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Samuel N Heyman - One of the best experts on this subject based on the ideXlab platform.
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Concerns about KIM-1 as a urinary biomarker for acute Tubular Necrosis (ATN)
Kidney international, 2003Co-Authors: Seymour Rosen, Samuel N HeymanAbstract:To the Editor: In a recent issue of Kidney International, Han et al1, regarding kidney injury molecule-1 (KIM-1) as a urinary biomarker for human proximal tubule injury, requires clarification. First, the selection of biopsied patients with putative acute Tubular Necrosis (ATN) is problematic. The authors include "ischemia" with minimal change, interstitial nephritis, and membranous nephropathy [with nonsteroidal anti-inflammatory drugs (NSAIDs)] and state that all patients had a confirmed pathologic diagnosis of ATN. Interstitial nephritis, membranous nephropathy (with NSAIDs), and minimal change disease are not commonly associated with ATN. Even in renal biopsies done within days after transplantation, changes of overt Tubular Necrosis are usually very limited2.
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animal models of acute Tubular Necrosis
Current Opinion in Critical Care, 2002Co-Authors: Samuel N Heyman, Wilfred Lieberthal, Peter Rogiers, Joseph V BonventreAbstract:: The evaluation and management of acute renal failure in the ICU patient remains a formidable task because of the complexity of this condition. Clinical and physiologic assessment and complementing laboratory and imaging tests are currently insufficient to differ between true renal parenchymal damage (acute Tubular Necrosis; it is important to realize that this term does not necessarily imply widespread injury, because whole organ dysfunction in humans has often been associated with very limited parenchymal cellular Necrosis) and prerenal azotemia (decreased renal blood flow with altered glomerular hemodynamics and subsequently diminished glomerular filtration, without significant epithelial cell injury). Moreover, Tubular damage and altered glomerular hemodynamics may coexist or lead to each other, and their relative contribution to the evolving renal dysfunction has not been unequivocally established. The limited data regarding the renal pathology of such patients and the scant information about human morphologic and functional correlates further undermine our knowledge about diagnostic and therapeutic approaches to these patients. Advanced techniques are critically needed to establish noninvasively the dynamic status of renal parenchymal microcirculation and the distribution of intrarenal oxygenation and to identify evolving cellular energy depletion and Tubular cell damage. A few technologies are potentially promising, such as blood oxygen level dependent magnetic resonance imaging, positron emission tomography, and kidney injury molecule-1 detection in patients' urine. Because of the difficulties in analyzing the pathophysiology in humans, clinicians continue to rely largely on animal models to guide understanding and rationale for the identification of therapeutic targets. Data from such animal studies are complemented by studies in isolated perfused kidneys, isolated tubules, and Tubular epithelial cell cultures. In this report, we summarize some concepts of acute Tubular Necrosis that have evolved as a result of these studies, evaluate available animal models, and underscore controversies regarding experimental acute Tubular Necrosis.
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difficulties in understanding human acute Tubular Necrosis limited data and flawed animal models
Kidney International, 2001Co-Authors: Seymour Rosen, Samuel N HeymanAbstract:Difficulties in understanding human "acute Tubular Necrosis": Limited data and flawed animal models. This review summarizes the current understanding of the renal biopsy in "acute Tubular Necrosis" and the attempts to mimic this phenomenon in animal models. Paradoxically, only very limited Necrosis is present in the biopsy of patients with this condition and differences in biopsies of patients with sustained and recovering renal failure cannot be clearly defined. The small amount of material examined, the variation in timing of the biopsy, the ability of the nephron to recover from sublethal injury, and the complexity of the clinical situation compound the difficulties in understanding this condition. Morphological findings in the animal studies are not equivalent to those in the human biopsy of "acute Tubular Necrosis," because they either have too much proximal Tubular Necrosis (ischemia-reflow model) or show severe injury to distal nephron segments (distal nephron model), the degree of which has not been clearly documented, as yet, in human material. The direct relevance of animal models in part may be tested by new noninvasive methods that define and quantify excreted proteins that reflect nephron injury or measure the status of renal oxygenation by radiological imaging techniques. Finally, it may be time to re-examine the morphology of "acute Tubular Necrosis," utilizing new techniques that illustrate induction of heat shock proteins, sublethal and apoptotic cellular injury, and alteration of gene expression.
