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Book ; Online ; E-Book: Pediatric nephrology

Emma, Francesco / Goldstein, Stuart L. / Bagga, Arvind / Bates, Carlton M. / Shroff, Rukshana

(Springer nature reference)

2022

Institution	International Pediatric Nephrology Association
Author's details	Francesco Emma, Stuart L. Goldstein, Arvind Bagga, Carlton M. Bates, Rukshana Shroff editors
Series title	Springer nature reference
Keywords	Pediatric nephrology
Language	English
Size	1 Online-Ressource (xxviii, 2134 Seiten), Illustrationen, Diagramme
Edition	Eight edition
Publisher	Springer
Publishing place	Cham
Publishing country	Switzerland
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT021871419
ISBN	978-3-030-52719-8 ; 9783030527181 ; 3-030-52719-0 ; 3030527182
DOI	10.1007/978-3-030-52719-8
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Implementing Pediatric Surviving Sepsis Campaign Guidelines: Improving Compliance With Lactate Measurement in the PICU.

Mazloom, Anisha / Sears, Stacey M / Carlton, Erin F / Bates, Katherine E / Flori, Heidi R

Critical care explorations

2023 Volume 5, Issue 4, Page(s) e0906

Abstract: The 2020 pediatric Surviving Sepsis Campaign (pSSC) recommends measuring lactate during the first hour of resuscitation for severe sepsis/shock. We aimed to improve compliance with this recommendation for patients who develop severe sepsis/shock while ... ...

Abstract	The 2020 pediatric Surviving Sepsis Campaign (pSSC) recommends measuring lactate during the first hour of resuscitation for severe sepsis/shock. We aimed to improve compliance with this recommendation for patients who develop severe sepsis/shock while admitted to the PICU. Design: Structured, quality improvement initiative. Setting: Single-center, 26-bed, quaternary-care PICU. Patients: All patients with PICU-onset severe sepsis/shock from December 2018 to December 2021. Interventions: Creation of a multidisciplinary local sepsis improvement team, education program targeting frontline providers (nurse practitioners, resident physicians), and peer-to-peer nursing education program with feedback to key stakeholders. Measurements and main results: The primary outcome measure was compliance with obtaining a lactate measurement within 60 minutes of the onset of severe sepsis/shock originating in our PICU using a local Improving Pediatric Sepsis Outcomes database and definitions. The process measure was time to first lactate measurement. Secondary outcomes included number of IV antibiotic days, number of vasoactive days, number of ICU days, and number of ventilator days. A total of 166 unique PICU-onset severe sepsis/shock events and 156 unique patients were included. One year after implementation of our first interventions with subsequent Plan-Do-Study-Act cycles, overall compliance increased from 38% to 47% (24% improvement) and time to first lactate decreased from 175 to 94 minutes (46% improvement). Using a statistical process control I chart, the preshift mean for time to first lactate measurement was noted to be 179 minutes and the postshift mean was noted to be 81 minutes demonstrating a 55% improvement. Conclusions: This multidisciplinary approach led to improvement in time to first lactate measurement, an important step toward attaining our target of lactate measurement within 60 minutes of septic shock identification. Improving compliance is necessary for understanding implications of the 2020 pSSC guidelines on sepsis morbidity and mortality.
Language	English
Publishing date	2023-04-21
Publishing country	United States
Document type	Journal Article
ISSN	2639-8028
ISSN (online)	2639-8028
DOI	10.1097/CCE.0000000000000906
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Article ; Online: AKT Signaling Downstream of KGF Is Necessary and Sufficient for Blocking Cyclophosphamide Bladder Injury.

Narla, Sridhar T / Bushnell, Daniel S / Duara, Joanne L / Bates, Carlton M

The American journal of pathology

2022 Volume 192, Issue 4, Page(s) 604–612

Abstract: Keratinocyte growth factor (KGF) drives phosphorylated (activated) AKT (pAKT) in bladder urothelium, which correlates with cytoprotection from cyclophosphamide. The current study determined whether: i) KGF modifies AKT targets [B-cell lymphoma protein 2- ... ...

