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  1. Article ; Online: Uromodulin fights UTI with sugars.

    Beenken, Andrew / Al-Awqati, Qais

    Kidney international

    2021  Volume 99, Issue 5, Page(s) 1057–1059

    MeSH term(s) Humans ; Sugars ; Urinary Tract Infections ; Uromodulin/genetics
    Chemical Substances Sugars ; Uromodulin
    Language English
    Publishing date 2021-02-05
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2020.12.035
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  2. Article ; Online: Kidney growth and hypertrophy: the role of mTOR and vesicle trafficking.

    Al-Awqati, Qais

    The Journal of clinical investigation

    2015  Volume 125, Issue 8, Page(s) 3304

    Language English
    Publishing date 2015-08-03
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI83542
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  3. Article ; Online: Kidney growth and hypertrophy: the role of mTOR and vesicle trafficking.

    Al-Awqati, Qais

    The Journal of clinical investigation

    2015  Volume 125, Issue 6, Page(s) 2267–2270

    Abstract: ... kidney is removed, the remaining one hypertrophies. In a comprehensive series of studies, Chen et al ...

    Abstract The kidney, like other organs, grows in constant proportion to the rest of the body. When one kidney is removed, the remaining one hypertrophies. In a comprehensive series of studies, Chen et al. show that growth during maturation is mediated by the mTORC1 signaling pathway, which is induced by EGF-like peptides, and requires PI3K, PDK, AKT, mTORC2, and activation of mTORC1 through the combined effects of TSC and RHEB as part of a multiprotein complex localized on lysosomes. However, compensatory growth is mediated by amino acids, which act on mTORC1 independently of the previous pathway, and requires a class III PI3K (VPS34) that is known to be involved in vesicle trafficking to the lysosomes.
    MeSH term(s) Animals ; Kidney/enzymology ; Kidney/pathology ; Kidney Diseases/enzymology ; Kidney Diseases/pathology ; Phosphatidylinositol 3-Kinases/metabolism ; Signal Transduction
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
    Language English
    Publishing date 2015-06
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI81508
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  4. Article ; Online: Lactate dehydrogenase 5: identification of a druggable target to reduce oxaluria.

    Stevens, Jacob S / Al-Awqati, Qais

    The Journal of clinical investigation

    2019  Volume 129, Issue 6, Page(s) 2201–2204

    Abstract: Excessive excretion of oxalate in the urine results in the formation of calcium oxalate crystals and subsequent kidney stone formation. Severe forms of hyperoxaluria, including genetic forms and those that result from ethylene glycol poisoning, can ... ...

    Abstract Excessive excretion of oxalate in the urine results in the formation of calcium oxalate crystals and subsequent kidney stone formation. Severe forms of hyperoxaluria, including genetic forms and those that result from ethylene glycol poisoning, can result in end-stage renal disease. Therapeutic interventions are limited and often rely on dietary intervention. In this issue of the JCI, Le Dudal and colleagues demonstrate that the lactate dehydrogenase 5 inhibitor (LDH5) stiripentol reduces urinary oxalate excretion. Importantly, stiripentol treatment of a single individual with primary hyperoxaluria reduced the urinary oxalate excretion. Together, these results support further evaluation of LDH5 as a therapeutic target for hyperoxaluria.
    MeSH term(s) Calcium Oxalate ; Dioxolanes ; Ethylene Glycols ; Humans ; Hyperoxaluria ; Lactate Dehydrogenase 5
    Chemical Substances Dioxolanes ; Ethylene Glycols ; Calcium Oxalate (2612HC57YE) ; Lactate Dehydrogenase 5 (EC 1.1.1.27.-) ; stiripentol (R02XOT8V8I)
    Language English
    Publishing date 2019-05-20
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI128709
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  5. Article ; Online: Basic research: Salt wasting in distal renal tubular acidosis-new look, old problem.

    Al-Awqati, Qais

    Nature reviews. Nephrology

    2013  Volume 9, Issue 12, Page(s) 712–713

    Abstract: Acidosis affects sodium and potassium excretion, likely via the pH sensitivity of ion transporters. A recent paper shows that β-intercalated cells with deleted H(+)-ATPase release ATP into urine, which induces the production of prostaglandin E2 (PGE2). ... ...

    Abstract Acidosis affects sodium and potassium excretion, likely via the pH sensitivity of ion transporters. A recent paper shows that β-intercalated cells with deleted H(+)-ATPase release ATP into urine, which induces the production of prostaglandin E2 (PGE2). PGE2 then reduces sodium absorption in the principal cells of the cortical collecting tubule and increases potassium secretion.
    MeSH term(s) Animals ; Kidney Tubules, Collecting/metabolism ; Potassium, Dietary/blood ; Sodium, Dietary/blood ; Water-Electrolyte Balance
    Chemical Substances Potassium, Dietary ; Sodium, Dietary
    Language English
    Publishing date 2013-11-05
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/nrneph.2013.235
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  6. Article ; Online: Cell biology of the intercalated cell in the kidney.

    Al-Awqati, Qais

    FEBS letters

    2013  Volume 587, Issue 13, Page(s) 1911–1914

    Abstract: The intercalated cell of the collecting tubule of the mammalian kidney is specialized for the transport of H(+) and HCO3. They exist in two forms; one specialized for acid secretion and the other secretes HCO3 into the urine. We discovered many years ago ...

