acute tubular necrosis


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Related to acute tubular necrosis: Acute interstitial nephritis

acute tubular necrosis

[ə′kyüt ′tüb·yə·lər nə′krō·səs]
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Table 1: Etiologies of Acute Kidney Injury in Lymphoma Pre-renal Intravascular volume depletion Nausea, emesis, diarrhea Hemorrhage Reduced kidney perfusion Vasoconstriction Sepsis Liver disease Medications (diuretics, nonsteroidal anti-inflammatory drugs) Renal Acute tubular necrosis Kidney ischemia Tumour lysis syndrome Medications (acetaminophen, nonsteroidal anti-inflammatory drugs, aminoglycosides) Tubulointerstitial disorders Secondary kidney infiltration Primary kidney lymphoma Glomerular disorders Amyloidosis IgA nephropathy Renovascular disorders Renal vein thrombosis Thrombotic microangiopathy Post-Renal Obstruction Exterior compression (lymphadenopathy, obstructing tumour) Internal obstruction (nephrolithiasis, crystalluria) (*)Adapted from Luciano & Brewster (2014).
Data concerning the classification of acute tubular necrosis presented in this study were not consistent with the protocols described in KHAN's study.
In patients who have tubular manifestations with light microscopic features of acute tubular necrosis (proximal tubulopathy without cytoplasmic inclusions), the endosomes unable to adequately process those peculiar light chains direct them to the lysosomal compartment.
Two cases (both falciparum oliguric renal failure) had isolated MPGN while it was seen along with changes of acute tubular necrosis (ATN) in 10 cases (falciparum 9 out of those 6 were oliguric, 3 nonoliguric and one case of nonoliguric vivax malaria).
The pathophysiologic mechanisms could be the increased free radical formation [4], skeletal and cardiac muscle necrosis (scattered coagulation necrosis) [3], formation of highly nephrotoxic quinonediamine (an oxidation product of PPD metabolites), renal tubular occlusion due to myoglobin casts, and acute tubular necrosis [5].
It has been observed that acute tubular necrosis can develop due to the edematous obstruction or acute renal failure caused by the intravesicle formalin used for the treatment of chronic hemorrhagic cystitis.
Renal biopsies, performed for 4 patients, detected patchy cortical necrosis in 3 (Figure 2) and acute tubular necrosis in 1.
These conditions may also cause ischaemia of the renal tubules, triggering acute tubular necrosis, a form of intrinsic AKI.
We did not encounter acute tubular necrosis or delayed graft function probably because all of our grafts were from living donors.
Acute tubular necrosis is usually caused by direct drug toxicity, but prolonged impaired renal perfusion as described above may also cause tubular damage.
It is thought that one mechanism through which they cause acute tubular necrosis (and Fanconi's syndrome) is tubular mitochondrial toxicity.
The most common forms of intrinsic kidney injury are acute tubular necrosis (ATN), acute interstitial nephritis (AIN), and contrast-induced nephropathy (CIN).

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