Abstract	Keratinocyte growth factor (KGF) drives phosphorylated (activated) AKT (pAKT) in bladder urothelium, which correlates with cytoprotection from cyclophosphamide. The current study determined whether: i) KGF modifies AKT targets [B-cell lymphoma protein 2-associated agonist of cell death (BAD) and mammalian target of rapamycin complex (mTORC)-1] that could block apoptosis; ii) AKT signaling is required for KGF cytoprotection; iii) direct AKT activation drives cytoprotection; iv) co-administration of KGF and an AKT inhibitor blocks urothelial cytoprotection and AKT and AKT-target activation; and v) an AKT agonist prevents cyclophosphamide-induced urothelial apoptosis. Mice were given KGF and cyclophosphamide (or sham injury), and pBAD (readout of BAD inhibition) or p-p70S6k (pS6, readout of mTORC1 signaling) was assessed. KGF induced pBAD urothelial staining and prevented cyclophosphamide-induced loss of urothelial pS6 staining (likely stabilizing mTORC1 activity). Co-administration of KGF and AKT inhibitor blocked KGF-driven urothelial cytoprotection from cyclophosphamide and prevented pAKT, pBAD, and pS6 urothelial expression. Conversely, systemic AKT agonist blocked cyclophosphamide-induced urothelial apoptosis and induced pAKT, pBAD, and pS6, similar to KGF. Thus, the KGF-AKT signaling axis appeared to phosphorylate (suppress) BAD and prevent cyclophosphamide-induced loss of mTORC1 signaling, both of which likely suppress apoptosis. Additionally, AKT signaling was required for KGF-driven cytoprotection, and direct AKT activation was sufficient for blocking apoptosis. Thus, AKT may be a therapeutic target for blocking urothelial apoptosis from cyclophosphamide.
MeSH term(s)	Animals ; Apoptosis ; Cyclophosphamide ; Fibroblast Growth Factor 7/metabolism ; Fibroblast Growth Factor 7/pharmacology ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Proto-Oncogene Proteins c-akt/metabolism ; Urinary Bladder/metabolism
Chemical Substances	Fibroblast Growth Factor 7 (126469-10-1) ; Cyclophosphamide (8N3DW7272P) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2022.01.004
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Article ; Online: Urothelial progenitors in development and repair.

Jackson, Ashley R / Narla, Sridhar T / Bates, Carlton M / Becknell, Brian

Pediatric nephrology (Berlin, Germany)

2021 Volume 37, Issue 8, Page(s) 1721–1731

Abstract: Urothelium is a specialized multilayer epithelium that lines the urinary tract from the proximal urethra to the kidney. In addition to proliferation and differentiation during development, urothelial injury postnatally triggers a robust regenerative ... ...

Abstract	Urothelium is a specialized multilayer epithelium that lines the urinary tract from the proximal urethra to the kidney. In addition to proliferation and differentiation during development, urothelial injury postnatally triggers a robust regenerative capacity to restore the protective barrier between the urine and tissue. Mounting evidence supports the existence of dedicated progenitor cell populations that give rise to urothelium during development and in response to injury. Understanding the cellular and molecular basis for urothelial patterning and repair will inform tissue regeneration therapies designed to ameliorate a number of structural and functional defects of the urinary tract. Here, we review the current understanding of urothelial progenitors and the signaling pathways that govern urothelial development and repair. While most published studies have focused on bladder urothelium, we also discuss literature on upper tract urothelial progenitors. Furthermore, we discuss evidence supporting existence of context-specific progenitors. This knowledge is fundamental to the development of strategies to regenerate or engineer damaged or diseased urothelium.
MeSH term(s)	Cell Differentiation ; Humans ; Stem Cells ; Urinary Bladder ; Urinary Tract ; Urothelium/metabolism
Language	English
Publishing date	2021-09-02
Publishing country	Germany
Document type	Journal Article ; Review ; 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/s00467-021-05239-w
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Zs.A 2196: Show issues

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Article ; Online: Pkd2 Deficiency in Embryonic Aqp2 + Progenitor Cells Is Sufficient to Cause Severe Polycystic Kidney Disease.