    Abstract The intercalated cell of the collecting tubule of the mammalian kidney is specialized for the transport of H(+) and HCO3. They exist in two forms; one specialized for acid secretion and the other secretes HCO3 into the urine. We discovered many years ago that feeding animals an acid diet converts the HCO3 secreting form to an acid secreting type. Here I discuss the molecular basis of this transformation. The conversion of the cell types is mediated by an extracellular matrix protein hensin (also known as DMBT1). However much remains to be identified in the differentiation of these cells.
    MeSH term(s) Adult Stem Cells/physiology ; Animals ; Bicarbonates/metabolism ; Cell Differentiation ; Extracellular Matrix Proteins/metabolism ; Humans ; Kidney/cytology ; Kidney Tubules, Collecting/cytology ; Kidney Tubules, Collecting/metabolism
    Chemical Substances Bicarbonates ; Extracellular Matrix Proteins
    Language English
    Publishing date 2013-05-16
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2013.05.007
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  7. Article ; Online: Basic research in nephrology: are we in decline?

    Al-Awqati, Qais

    Journal of the American Society of Nephrology : JASN

    2012  Volume 23, Issue 10, Page(s) 1611–1616

    MeSH term(s) Animals ; Humans ; Nephrology/trends ; Publishing/trends ; Research/trends ; United States
    Language English
    Publishing date 2012-08-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2012060553
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  8. Article ; Online: Forty years and counting...

    Al-Awqati, Qais

    Kidney international

    2012  Volume 81, Issue 1, Page(s) 3–4

    MeSH term(s) History, 20th Century ; History, 21st Century ; Humans ; Internationality ; Nephrology/history ; Publishing/history ; Societies, Medical/history
    Language English
    Publishing date 2012-01
    Publishing country United States
    Document type Editorial ; Historical Article
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1038/ki.2011.395
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  9. Article ; Online: Low nephron endowment increases susceptibility to renal stress and chronic kidney disease.

    Good, Pamela I / Li, Ling / Hurst, Holly A / Serrano Herrera, Ileana / Xu, Katherine / Rao, Meenakshi / Bateman, David A / Al-Awqati, Qais / D'Agati, Vivette D / Costantini, Frank / Lin, Fangming

    JCI insight

    2023  Volume 8, Issue 3

    Abstract: Preterm birth results in low nephron endowment and increased risk of acute kidney injury (AKI) and chronic kidney disease (CKD). To understand the pathogenesis of AKI and CKD in preterm humans, we generated potentially novel mouse models with a 30%-70% ... ...

    Abstract Preterm birth results in low nephron endowment and increased risk of acute kidney injury (AKI) and chronic kidney disease (CKD). To understand the pathogenesis of AKI and CKD in preterm humans, we generated potentially novel mouse models with a 30%-70% reduction in nephron number by inhibiting or deleting Ret tyrosine kinase in the developing ureteric bud. These mice developed glomerular and tubular hypertrophy, followed by the transition to CKD, recapitulating the renal pathological changes seen in humans born preterm. We injected neonatal mice with gentamicin, a ubiquitous nephrotoxic exposure in preterm infants, and detected more severe proximal tubular injury in mice with low nephron number compared with controls with normal nephron number. Mice with low nephron number had reduced proliferative repair with more rapid development of CKD. Furthermore, mice had more profound inflammation with highly elevated levels of MCP-1 and CXCL10, produced in part by damaged proximal tubules. Our study directly links low nephron endowment with postnatal renal hypertrophy, which in this model is maladaptive and results in CKD. Underdeveloped kidneys are more susceptible to gentamicin-induced AKI, suggesting that AKI in the setting of low nephron number is more severe and further increases the risk of CKD in this vulnerable population.
    MeSH term(s) Animals ; Female ; Humans ; Mice ; Acute Kidney Injury/pathology ; Gentamicins ; Hypertrophy/pathology ; Infant, Premature ; Kidney/pathology ; Nephrons/pathology ; Premature Birth/pathology ; Renal Insufficiency, Chronic/pathology
    Chemical Substances Gentamicins
    Language English
    Publishing date 2023-02-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.161316
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  10. Article ; Online: Terminal differentiation in epithelia: the role of integrins in hensin polymerization.

    Al-Awqati, Qais

    Annual review of physiology

    2011  Volume 73, Page(s) 401–412

    Abstract: Epithelia, the most abundant cell type, differentiate to protoepithelia from stem cells by developing apical and basolateral membrane domains and form sheets of cells connected by junctions. Following this differentiation step, the cells undergo a second ...

    Abstract Epithelia, the most abundant cell type, differentiate to protoepithelia from stem cells by developing apical and basolateral membrane domains and form sheets of cells connected by junctions. Following this differentiation step, the cells undergo a second step (terminal differentiation), during which they acquire a mature phenotype, which unlike the protoepithelial one is tissue and organ specific. An extracellular matrix (ECM) protein termed hensin (DMBT1) mediates this differentiation step in the kidney intercalated cells. Although hensin is secreted as a soluble monomer, it requires polymerization and deposition in the ECM to become active. The polymerization step is mediated by the activation of inside-out signaling by integrins and by the secretion of two proteins: cypA (a cis-trans prolyl isomerase) and galectin 3.
    MeSH term(s) Animals ; Cell Differentiation/physiology ; Cyclophilin A/physiology ; Epithelium/physiology ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Galectin 3/physiology ; Humans ; Integrins/physiology ; Kidney/physiology ; Polymerization ; Rabbits ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Receptors, Scavenger/genetics ; Receptors, Scavenger/metabolism ; Signal Transduction/physiology
    Chemical Substances DMBT1 protein, human ; Extracellular Matrix Proteins ; Galectin 3 ; Integrins ; Receptors, Cell Surface ; Receptors, Scavenger ; hensin protein, rabbit ; Cyclophilin A (EC 5.2.1.-)
    Language English
    Publishing date 2011
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 207933-1
    ISSN 1545-1585 ; 0066-4278
    ISSN (online) 1545-1585
    ISSN 0066-4278
    DOI 10.1146/annurev-physiol-012110-142253
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