acute tubular necrosis

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acute tubular necrosis

[ə′kyüt ′tüb·yə·lər nə′krō·səs]
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Control group I Group II Group III Group IV N= 10 N= 10 N= 10 N= 10 Tubular degeneration (-) (+) (+) (+++) and widening Tubular necrosis (-) (-) (+) (+++) Atrophy (-) (-) (-) (+) Nuclear pyknosis (-) (-) (-) (++) Mononuclear cell (-) (-) (-) (+) infiltration Congested vessels (-) (+) (+) (+) Reaction to PAS (++) (++) (+) (+) Fibrous tissue (-) (+) (+) (++) Changes were graded as follows: (-) showing no change and (+), (++) and (+++) indicating mild, moderate and severe changes respectively.
The most established mechanism for VCM nephrotoxicity as authenticated in animal studies, can be at least moderately stated to be an enhanced production of reactive oxygen species, oxidative stress with tubular necrosis, interstial inflammation mitochondrial dysfunction and cellular apoptosis15,16.
Fisher's Exact Test= 42.45; p-value 50% necrosis in mice of group C, B and A, as well as a few of them showed tubular necrosis upto 25-50% (Figure 7)and these consequence of cadmium are well established.21
Diffuse parenchymal abnormalities include acute tubular necrosis, hyperacute rejection, acute rejection, chronic rejection, and drug-induced nephrotoxicity.
Intrarenal cause of acute kidney injury in lymphoma can be due to ischemic or nonischemic acute tubular necrosis, direct tumor infiltrates, and renovascular disorder due to the prothrombotic state associated with malignancy or glomerulopathy.
Tubular injury contained the typical degenerative changes of acute tubular necrosis. Many studies indicate cytotoxins and [PLA.sub.2] as the mediators of venom induced nephropathy [13, 53].
In this case, the patient initially presented with symptoms of nonoliguric acute tubular necrosis (ATN).
Similarly, among DM animals, a reduction in tubular necrosis was found in the MSC-treated group at 24 (P < 0.05) and 48 hours (P < 0.001, Figure 2(c)).
Schrier, "Diagnosis and treatment of acute tubular necrosis," Annals of Internal Medicine, vol.
Acute tubular necrosis was found to be the most common pathophysiological process responsible for AKI.
The suspects' medical experts appeared to be 'unanimous' in saying that Horacio's death could not be attributed to acute tubular necrosis and congestion, according to lawyer Paterno Esmaquel, Solano's legal counsel.
Only 40 patients (48%) had abnormal histological changes, which included glomerulosclerosis (GS, 25%),interstitial fibrosis (IF, 13%), acute tubular necrosis (ATN, 5%), and focal tubal atrophy (FTA, 5%) (Table 1).