Tsilosani, Akaki / Gao, Chao / Chen, Enuo / Lightle, Andrea R / Shehzad, Sana / Sharma, Madhulika / Tran, Pamela V / Bates, Carlton M / Wallace, Darren P / Zhang, Wenzheng

Journal of the American Society of Nephrology : JASN

2024 Volume 35, Issue 4, Page(s) 398–409

Abstract: Significance statement: Autosomal dominant polycystic kidney disease (ADPKD) is a devastating disorder caused by mutations in polycystin 1 ( PKD1 ) and polycystin 2 ( PKD2 ). Currently, the mechanism for renal cyst formation remains unclear. Here, we ... ...

Abstract	Significance statement: Autosomal dominant polycystic kidney disease (ADPKD) is a devastating disorder caused by mutations in polycystin 1 ( PKD1 ) and polycystin 2 ( PKD2 ). Currently, the mechanism for renal cyst formation remains unclear. Here, we provide convincing and conclusive data in mice demonstrating that Pkd2 deletion in embryonic Aqp2 + progenitor cells (AP), but not in neonate or adult Aqp2 + cells, is sufficient to cause severe polycystic kidney disease (PKD) with progressive loss of intercalated cells and complete elimination of α -intercalated cells, accurately recapitulating a newly identified cellular phenotype of patients with ADPKD. Hence, Pkd2 is a new potential regulator critical for balanced AP differentiation into, proliferation, and/or maintenance of various cell types, particularly α -intercalated cells. The Pkd2 conditional knockout mice developed in this study are valuable tools for further studies on collecting duct development and early steps in cyst formation. The finding that Pkd2 loss triggers the loss of intercalated cells is a suitable topic for further mechanistic studies. Background: Most cases of autosomal dominant polycystic kidney disease (ADPKD) are caused by mutations in PKD1 or PKD2. Currently, the mechanism for renal cyst formation remains unclear. Aqp2 + progenitor cells (AP) (re)generate ≥5 cell types, including principal cells and intercalated cells in the late distal convoluted tubules (DCT2), connecting tubules, and collecting ducts. Methods: Here, we tested whether Pkd2 deletion in AP and their derivatives at different developmental stages is sufficient to induce PKD. Aqp2Cre Pkd2f/f ( Pkd2AC ) mice were generated to disrupt Pkd2 in embryonic AP. Aqp2ECE/+Pkd2f/f ( Pkd2ECE ) mice were tamoxifen-inducted at P1 or P60 to inactivate Pkd2 in neonate or adult AP and their derivatives, respectively. All induced mice were sacrificed at P300. Immunofluorescence staining was performed to categorize and quantify cyst-lining cell types. Four other PKD mouse models and patients with ADPKD were similarly analyzed. Results: Pkd2 was highly expressed in all connecting tubules/collecting duct cell types and weakly in all other tubular segments. Pkd2AC mice had obvious cysts by P6 and developed severe PKD and died by P17. The kidneys had reduced intercalated cells and increased transitional cells. Transitional cells were negative for principal cell and intercalated cell markers examined. A complete loss of α -intercalated cells occurred by P12. Cysts extended from the distal renal segments to DCT1 and possibly to the loop of Henle, but not to the proximal tubules. The induced Pkd2ECE mice developed mild PKD. Cystic α -intercalated cells were found in the other PKD models. AQP2 + cells were found in cysts of only 13/27 ADPKD samples, which had the same cellular phenotype as Pkd2AC mice. Conclusions: Hence, Pkd2 deletion in embryonic AP, but unlikely in neonate or adult Aqp2 + cells (principal cells and AP), was sufficient to cause severe PKD with progressive elimination of α -intercalated cells, recapitulating a newly identified cellular phenotype of patients with ADPKD. We proposed that Pkd2 is critical for balanced AP differentiation into, proliferation, and/or maintenance of cystic intercalated cells, particularly α -intercalated cells.
MeSH term(s)	Adult ; Animals ; Humans ; Mice ; Aquaporin 2/deficiency ; Aquaporin 2/genetics ; Cysts ; Kidney/metabolism ; Mice, Knockout ; Polycystic Kidney Diseases/genetics ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/metabolism ; Renal Insufficiency, Chronic ; Stem Cells/metabolism ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism
Chemical Substances	Aqp2 protein, mouse ; Aquaporin 2 ; TRPP Cation Channels
Language	English
Publishing date	2024-01-23
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.0000000000000309
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Article ; Online: Perspective commentary from the Society for Pediatric Research: supporting early-stage pediatric physician-scientist success.

