Medical condition
Acute tubular necrosis
(
ATN
) is a medical condition involving the
death
of tubular
epithelial
cells
that form the
renal tubules
of the
kidneys
. Because necrosis is often not present, the term acute tubular injury (ATI) is preferred by pathologists over the older name acute tubular necrosis (ATN).
[1]
ATN presents with
acute kidney injury
(AKI) and is one of the most common causes of AKI.
[2]
Common causes of ATN include
low blood pressure
and use of
nephrotoxic
drugs.
[2]
The presence of "muddy brown
casts
" of epithelial cells found in the urine during
urinalysis
is
pathognomonic
for ATN.
[3]
Management relies on aggressive treatment of the factors that precipitated ATN (e.g.
hydration
and cessation of the offending drug). Because the tubular cells continually replace themselves, the overall
prognosis
for ATN is quite good if the underlying cause is corrected, and recovery is likely within 7 to 21 days.
[2]
Classification
[
edit
]
ATN 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
.
[4]
Due to several reasons, the proximal portion of the renal tubule is most commonly injured in ATN.
Diagnosis
[
edit
]
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 (a type of
granular cast
) 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.
[5]
Proximal tubule cells can shed with variable viability and not be purely "necrotic".
[6]
[7]
[8]
[9]
[10]
Toxic ATN
[
edit
]
Toxic ATN can be caused by free
hemoglobin
or
myoglobin
, by medication including
antibiotics
such as
aminoglycoside
,
[11]
statins
such as
atorvastatin
,
bisphosphonates
like
pamidronate
[12]
and
cytotoxic
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 kidney failure. Basement membrane is intact,
[
citation needed
]
so the tubular epithelium regeneration is possible.
Glomeruli
are not affected.
[2]
Ischemic ATN
[
edit
]
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. Given their importance in massive nutrient and electrolyte reabsorption, the proximal tubule and medullary thick ascending limb require significant ATP and are most susceptible to ischemic damage. Thus, ischemic ATN specifically causes
skip lesions
through the tubules.
[3]
See also
[
edit
]
References
[
edit
]
- ^
Desanti De Oliveira, B., Xu, K., Shen, T.H. et al. Molecular nephrology: types of acute tubular injury. Nat Rev Nephrol 15, 599?612 (2019).
https://doi.org/10.1038/s41581-019-0184-x
- ^
a
b
c
d
"Acute Tubular Necrosis (ATN)"
.
Nephrology Channel
. HealthCommunities.com. 2008
. Retrieved
2008-09-23
.
- ^
a
b
Goldman, Lee; Cecil, Russell L. (2008).
Cecil medicine
. Philadelphia, PA: Saunders Elsevier. p. 705.
ISBN
978-0-8089-2377-0
.
OCLC
191854838
.
- ^
Goldman, Lee; Cecil, Russell L. (2008).
Cecil medicine
. Philadelphia, PA: Saunders Elsevier.
ISBN
978-0-8089-2377-0
.
OCLC
191854838
.
[
page needed
]
- ^
TheFreeDictionary > tubulorrhexis
Citing: The American Heritage Medical Dictionary 2007
- ^
Glynne PA, Picot J, Evans TJ (November 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.
doi
:
10.1681/ASN.V12112370
.
PMID
11675413
.
- ^
Glynne PA, Evans TJ (June 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
.
- ^
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
.
S2CID
39727538
.
- ^
Solez K, Racusen LC, Marcussen N, et al. (May 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
.
- ^
Racusen LC, Fivush BA, Li YL, Slatnik I, Solez K (April 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
.
- ^
Tulkens, P.M. (March 1989).
"Nephrotoxicity of aminoglycoside antibiotics"
.
Toxicology Letters
.
46
(1?3): 107?123.
doi
:
10.1016/0378-4274(89)90121-5
.
PMID
2650018
.
- ^
Banerjee, Debasish; Asif, Arif (May 2003).
"Short-Term, High-Dose Pamidronate-Induced Acute Tubular Necrosis: The Postulated Mechanisms of Bisphosphonate Nephrotoxicity"
.
American Journal of Kidney Diseases
.
41
(5): e18.1?e18.6.
doi
:
10.1016/S0272-6386(03)00214-2
.
PMID
12778436
.
External links
[
edit
]
Classification
| |
---|
External resources
| |
---|