosporine-treated renal allograft recipients". Kidney International. 43 (5): 1058–67. doi:10.1038/ki.1993.148. PMID 8510383. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  9. ^ Racusen LC, Fivush BA, Li YL, Slatnik I, Solez K (1991). "Dissociation of tubular cell detachment and tubular cell death in clinical and experimental 'acute tubular necrosis'". Laboratory Investigation. 64 (4): 546–56. PMID 1673163. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)


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