Hurley, Edward / Peeples, Eric S / Bates, Carlton M / Hunstad, David A / Barkin, Shari L

Pediatric research

2020 Volume 87, Issue 5, Page(s) 834–838

MeSH term(s)	Biomedical Research/education ; Biomedical Research/trends ; Humans ; Mentors ; National Institutes of Health (U.S.) ; Pediatrics/education ; Pediatrics/trends ; Peer Group ; Physicians ; Research Personnel ; Societies, Medical ; Training Support ; United States
Language	English
Publishing date	2020-01-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	4411-8
ISSN	1530-0447 ; 0031-3998
ISSN (online)	1530-0447
ISSN	0031-3998
DOI	10.1038/s41390-019-0745-5
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Zs.A 564: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Role of fibroblast growth factor receptor signaling in kidney development.

Bates, Carlton M

American journal of physiology. Renal physiology

2011 Volume 301, Issue 2, Page(s) F245–51

Abstract: Fibroblast growth factor receptors (Fgfrs) consist of four signaling family members and one nonsignaling "decoy" receptor, Fgfr-like 1 (Fgfrl1), all of which are expressed in the developing kidney. Several studies have shown that exogenous fibroblast ... ...

Abstract	Fibroblast growth factor receptors (Fgfrs) consist of four signaling family members and one nonsignaling "decoy" receptor, Fgfr-like 1 (Fgfrl1), all of which are expressed in the developing kidney. Several studies have shown that exogenous fibroblast growth factors (Fgfs) affect growth and maturation of the metanephric mesenchyme (MM) and ureteric bud (UB) in cultured tissues. Transgenic and conditional knockout approaches in whole animals have shown that Fgfr1 and Fgfr2 (predominantly the IIIc isoform) in kidney mesenchyme are critical for early MM and UB formation. Conditional deletion of the ligand, Fgf8, in nephron precursors or global deletion of Fgfrl1 interrupts nephron formation. Fgfr2 (likely the IIIb isoform signaling downstream of Fgf7 and Fgf10) is critical for ureteric morphogenesis. Moreover, Fgfr2 appears to act independently of Frs2α (the major signaling adapter for Fgfrs) in regulating UB branching. Loss of Fgfr2 in the MM leads to many kidney and urinary tract anomalies, including vesicoureteral reflux. Thus Fgfr signaling is critical for patterning of virtually all renal lineages at early and later stages of development.
MeSH term(s)	Animals ; Body Patterning ; Humans ; Kidney/embryology ; Kidney/metabolism ; Receptors, Fibroblast Growth Factor/metabolism ; Signal Transduction
Chemical Substances	Receptors, Fibroblast Growth Factor
Language	English
Publishing date	2011-05-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00186.2011
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Article ; Online: Role of fibroblast growth factor receptor signaling in kidney development.

Bates, Carlton M

Pediatric nephrology (Berlin, Germany)

2011 Volume 26, Issue 9, Page(s) 1373–1379

Abstract: Fibroblast growth factor receptors (Fgfrs) are expressed throughout the developing kidney. Several early studies have shown that exogenous fibroblast growth factors (Fgfs) affect growth and maturation of the metanephric mesenchyme (MM) and ureteric bud ( ... ...

