acute tubular necrosis

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acute tubular necrosis

[ə′kyüt ′tüb·yə·lər nə′krō·səs]
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Specimens were examined for tubular necrosis which was graded as follows11:, 0=No cell necrosis, 1=Mild, only single cell necrosis in sparse tubules, 2=Moderate, more than one cell involved in sparse tubules, 3=Marked, tubules exhibiting total necrosis in almost every power field, 4=Massive total necrosis.
Effect of various histological changes on graft function at 1 month Histological changes if Number of Effect on graft function cortical biopsy patients (out of 84) Normal histology 48 (58%) No effect Glomerulosclerosis 21 (25%) No effect Interstitial fibrosis 11 (13%) Delayed graft function: 4 Acute tubular necrosis 4 (5%) Acute rejection: 2 Delayed graft function: 2 Focal tubal atrophy 4 (5%) No effect Table 2.
Acute tubular necrosis is the most common renal AKI seen in lymphoma patients, with lysozyme-induced tubular necrosis and tumour lysis syndrome being common etiologies (Luciano & Brewster, 2014).
Acute CsA induced nephrotoxicity is characterised by arteriolar hyalinisation and stripped tubular necrosis and interstitial infilteration.
In other words, mild, moderate, and very severe-degree changes of renal tubular necrosis, glomerular oedema and haemorrhage and necrosis, interstitial haemorrhage, oedema and inflammation.
Tubular injury may result from acute tubular necrosis due to sepsis, shock, or nephrotoxic drugs, from drug-induced interstitial nephritis, or from other disorders that occur in patients with and without cancer.
SV40 has been associated with two kidney diseases: focal and segmental glomerulosclerosis (FSGS) and tubular necrosis.
Decreased renal blood flow occurs due to babesiosis results in reduced amounts of oxygen and metabolic substrates presented to tubular cells and this 'cellular starvation' initiates development of acute tubular necrosis with consequent ARF.
Epithelial cells, particularly those of the S3 segment of the proximal tubule in the outer renal medulla, are particularly exposed to both ischemia and reperfusion phases of I/R injury, which can lead to acute tubular necrosis [69,70]; on the contrary, glomerular vessels degeneration was described only in the reperfusion phase [69].
These findings are not specific, however, as they can also be seen with acute tubular necrosis, acute rejection, and urinary obstruction [2, 4].
Renal biopsy was carried out in 15 patients, findings were acute tubular necrosis in 6, cortical necrosis in 4, tubulointerstitial nephritis in 2 and 2 had crescentic glomerulonephritis.