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Difficulties in understanding human "acute Tubular Necrosis": limited data and flawed animal models.
Kidney international, 2001Co-Authors: Seymour Rosen, Samuel N HeymanAbstract:This review summarizes the current understanding of the renal biopsy in "acute Tubular Necrosis" and the attempts to mimic this phenomenon in animal models. Paradoxically, only very limited Necrosis is present in the biopsy of patients with this condition and differences in biopsies of patients with sustained and recovering renal failure cannot be clearly defined. The small amount of material examined, the variation in timing of the biopsy, the ability of the nephron to recover from sublethal injury, and the complexity of the clinical situation compound the difficulties in understanding this condition. Morphological findings in the animal studies are not equivalent to those in the human biopsy of "acute Tubular Necrosis," because they either have too much proximal Tubular Necrosis (ischemia-reflow model) or show severe injury to distal nephron segments (distal nephron model), the degree of which has not been clearly documented, as yet, in human material. The direct relevance of animal models in part may be tested by new noninvasive methods that define and quantify excreted proteins that reflect nephron injury or measure the status of renal oxygenation by radiological imaging techniques. Finally, it may be time to re-examine the morphology of "acute Tubular Necrosis," utilizing new techniques that illustrate induction of heat shock proteins, sublethal and apoptotic cellular injury, and alteration of gene expression.
Seymour Rosen - One of the best experts on this subject based on the ideXlab platform.
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Concerns about KIM-1 as a urinary biomarker for acute Tubular Necrosis (ATN)
Kidney international, 2003Co-Authors: Seymour Rosen, Samuel N HeymanAbstract:To the Editor: In a recent issue of Kidney International, Han et al1, regarding kidney injury molecule-1 (KIM-1) as a urinary biomarker for human proximal tubule injury, requires clarification. First, the selection of biopsied patients with putative acute Tubular Necrosis (ATN) is problematic. The authors include "ischemia" with minimal change, interstitial nephritis, and membranous nephropathy [with nonsteroidal anti-inflammatory drugs (NSAIDs)] and state that all patients had a confirmed pathologic diagnosis of ATN. Interstitial nephritis, membranous nephropathy (with NSAIDs), and minimal change disease are not commonly associated with ATN. Even in renal biopsies done within days after transplantation, changes of overt Tubular Necrosis are usually very limited2.
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difficulties in understanding human acute Tubular Necrosis limited data and flawed animal models
Kidney International, 2001Co-Authors: Seymour Rosen, Samuel N HeymanAbstract:Difficulties in understanding human "acute Tubular Necrosis": Limited data and flawed animal models. This review summarizes the current understanding of the renal biopsy in "acute Tubular Necrosis" and the attempts to mimic this phenomenon in animal models. Paradoxically, only very limited Necrosis is present in the biopsy of patients with this condition and differences in biopsies of patients with sustained and recovering renal failure cannot be clearly defined. The small amount of material examined, the variation in timing of the biopsy, the ability of the nephron to recover from sublethal injury, and the complexity of the clinical situation compound the difficulties in understanding this condition. Morphological findings in the animal studies are not equivalent to those in the human biopsy of "acute Tubular Necrosis," because they either have too much proximal Tubular Necrosis (ischemia-reflow model) or show severe injury to distal nephron segments (distal nephron model), the degree of which has not been clearly documented, as yet, in human material. The direct relevance of animal models in part may be tested by new noninvasive methods that define and quantify excreted proteins that reflect nephron injury or measure the status of renal oxygenation by radiological imaging techniques. Finally, it may be time to re-examine the morphology of "acute Tubular Necrosis," utilizing new techniques that illustrate induction of heat shock proteins, sublethal and apoptotic cellular injury, and alteration of gene expression.