Abstract	Fibroblast growth factor receptors (Fgfrs) are expressed throughout the developing kidney. Several early studies have shown that exogenous fibroblast growth factors (Fgfs) affect growth and maturation of the metanephric mesenchyme (MM) and ureteric bud (UB). Transgenic mice that over-express a dominant negative receptor isoform develop renal aplasia/severe dysplasia, confirming the importance of Fgfrs in renal development. Furthermore, global deletion of Fgf7, Fgf10, and Fgfr2IIIb (isoform that binds Fgf7 and Fgf10) in mice leads to small kidneys with fewer collecting ducts and nephrons. Deletion of Fgfrl1, a receptor lacking intracellular signaling domains, causes severe renal dysgenesis. Conditional targeting of Fgf8 from the MM interrupts nephron formation. Deletion of Fgfr2 from the UB results in severe ureteric branching and stromal mesenchymal defects, although loss of Frs2α (major signaling adapter for Fgfrs) in the UB causes only mild renal hypoplasia. Deletion of both Fgfr1 and Fgfr2 in the MM results in renal aplasia with defects in MM formation and initial UB elongation and branching. Loss of Fgfr2 in the MM leads to many renal and urinary tract anomalies as well as vesicoureteral reflux. Thus, Fgfr signaling is critical for patterning of virtually all renal lineages at early and later stages of development.
MeSH term(s)	Animals ; Fibroblast Growth Factors/metabolism ; Humans ; Kidney/abnormalities ; Kidney/embryology ; Kidney/metabolism ; Mice ; Mice, Transgenic ; Organogenesis ; Receptors, Fibroblast Growth Factor/genetics ; Receptors, Fibroblast Growth Factor/metabolism ; Signal Transduction/genetics ; Urogenital Abnormalities/embryology ; Urogenital Abnormalities/metabolism
Chemical Substances	Receptors, Fibroblast Growth Factor ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2011-01-11
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/s00467-010-1747-z
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Article: [Evolution and intelligent design].

Bates, Carlton M

The Pharos of Alpha Omega Alpha-Honor Medical Society. Alpha Omega Alpha

2007 Volume 70, Issue 2, Page(s) 66–67

MeSH term(s)	Biological Evolution ; Evolution, Molecular ; Humans ; Intelligence ; Peer Review, Research ; Religion and Science ; Research Design ; United States
Language	English
Publishing date	2007
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	604131-0
ISSN	0031-7179
ISSN	0031-7179
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Article ; Online: Keratinocyte Growth Factor Reduces Injury and Leads to Early Recovery from Cyclophosphamide Bladder Injury.

Narla, Sridhar T / Bushnell, Daniel S / Schaefer, Caitlin M / Nouraie, Mehdi / Bates, Carlton M

The American journal of pathology

2019 Volume 190, Issue 1, Page(s) 108–124

Abstract: Keratinocyte growth factor (KGF) improves cyclophosphamide-induced bladder injury. To understand the mechanisms, we subcutaneously administered KGF to mice 24 hours before i.p. cyclophosphamide administration, followed by histologic assays and ... ...

Abstract	Keratinocyte growth factor (KGF) improves cyclophosphamide-induced bladder injury. To understand the mechanisms, we subcutaneously administered KGF to mice 24 hours before i.p. cyclophosphamide administration, followed by histologic assays and immunostaining. In vehicle (phosphate-buffered saline)-pretreated mice, nonapoptotic superficial cell death from 2 to 6 hours and apoptosis in intermediate and basal cells from 4 to 24 hours was observed after cyclophosphamide. Despite superficial cell loss, KGF suppressed intermediate and basal cell apoptosis, likely via AKT signaling. At 6 and 24 hours after cyclophosphamide, KGF-pretreated mice also had apparent extracellular signal-regulated kinase (ERK)-driven proliferation of mostly keratin 5 (KRT5)
MeSH term(s)	Animals ; Antineoplastic Agents, Alkylating/toxicity ; Cell Proliferation ; Cyclophosphamide/toxicity ; Cystitis/chemically induced ; Cystitis/metabolism ; Cystitis/pathology ; Cystitis/prevention & control ; Cytoprotection ; Female ; Fibroblast Growth Factor 7/genetics ; Fibroblast Growth Factor 7/metabolism ; Mice ; Regeneration ; Urinary Bladder/injuries ; Urinary Bladder/metabolism ; Urinary Bladder/pathology
Chemical Substances	Antineoplastic Agents, Alkylating ; Fgf7 protein, mouse ; Fibroblast Growth Factor 7 (126469-10-1) ; Cyclophosphamide (8N3DW7272P)
Language	English
Publishing date	2019-10-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2019.09.015
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