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  1. Article ; Online: The Tubulointerstitial Pathophysiology of Progressive Kidney Disease.

    Schnaper, H William

    Advances in chronic kidney disease

    2017  Volume 24, Issue 2, Page(s) 107–116

    Abstract: Accumulating evidence suggests that the central locus for the progression of CKD is the renal proximal tubule. As injured tubular epithelial cells dedifferentiate in attempted repair, they stimulate inflammation and recruit myofibroblasts. At the same ... ...

    Abstract Accumulating evidence suggests that the central locus for the progression of CKD is the renal proximal tubule. As injured tubular epithelial cells dedifferentiate in attempted repair, they stimulate inflammation and recruit myofibroblasts. At the same time, tissue loss stimulates remnant nephron hypertrophy. Increased tubular transport workload eventually exceeds the energy-generating capacity of the hypertrophied nephrons, leading to anerobic metabolism, acidosis, hypoxia, endoplasmic reticulum stress, and the induction of additional inflammatory and fibrogenic responses. The result is a vicious cycle of injury, misdirected repair, maladaptive responses, and more nephron loss. Therapy that might be advantageous at one phase of this progression pathway could be deleterious during other phases. Thus, interrupting this downward spiral requires narrowly targeted approaches that promote healing and adequate function without generating further entry into the progression cycle.
    MeSH term(s) Acute Kidney Injury/complications ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Animals ; Cell Dedifferentiation ; Disease Progression ; Extracellular Matrix/metabolism ; Fibrosis ; Homeostasis ; Humans ; Hyperplasia/pathology ; Kidney Tubules, Proximal/metabolism ; Kidney Tubules, Proximal/pathology ; Nephritis, Interstitial/complications ; Nephritis, Interstitial/physiopathology ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/physiopathology
    Language English
    Publishing date 2017-03-09
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1548-5609 ; 1548-5595
    ISSN (online) 1548-5609
    ISSN 1548-5595
    DOI 10.1053/j.ackd.2016.11.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Remnant nephron physiology and the progression of chronic kidney disease.

    Schnaper, H William

    Pediatric nephrology (Berlin, Germany)

    2013  Volume 29, Issue 2, Page(s) 193–202

    Abstract: In chronic kidney disease, ongoing failure of individual nephrons leads to the progressive loss of renal function. This process results in part from a cellular and molecular response to injury that represents an attempt to maintain homeostasis but ... ...

    Abstract In chronic kidney disease, ongoing failure of individual nephrons leads to the progressive loss of renal function. This process results in part from a cellular and molecular response to injury that represents an attempt to maintain homeostasis but instead initiates a program that damages the nephron. As nephrons are lost, compensation by the remaining nephrons exacerbates glomerular pathophysiology. The delivery of excessive amounts of biologically active molecules to the distal nephron and tubulointerstitium generates inflammation and cellular dedifferentiation. Energy requirements of hyperfunctioning nephrons exceed the metabolic substrate available to the renal tubule, and inadequacy of the local vascular supply promotes hypoxia/ischemia and consequent acidosis and reactive oxygen species generation. In this way, mechanisms activated to maintain biological balance ultimately lead to demise of the nephron.
    MeSH term(s) Disease Progression ; Humans ; Nephrons/pathology ; Nephrons/physiopathology ; Renal Insufficiency, Chronic/pathology ; Renal Insufficiency, Chronic/physiopathology
    Language English
    Publishing date 2013-05-29
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-013-2494-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Keeping the customers stratified: moving toward genetics-based treatment options in childhood NS.

    Puckelwartz, Megan / Schnaper, H William

    Kidney international

    2017  Volume 91, Issue 4, Page(s) 781–783

    Abstract: In this issue, Bierzynska et al. report the results of analyzing a cohort of children with steroid-resistant nephrotic syndrome (SRNS) of childhood, correlating genetic studies with clinical outcomes. This approach has the potential to advance both our ... ...

