Acute tubular necrosis – Wikipedia

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The acute tubular necrosis (NTA or ATN) is a form of acute renal failure due to the death of tubular epithelial cells which form the renal tubule carrying the urine from glomerule to ureter and reabsorbent approximately 99% of water filtered by the kidneys ( This makes it possible to strongly concentrate salts and metabolic waste). Tubular cells are constantly renewing, if the cause of the NTA is deleted, renal recovery is likely. The NTA presents itself as an acute renal failure (IRA) and is one of the most common causes [ first ] . The presence of “pigmented grainy cylinders” in urine during urine analyzes is pathognomonic of an NTA [ 2 ] .

They can be classified according to their causes in toxic or ischemic. The toxic NTAs occur when the tubular cells are exposed to a toxic substance. Ischemic NTAs occur when tubular cells do not receive enough oxygen, a situation to which they are very sensitive because of their very high metabolism [ 3 ] .

The NTA is considered to be a “renal” disease (therefore not “pre-renal” or “post-renal”) causes acute renal failure. The diagnosis can be made by measuring the FENA (fraction of excretion of the filtered sodium) greater than 3 and the presence of pigmented granular cylinders with urine analysis. It should be noted that the proximal tube cells can defolish at a variable stage and are not purely “necrotic” [ 4 ] , [ 5 ] , [ 6 ] , [ 7 ] , [ 8 ] .

The toxic NTAs can be caused by free hemoglobin or myoglobin, by drugs such as antibiotics, iodized consistent products and cytostatic drugs, or by poisoning with glycol ethylene (“anti-gel”).

In histopathology, the toxic NTA is characterized by necrosis of proximal tubular epithelium (absence of nuclei with intense homogeneous cytoplasmic coloring and preserved form) due to toxic substances (poisons, organic solvents, drugs, heavy metals). Necrotic cells fall into the tubular light, obstruct it and cause acute renal failure. The basal membrane is intact, so that the regeneration of the tubular epithelium is possible. Glomerules are not affected [ first ] .

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The ischemic NTAs occur when the kidneys are not sufficiently infused for a long period of time (by stenosis of the renal artery or during a shock). A hypoperfusion can also be caused by an embolism of the renal artery. The ischemic NTA cause specific lesions of the tubules ( skip lesions ) [ 2 ] .

  1. ↑ a et b (in) ‘ Acute Tubular Necrosis (ATN)» , Nephrology Channel , Healthcommunities.com, (consulted the )
  2. ↑ a et b (in) Lee Goldman, Russell L. Cecil;, Cecil medicine , Philadelphia, PA, Saunders Elsevier, , 23 It is ed. , 3078 p. (ISBN  978-0-8089-2377-0 , OCLC  191854838 , LCCN 2006047505 ) , p. 705
  3. ↑ (in) Lee Goldman, Russell L. Cecil;, Cecil medicine , Philadelphia, PA, Saunders Elsevier, , 23 It is ed. , 3078 p. (ISBN  978-0-8089-2377-0 , OCLC  191854838 , LCCN 2006047505 )
  4. ↑ (in) P. Glynne, J. Picot, T. Evans, ‘ Coexpressed nitric oxide synthase and apical beta(1) integrins influence tubule cell adhesion after cytokine-induced injury » , Journal of the American Society of Nephrology , vol. twelfth, n O 11, , p. 2370–83 (PMID  11675413, read online )
  5. ↑ (in) P. Glynne, T. Evans, ‘ Inflammatory cytokines induce apoptotic and necrotic cell shedding from human proximal tubular epithelial cell monolayers » , Kidney International , vol. 55, n O 6, , p. 2573–97 (PMID  10354308, DOI  10.1046/j.1523-1755.2002.t01-1-00456.x)
  6. ↑ (in) L. Racusen, ‘ Epithelial cell shedding in acute renal injury » , Clinical and Experimental Pharmacology & Physiology , vol. 25, n you 3-4, , p. 273–5 (PMID  9590582, DOI  10.1111/j.1440-1681.1998.t01-3-.x)
  7. ↑ (in) K. Solez, L. Racusen, N. Marcussen et al. , ‘ Morphology of ischemic acute renal failure, normal function, and cyclosporine toxicity in cyclosporine-treated renal allograft recipients » , Kidney International , vol. 43, n O 5, , p. 1058–67 (PMID  8510383, DOI  10.1038/ki.1993.148)
  8. ↑ (in) L. Racusen, B. Fivush, Y. Li, et al. , ‘ Dissociation of tubular cell detachment and tubular cell death in clinical and experimental “acute tubular necrosis” » , Laboratory Investigation , vol. sixty four, n O 4, , p. 546–56 (PMID  1673163)

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