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Difficulties in understanding human "acute Tubular Necrosis": limited data and flawed animal models.
Kidney international, 2001Co-Authors: Seymour Rosen, Samuel N HeymanAbstract:This review summarizes the current understanding of the renal biopsy in "acute Tubular Necrosis" and the attempts to mimic this phenomenon in animal models. Paradoxically, only very limited Necrosis is present in the biopsy of patients with this condition and differences in biopsies of patients with sustained and recovering renal failure cannot be clearly defined. The small amount of material examined, the variation in timing of the biopsy, the ability of the nephron to recover from sublethal injury, and the complexity of the clinical situation compound the difficulties in understanding this condition. Morphological findings in the animal studies are not equivalent to those in the human biopsy of "acute Tubular Necrosis," because they either have too much proximal Tubular Necrosis (ischemia-reflow model) or show severe injury to distal nephron segments (distal nephron model), the degree of which has not been clearly documented, as yet, in human material. The direct relevance of animal models in part may be tested by new noninvasive methods that define and quantify excreted proteins that reflect nephron injury or measure the status of renal oxygenation by radiological imaging techniques. Finally, it may be time to re-examine the morphology of "acute Tubular Necrosis," utilizing new techniques that illustrate induction of heat shock proteins, sublethal and apoptotic cellular injury, and alteration of gene expression.
Wenjuan Wang - One of the best experts on this subject based on the ideXlab platform.
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proliferative capacity of stem progenitor like cells in the kidney may associate with the outcome of patients with acute Tubular Necrosis
Human Pathology, 2011Co-Authors: Youxin Ye, Bingyin Wang, Yingjuan Ying, Weiming Hu, Xinxin Jiang, Hua Li, Jian Feng, Wenjuan WangAbstract:Summary Animal studies indicate that adult renal stem/progenitor cells can undergo rapid proliferation in response to renal injury, but whether the same is true in humans is largely unknown. To examine the profile of renal stem/progenitor cells responsible for acute Tubular Necrosis in human kidney, double and triple immunostaining was performed using proliferative marker and stem/progenitor protein markers on sections from 10 kidneys with acute Tubular Necrosis and 4 normal adult kidneys. The immunopositive cells were recorded using 2-photon confocal laser scanning microscopy. We found that dividing cells were present in the tubules of the cortex and medulla, as well as the glomerulus in normal human kidney. Proliferative cells in the parietal layer of Bowman capsule expressed CD133, and dividing cells in the tubules expressed immature cell protein markers paired box gene 2, vimentin, and nestin. After acute Tubular Necrosis, Ki67-positive cells in the cortex tubules significantly increased compared with normal adult kidney. These Ki67-positive cells expressed CD133 and paired box gene 2, but not the cell death marker, activated caspase-3. In addition, the number of dividing cells increased significantly in patients with acute Tubular Necrosis who subsequently recovered, compared with patients with acute Tubular Necrosis who consequently developed protracted acute Tubular Necrosis or died. Our data suggest that renal stem/progenitor cells may reside not only in the parietal layer of Bowman capsule but also in the cortex and medulla in normal human kidney, and the proliferative capacity of renal stem/progenitor cells after acute Tubular Necrosis may be an important determinant of a patient's outcome.
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Proliferative capacity of stem/progenitor-like cells in the kidney may associate with the outcome of patients with acute Tubular Necrosis.