    Abstract In this issue, Bierzynska et al. report the results of analyzing a cohort of children with steroid-resistant nephrotic syndrome (SRNS) of childhood, correlating genetic studies with clinical outcomes. This approach has the potential to advance both our research into the causes and treatments of childhood SRNS and our ability to stratify patients into groups that are likely to be responsive to specific treatments. Here, we discuss some of the strengths and limitations of this report.
    Language English
    Publishing date 2017-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2016.12.032
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Defining new surrogate markers for CKD progression.

    Schnaper, H William / Furth, Susan L / Yao, Lynne P

    Pediatric nephrology (Berlin, Germany)

    2015  Volume 30, Issue 2, Page(s) 193–198

    Abstract: At a recent meeting of international experts on clinical aspects of progressive chronic kidney disease (CKD), an extensive analysis of extant clinical trials was used to develop more effective and economical surrogate markers for CKD outcomes in adults. ... ...

    Abstract At a recent meeting of international experts on clinical aspects of progressive chronic kidney disease (CKD), an extensive analysis of extant clinical trials was used to develop more effective and economical surrogate markers for CKD outcomes in adults. This article describes the reasons for this undertaking, the methods and conclusions of the meeting, and the relevance of these findings to pediatric nephrology.
    MeSH term(s) Adult ; Biomarkers/analysis ; Child ; Disease Progression ; Female ; Glomerular Filtration Rate ; Humans ; Male ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/pathology ; Treatment Outcome
    Chemical Substances Biomarkers
    Language English
    Publishing date 2015-02
    Publishing country Germany
    Document type Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-014-2995-0
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  5. Article: Renal fibrosis.

    Schnaper, H William

    Methods in molecular medicine

    2005  Volume 117, Page(s) 45–68

    Abstract: The kidney has unique attributes that are related to its complex structure and that affect the nature of fibrogenesis in this organ. It is divided into functional units, called nephrons, that have both a filtering and a reabsorbing component. Sclerosis ... ...

    Abstract The kidney has unique attributes that are related to its complex structure and that affect the nature of fibrogenesis in this organ. It is divided into functional units, called nephrons, that have both a filtering and a reabsorbing component. Sclerosis may initiate in the sites of either of these components but ultimately involves both. The epidemiology and clinical manifestations of renal fibrosis suggest complex genetic and environmental influences on the development of fibrosis. Further, the different structures in the kidney manifest different mechanisms of fibrogenesis. These are determined by a combination of differences in the biology of the affected cells and the physical effects of nephron failure. Although therapy for renal fibrosis remains somewhat problematic, new insights into the mechanisms of the underlying diseases offer the promise of improved approaches to treatment.
    MeSH term(s) Animals ; Basement Membrane/metabolism ; Cell Differentiation ; Disease Models, Animal ; Fibrosis/diagnosis ; Fibrosis/epidemiology ; Fibrosis/pathology ; Glomerulonephritis/diagnosis ; Glomerulonephritis/epidemiology ; Humans ; Kidney Diseases/diagnosis ; Kidney Diseases/epidemiology ; Kidney Diseases/pathology ; Nephrons/anatomy & histology ; Nephrons/metabolism ; Rats ; Renal Insufficiency ; Transforming Growth Factor beta/metabolism
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2005
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S. ; Review
    ISSN 1543-1894
    ISSN 1543-1894
    DOI 10.1385/1-59259-940-0:045
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Tubulointerstitial injury and the progression of chronic kidney disease.

    Hodgkins, Kavita S / Schnaper, H William

    Pediatric nephrology (Berlin, Germany)

    2011  Volume 27, Issue 6, Page(s) 901–909

    Abstract: In chronic kidney disease (CKD), once injury from any number of disease processes reaches a threshold, there follows an apparently irreversible course toward decline in kidney function. The tubulointerstitium may play a key role in this common ... ...

