Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to clarify the participations of cellular immunity in the development of tubulo-interstitial lesions, aberrant expressions of major histocompatibility complex (MHC) class II antigens and Ki-67 nuclear antigen on the renal tubular epithelial cells were studied. Ki-67 antigen was known to appear in all phases of cell cycle except for Go. Nine normal kidney specimens (4 males and 5 females) and 117 kidney specimens obtained from patients with kidney diseases (54 males and 63 females) were examined with the indirect immunofluorescence technique using murine monoclonal antibodies against HLA-DR (lal), HLA-DQ (Leu10) and Ki-67 nuclear antigen. Patients included 100 with glomerular diseases, and 16 with tubulo-interstitial diseases consisting of 4 acute tubular necrosis (ATN), 7 acute tubulo-interstitial nephritis (AIN), one renal allograft rejection and 4 sarcoidosis. In normal kidney, HLA-DR was solely noted in only two specimens (22.2%) at the basal portion of proximal tubular epithelial cells. In tubulo-interstitial diseases 11 (68.8%) out of 16 patients showed diffuse and intense expressions of HLA-DR concomitant with HLA-DQ in 6 of 13 (42.9%), and 11 of 13 (84.6%) were positive for Ki-67 nuclear antigen. Especially, in AIN and allograft rejection, intense expression of HLA-DR, DQ and Ki-67 nuclear antigen were observed in 100%, 86%, 100%, respectively. In ATN 3(75%) were positive for HLA-DR and Ki-67, but not for HLA-DQ. In contrast, only 12(15.6%). 2(2.6%) and 2(4.8%) of primary glomerular disease were weakly positive for HLA-DR, DQ and Ki-67 nuclear antigen, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Aberrant expression of major histocompatibility complex class II. (HLA-DR/DQ) antigens and proliferative nuclear antigen. (Ki-67) in renal tubular epithelial cells]. 262 37

A model of para-aminophenol (PAP) nephrotoxicity in Sprague-Dawley rats was utilized to characterize potential indicators of toxicity in the kidney and in biofluids, and to chronicle the progression of acute renal injury. Rats were administered PAP at a low or high dose and examined terminally at 6, 24 and 48 hours (4 animals/group with matching controls). Acute tubular necrosis was observed in the medullary rays (low and high doses) and the outer stripe of outer medulla (high dose only) as early as 6 hours postdosing. Starting at 24 hours, regeneration of the tubular epithelium was evident in both low and high dose studies. Associated with the tubular lesions, we observed elevation of urinary alpha -glutathione S-transferase levels, an indicator of proximal tubular injury. By immunohistochemistry of the kidney, decreased gamma -glutamylcysteine synthetase expression correlated with tubular injury, especially at high dose, whereas elevation of vimentin, osteopontin, and Ki-67 expression was concurrent with tubular regeneration. Clusterin and kidney injury molecule-1 displayed expression patterns characteristic of both renal injury and regeneration. Taken together, this study provided insight into the progression of nephrotoxicity, and allowed the evaluation of potential urinary and tissue protein biomarkers that could complement the early detection of acute tubular injury.
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PMID:Clinicopathological and tissue indicators of para-aminophenol nephrotoxicity in sprague-dawley rats. 1756 85

The existence of adult renal stem cells has long been suspected because the kidney is capable of regeneration in response to injury, such as acute tubular necrosis (ATN), but their location, or niche, has not been fully defined yet. The aim of this study was to identify the niche of adult renal stem cells responsible for the tubular regeneration. The location of label-retaining cells (LRCs) was studied in adult mouse kidneys after administration of a pulse of bromodeoxyuridine (BrdU) during embryonic period. To study regional participation in renal tubular regeneration, the expression of the proliferation marker Ki-67 was examined after induction of unilateral ATN in mouse kidneys. Regional colony-forming capacity was examined using cultured cells derived from normal mouse and human kidneys and their multipotency was examined in human kidneys. LRCs in adult mouse kidneys were mostly tubular epithelial cells and concentrated constantly in the outer stripe of the corticomedullary junction (CMJ). In the ATN model, Ki-67 positive cells were concentrated in the tubular epithelial cells of the outer stripe, not only in the ATN kidneys but also in the contralateral non-ATN kidneys. High colony-forming capacity was noted in the CMJ of mouse and human kidneys. Cultured cells derived from a single human CMJ cell revealed multipotency, differentiating not only into tubular cells but also into glomerular podocytes. These results demonstrate that the CMJ of the kidney contains label-retaining, renal-repairing, highly colony-forming multipotent stem cell-like tubular cells, suggesting the CMJ as the niche of adult renal stem cells.
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PMID:Adult stem cell-like tubular cells reside in the corticomedullary junction of the kidney. 1878 15

We investigate the morphological characteristics that may differentiate between ischemic acute tubular necrosis (ATN) and autolysis in postmortem samples. Renal tissue from 57 postmortem cases with an antemortem diagnosis of ATN and 57 age-/sex-matched control cases were examined for 10 morphological characteristics: epithelial proliferation (Ki-67 immunoperoxidase positivity), fibrin thrombi, tubular epithelial whorls, mitoses, casts, autolysis, tubulorrhexis, epithelial flattening, interstitial inflammation, and interstitial expansion. Tubular epithelial whorls were found in 16 ATN cases and were absent in controls. These findings suggest that specific morphological criteria may distinguish ischemic ATN from autolysis. Diagnoses of ATN may be confirmed using these combined criteria as contributing to cause of death and/or to ascertain previously undiagnosed cases of ATN postmortem.
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PMID:Can renal acute tubular necrosis be differentiated from autolysis at autopsy? 1920 86