نتایج جستجو برای: induced renal tubular injury

تعداد نتایج: 1420420  

Journal: :American journal of physiology. Renal physiology 2014
Tatiana Novitskaya Lee McDermott Ke Xin Zhang Takuto Chiba Paisit Paueksakon Neil A Hukriede Mark P de Caestecker

Phenylthiobutanoic acids (PTBAs) are a new class of histone deacetylase (HDAC) inhibitors that accelerate recovery and reduce postinjury fibrosis after ischemia-reperfusion-induced acute kidney injury. However, unlike the more common scenario in which patients present with protracted and less clearly defined onset of renal injury, this model of acute kidney injury gives rise to a clearly define...

Journal: :The American journal of physiology 1987
M Levi B A Molitoris T J Burke R W Schrier F R Simon

Increases in intracellular and mitochondrial calcium content that accompany ischemic and toxic acute renal failure have been suggested to mediate renal tubular cell injury and dysfunction, but the mechanism(s) are unknown. We studied the effects of in vivo vitamin D-induced chronic hypercalcemia on rat renal cortical brush-border and basolateral membranes and mitochondria. In the brush-border m...

Journal: :Hypertension 2017
Lionel Lattenist Sebastian M Lechner Smail Messaoudi Alan Le Mercier Soumaya El Moghrabi Sonia Prince Norma A Bobadilla Peter Kolkhof Frédéric Jaisser Jonatan Barrera-Chimal

Acute kidney injury induced by ischemia/reperfusion (IR) is a frequent complication in hospitalized patients. Mineralocorticoid receptor antagonism has shown to be helpful against renal IR consequences; however, the potential benefit of novel nonsteroidal mineralocorticoid receptor antagonists such as finerenone has to be further explored. In this study, we evaluated the efficacy of finerenone ...

2012
Nirmala Parajuli Lia H. Campbell Akira Marine Kelvin G. M. Brockbank Lee Ann MacMillan-Crow

Cold preservation has greatly facilitated the use of cadaveric kidneys for transplantation but damage occurs during the preservation episode. It is well established that oxidant production increases during cold renal preservation and mitochondria are a key target for injury. Our laboratory has demonstrated that cold storage of renal cells and rat kidneys leads to increased mitochondrial superox...

Journal: :پژوهنده 0
رعنا غزنوی ghaznavi r msc., dept. of physiology, tehran university of medical sciencesتهران ، خیابان 16 آذر ، دانشگاه علـوم پزشکی تهران دانشکده پزشکی ، گروه فیزیولوژی . تلفن و دورنما : 66419484 . دکتر مهری کدخدایی kadkhodaei m prof., dept. of physiology, tehran university of medical sciencesاستاد ، گروه فیزیولوژی ، دانشگاه علوم پزشکی تهران

background: all the three nitric oxide synthase (nos) isoforms are presented in the kidney. some data provided evidences that enos activity leads to restoration of renal function after injury, but activation of inos aggravates renal failure. in the present study, we investigated that whether in gentamicin-induced renal failure selective inos blockade is beneficial. materials and methods: four g...

2000
Bruce A. Molitoris Robert Bacallao

Ischemia remains the major cause of acute renal failure (ARF) in the adult population [1]. Clinically a reduction in glomerular filtration rate (GFR) secondary to reduced renal blood flow can reflect prerenal azotemia or acute tubular necrosis (ATN). More appropriate terms for ATN are acute tubular dysfunction or acute tubular injury, as necrosis only rarely is seen in renal biopsies, and renal...

Journal: :American journal of physiology. Renal physiology 2014
Qiongzhen Lin Ying Chen Jicheng Lv Hong Zhang Jiawei Tang Lakshman Gunaratnam Xiaomei Li Li Yang

Tubulointerstitial injury plays an important role in the development and progression of chronic kidney disease (CKD). Kidney injury molecule (KIM)-1 is induced in damaged proximal tubules in both acute renal injury and CKD. However, the dynamics of KIM-1 in CKD and effects of KIM-1 expression on disease progression are unknown. Here, we aimed to determine the associations between tubular KIM-1 ...

2005
R. A. Zager

Intracellular iron reportedly mediates many forms of tissue injury, including ischemic and myohemoglobinuric acute renal failure. This action may be explained by the ability of iron to catalyze the formation of the highly toxic hydroxyl radical (.OH) from H202 via the Fenton/Haber-Weiss reactions. To assess whether renal tubular myoglobin/iron loading, induced by a physiological mechanism (endo...

Journal: :The Journal of clinical investigation 2009
Julia Menke Yasunori Iwata Whitney A Rabacal Ranu Basu Yee G Yeung Benjamin D Humphreys Takashi Wada Andreas Schwarting E Richard Stanley Vicki R Kelley

Tubular damage following ischemic renal injury is often reversible, and tubular epithelial cell (TEC) proliferation is a hallmark of tubular repair. Macrophages have been implicated in tissue repair, and CSF-1, the principal macrophage growth factor, is expressed by TECs. We therefore tested the hypothesis that CSF-1 is central to tubular repair using an acute renal injury and repair model, isc...

2017
Muhammad Mansyur Romi Nur Arfian Untung Tranggono Wiwit Ananda Wahyu Setyaningsih Dwi Cahyani Ratna Sari

BACKGROUND Uric acid (UA) plays important roles in inducing renal inflammation, intra-renal vasoconstriction and renal damage. Endothelin-1 (ET-1) is a well-known profibrotic factor in the kidney and is associated with fibroblast expansion. We examined the role of hyperuricemia conditions in causing elevation of ET-1 expression and kidney injury. METHODS Hyperuricemia was induced in mice usin...

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