    Abstract In chronic kidney disease (CKD), once injury from any number of disease processes reaches a threshold, there follows an apparently irreversible course toward decline in kidney function. The tubulointerstitium may play a key role in this common progression pathway. Direct injury, high metabolic demands, or stimuli from various other forms of renal dysfunction activate tubular cells. These, in turn, interact with interstitial tissue elements and inflammatory cells, causing further pathologic changes in the renal parenchyma. The tissue response to these changes thus generates a feed-forward loop of kidney injury and progressive loss of function. This article reviews the mechanisms of this negative cycle mediating CKD.
    MeSH term(s) Cell Communication ; Chronic Disease ; Disease Progression ; Feedback, Physiological ; Fibrosis ; Humans ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; Kidney Diseases/physiopathology ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Kidney Tubules/physiopathology ; Nephritis, Interstitial/metabolism ; Nephritis, Interstitial/pathology ; Signal Transduction
    Language English
    Publishing date 2011-09-27
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-011-1992-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Hypoxia-inducible factor-1α promotes glomerulosclerosis and regulates COL1A2 expression through interactions with Smad3.

    Baumann, Bethany / Hayashida, Tomoko / Liang, Xiaoyan / Schnaper, H William

    Kidney international

    2016  Volume 90, Issue 4, Page(s) 797–808

    Abstract: The function of hypoxia-inducible factor-1α (HIF-1α) in chronic kidney disease is disputed. Here we report that interactions of HIF-1α with transforming growth factor-β (TGF-β) signaling may promote its fibrotic effects. Knockout of HIF-1α is protective ... ...

    Abstract The function of hypoxia-inducible factor-1α (HIF-1α) in chronic kidney disease is disputed. Here we report that interactions of HIF-1α with transforming growth factor-β (TGF-β) signaling may promote its fibrotic effects. Knockout of HIF-1α is protective against glomerulosclerosis and glomerular type-I collagen accumulation in a mouse podocyte ablation model. Transcriptional analysis of cultured renal cells showed that α2(I) collagen expression is directly regulated by HIF-1α binding to a functional hypoxia-responsive element in its promoter at -335 relative to the transcription start site. Activation of COL1A2 transcription by HIF-1α occurred in the absence of hypoxia and is strongly enhanced by TGF-β signaling. TGF-β, in addition to increasing HIF-1α levels, increased both HIF-1α binding to the COL1A2 promoter and HIF-1α N-terminal transactivation domain activity. These effects of TGF-β on HIF-1α were inhibited in Smad3-null mouse embryonic fibroblasts, suggesting a requirement for Smad3. Phosphorylated Smad3 also associated with the -335 hypoxia-responsive element of the COL1A2 promoter independent of a Smad DNA binding sequence. Smad3 binding to the -335 hypoxia-responsive element required HIF-1α both in vitro and in kidney lysate from the disease model, suggesting formation of an HIF-1α-Smad3 transcriptional complex. Thus, HIF-1α-Smad3 has a novel interaction in glomerulosclerosis.
    MeSH term(s) Animals ; Cells, Cultured ; Collagen Type I/metabolism ; Disease Models, Animal ; Fibroblasts ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Kidney Glomerulus/cytology ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Kidney Tubules, Proximal/cytology ; Kidney Tubules, Proximal/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phosphorylation ; Podocytes ; Promoter Regions, Genetic ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Sclerosis ; Signal Transduction ; Smad3 Protein/genetics ; Smad3 Protein/metabolism ; Transforming Growth Factor beta1/metabolism
    Chemical Substances Col1a2 protein, mouse ; Collagen Type I ; Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Smad3 Protein ; Smad3 protein, mouse ; Transforming Growth Factor beta1
    Language English
    Publishing date 2016-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2016.05.026
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  8. Article: Idiopathic focal segmental glomerulosclerosis.