Human Pathology, 2011Co-Authors: Youxin Ye, Bingyin Wang, Yingjuan Ying, Weiming Hu, Xinxin Jiang, Hua Li, Jian Feng, Wenjuan WangAbstract:Summary Animal studies indicate that adult renal stem/progenitor cells can undergo rapid proliferation in response to renal injury, but whether the same is true in humans is largely unknown. To examine the profile of renal stem/progenitor cells responsible for acute Tubular Necrosis in human kidney, double and triple immunostaining was performed using proliferative marker and stem/progenitor protein markers on sections from 10 kidneys with acute Tubular Necrosis and 4 normal adult kidneys. The immunopositive cells were recorded using 2-photon confocal laser scanning microscopy. We found that dividing cells were present in the tubules of the cortex and medulla, as well as the glomerulus in normal human kidney. Proliferative cells in the parietal layer of Bowman capsule expressed CD133, and dividing cells in the tubules expressed immature cell protein markers paired box gene 2, vimentin, and nestin. After acute Tubular Necrosis, Ki67-positive cells in the cortex tubules significantly increased compared with normal adult kidney. These Ki67-positive cells expressed CD133 and paired box gene 2, but not the cell death marker, activated caspase-3. In addition, the number of dividing cells increased significantly in patients with acute Tubular Necrosis who subsequently recovered, compared with patients with acute Tubular Necrosis who consequently developed protracted acute Tubular Necrosis or died. Our data suggest that renal stem/progenitor cells may reside not only in the parietal layer of Bowman capsule but also in the cortex and medulla in normal human kidney, and the proliferative capacity of renal stem/progenitor cells after acute Tubular Necrosis may be an important determinant of a patient's outcome.
U. Binswanger - One of the best experts on this subject based on the ideXlab platform.
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Serum hippuric acid concentration in renal allograft rejection, ureter obstruction, and Tubular Necrosis
Transplant International, 1994Co-Authors: A. Knoflach, U. BinswangerAbstract:Plasma from 35 renal allograft recipients (21 males and 14 females) was sampled daily and analyzed for hippuric acid (HA) by highperformance liquid chromatography (HPLC) and serum creatinine. Twelve of these patients experienced an acute renal allograft rejection or a ureter obstruction as proven by clinical signs and biopsy, as well as by radiography or ultrasound, respectively. Two patients suffered from Tubular Necrosis followed by rejection during the postoperative period. Mean serum HA increased by 39.9 μmol/l from baseline (range 20.4–115.5 μmol/l) in patients with acute rejection 3 days after an initial increase that was observed 24 h before the mean serum creatinine increased by 107.1 μmol/l (range 21–193 μmol/l). In cases of ureter obstruction, HA rose by 1.6 μmol/l (range 1–8.2 μmol/l), significantly less than elevations due to rejection. The increase in creatinine, however, amounted to 65.3 μmol/l (range 22–140 μmol/l) and was not different from the change in rejecting patients. Successful antirejection treatment coincided with a decrease in serum HA starting 24 h earlier than the decrease in the serum creatinine concentration. Of special interest was the observation of a parallel decrease in HA with creatinine concentration in patients with Tubular Necrosis after allotransplantation; HA increased in cases of an additional rejection. Our data suggest that HA, which is excreted by Tubular secretion and glomerular filtration, could be a sensitive and early marker of acute allograft rejection. Furthermore, it seems to discriminate between acute renal allograft rejection and ureter obstruction. It might, therefore, be of value in the diagnosis of rejection complicating Tubular Necrosis after transplantation.
Carl M Kjellstrand - One of the best experts on this subject based on the ideXlab platform.
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Influence of Splenectomy on Human Acute Tubular Necrosis
Nephron, 2008Co-Authors: David S. Fryd, Carl M KjellstrandAbstract:The incidence of acute Tubular Necrosis (need for hemodialysis immediately after transplantation) and its severity (the number of days dialysis was needed) were studied in 299 patients who were randomized prior to transplantation into undergoing splenectomy or not having splenectomy. There was no difference in the incidence of acute Tubular Necrosis between splenectomized and nonsplenectomized patients who received cadaveric grafts or kidneys from living related donors. In those patients in the cadaveric group who had acute Tubular Necrosis, the duration of need for dialysis was significantly less (p