    Schnaper, H William

    Seminars in nephrology

    2003  Volume 23, Issue 2, Page(s) 183–193

    Abstract: Idiopathic focal segmental glomerulosclerosis (FSGS) is a primary glomerular disease that essentially represents a form of chronic, progressive renal fibrosis for which there is no discernible cause. Often presenting with or eventually manifesting the ... ...

    Abstract Idiopathic focal segmental glomerulosclerosis (FSGS) is a primary glomerular disease that essentially represents a form of chronic, progressive renal fibrosis for which there is no discernible cause. Often presenting with or eventually manifesting the nephrotic syndrome, this disease is increasing in incidence in both children and adults. Therapy continues to be a challenge, although some patients clearly respond to corticosteroids or cyclosporine with a decrease in, or remission of, proteinuria. A favorable response is associated with a decreased likelihood of progression to kidney failure. Given our clinical experience and recent advances in understanding the genetics of FSGS, a stochastic model of disease pathogenesis can be proposed.
    MeSH term(s) Disease Progression ; Glomerulosclerosis, Focal Segmental/diagnosis ; Glomerulosclerosis, Focal Segmental/etiology ; Glomerulosclerosis, Focal Segmental/therapy ; Humans ; Kidney Glomerulus/pathology ; Nephrotic Syndrome/diagnosis ; Nephrotic Syndrome/etiology ; Nephrotic Syndrome/therapy ; Renal Insufficiency/etiology
    Language English
    Publishing date 2003-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604652-6
    ISSN 1558-4488 ; 0270-9295
    ISSN (online) 1558-4488
    ISSN 0270-9295
    DOI 10.1053/snep.2003.50016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Book: Clinical pediatric nephrology

    Kher, Kanwal K / Schnaper, H. William / Greenbaum, Larry A

    2016  

    Author's details edited by Kanwal Kher, H. William Schnaper, Larry A. Greenbaum
    MeSH term(s) Kidney Diseases/diagnosis ; Kidney Diseases/therapy ; Kidney Diseases/complications ; Infant ; Child ; Adolescent
    Language English
    Size xv, 1093 pages :, illustrations
    Edition Third edition.
    Document type Book
    ISBN 9781482214628 ; 1482214628
    Database Catalogue of the US National Library of Medicine (NLM)

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  10. Article ; Online: Progression of glomerular and tubular disease in pediatrics.

    Woroniecki, Robert P / Schnaper, H William

    Seminars in nephrology

    2009  Volume 29, Issue 4, Page(s) 412–424

    Abstract: Chronic kidney disease may be stimulated by many different etiologies, but its progression involves a common, yet complex, series of events that lead to the replacement of normal tissue with scar. These events include altered physiology within the kidney ...

    Abstract Chronic kidney disease may be stimulated by many different etiologies, but its progression involves a common, yet complex, series of events that lead to the replacement of normal tissue with scar. These events include altered physiology within the kidney leading to abnormal hemodynamics, chronic hypoxia, inflammation, cellular dysfunction, and activation of fibrogenic biochemical pathways. The end result is the replacement of normal structures with extracellular matrix. Treatments presently are focused on delaying or preventing such progression, and are largely nonspecific. In pediatrics, such therapy is complicated further by pathophysiological issues that render children a unique population.
    MeSH term(s) Child ; Child, Preschool ; Cytokines/metabolism ; Disease Progression ; Extracellular Matrix/metabolism ; Fibrosis/pathology ; Humans ; Kidney Diseases/pathology ; Kidney Diseases/physiopathology ; Kidney Glomerulus/pathology ; Kidney Glomerulus/physiopathology ; Kidney Tubules/pathology ; Kidney Tubules/physiopathology ; Proteinuria/physiopathology
    Chemical Substances Cytokines
    Language English
    Publishing date 2009-07-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604652-6
    ISSN 1558-4488 ; 0270-9295
    ISSN (online) 1558-4488
    ISSN 0270-9295
    DOI 10.1016/j.semnephrol.2009.03.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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