LIVIVO - Search results -

Search results

Result 1 - 10 of total 37

Search options

Article ; Online: Acute Postinfectious Glomerulonephritis.

Duong, Minh Dien / Reidy, Kimberly J

2022 Volume 69, Issue 6, Page(s) 1051–1078

Abstract: Postinfectious glomerulonephritis (PIGN) is a leading cause of acute glomerulonephritis in children. The presentation of PIGN can vary from asymptomatic microscopic hematuria incidentally detected on routine urinalysis to nephritic syndrome and a rapidly ...

Abstract	Postinfectious glomerulonephritis (PIGN) is a leading cause of acute glomerulonephritis in children. The presentation of PIGN can vary from asymptomatic microscopic hematuria incidentally detected on routine urinalysis to nephritic syndrome and a rapidly progressive glomerulonephritis. Treatment involves supportive care with salt and water restriction, and the use of diuretic and/or antihypertensive medication, depending on the severity of fluid retention and the presence of hypertension. PIGN resolves completely and spontaneously in most children, and the long-term outcomes are typically good with preserved renal function and no recurrence.
MeSH term(s)	Child ; Humans ; Glomerulonephritis/diagnosis ; Glomerulonephritis/drug therapy ; Glomerulonephritis/etiology ; Antihypertensive Agents ; Diuretics ; Hematuria ; Hypertension
Chemical Substances	Antihypertensive Agents ; Diuretics
Language	English
Publishing date	2022-10-29
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	215711-1
ISSN	1557-8240 ; 0031-3955
ISSN (online)	1557-8240
ISSN	0031-3955
DOI	10.1016/j.pcl.2022.08.001
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Um IV Zs.147: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Re-energizing the kidney: targeting fatty acid metabolism protects against kidney fibrosis.

Reidy, Kimberly J / Ross, Michael J

Kidney international

2021 Volume 100, Issue 4, Page(s) 742–744

MeSH term(s)	Fatty Acids ; Fibrosis ; Humans ; Kidney/pathology ; Kidney Diseases/pathology ; Kidney Diseases/prevention & control ; Lipid Metabolism
Chemical Substances	Fatty Acids
Language	English
Publishing date	2021-06-17
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.2021.06.010
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 797: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Approach to the Child with Hematuria.

Brown, Denver D / Reidy, Kimberly J

Pediatric clinics of North America

2018 Volume 66, Issue 1, Page(s) 15–30

Abstract: The causes of macroscopic and microscopic hematuria overlap; both are often caused by urinary tract infections or urethral/bladder irritation. Coexistent hypertension and proteinuria should prompt investigation for glomerular disease. The most common ... ...

Abstract	The causes of macroscopic and microscopic hematuria overlap; both are often caused by urinary tract infections or urethral/bladder irritation. Coexistent hypertension and proteinuria should prompt investigation for glomerular disease. The most common glomerulonephritis in children is postinfectious glomerulonephritis. In most patients, and especially with isolated microscopic hematuria, the diagnostic workup reveals no clear underlying cause. In those cases whereby a diagnosis is made, the most common causes of persistent microscopic hematuria are thin basement membrane nephropathy, immunoglobulin A nephropathy, or idiopathic hypercalciuria. Treatment and long-term prognosis varies with the underlying disease.
MeSH term(s)	Child ; Diagnosis, Differential ; Glomerulonephritis, IGA/complications ; Hematuria/diagnosis ; Hematuria/etiology ; Humans ; Hypercalciuria/complications ; Hypertension/complications ; Kidney Diseases/complications ; Proteinuria/complications ; Urinary Tract Infections/complications
Language	English
Publishing date	2018-03-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	215711-1
ISSN	1557-8240 ; 0031-3955
ISSN (online)	1557-8240
ISSN	0031-3955
DOI	10.1016/j.pcl.2018.08.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Um IV Zs.147: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Genetic Syndromes Affecting Kidney Development.

Pal, Abhijeet / Reidy, Kimberly J

Results and problems in cell differentiation

2017 Volume 60, Page(s) 257–279

Abstract: Renal anomalies are common birth defects that may manifest as a wide spectrum of anomalies from hydronephrosis (dilation of the renal pelvis and calyces) to renal aplasia (complete absence of the kidney(s)). Aneuploidies and mosaicisms are the most ... ...

Abstract	Renal anomalies are common birth defects that may manifest as a wide spectrum of anomalies from hydronephrosis (dilation of the renal pelvis and calyces) to renal aplasia (complete absence of the kidney(s)). Aneuploidies and mosaicisms are the most common syndromes associated with CAKUT. Syndromes with single gene and renal developmental defects are less common but have facilitated insight into the mechanism of renal and other organ development. Analysis of underlying genetic mutations with transgenic and mutant mice has also led to advances in our understanding of mechanisms of renal development.
MeSH term(s)	Animals ; Genetic Predisposition to Disease ; Humans ; Kidney/embryology ; Kidney Diseases/congenital ; Kidney Diseases/genetics ; Organogenesis ; Syndrome
Language	English
Publishing date	2017
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	0080-1844
ISSN	0080-1844
DOI	10.1007/978-3-319-51436-9_10
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Preterm birth and neonatal acute kidney injury: implications on adolescent and adult outcomes.

Harer, Matthew W / Charlton, Jennifer R / Tipple, Trent E / Reidy, Kimberly J

Journal of perinatology : official journal of the California Perinatal Association

2020 Volume 40, Issue 9, Page(s) 1286–1295

Abstract: As a result of preterm birth, immature kidneys are exposed to interventions in the NICU that promote survival, but are nephrotoxic. Furthermore, the duration of renal development may be truncated in these vulnerable neonates. Immaturity and nephrotoxic ... ...

Abstract	As a result of preterm birth, immature kidneys are exposed to interventions in the NICU that promote survival, but are nephrotoxic. Furthermore, the duration of renal development may be truncated in these vulnerable neonates. Immaturity and nephrotoxic exposures predispose preterm newborns to acute kidney injury (AKI), particularly in the low birth weight and extremely preterm gestational age groups. Several studies have associated preterm birth as a risk factor for future chronic kidney disease (CKD). However, only a few publications have investigated the impact of neonatal AKI on CKD development. Here, we will review the evidence linking preterm birth and AKI in the NICU to CKD and highlight the knowledge gaps and opportunities for future research. For neonatal intensive care studies, we propose the inclusion of AKI as an important short-term morbidity outcome and CKD findings such as a reduced glomerular filtration rate in the assessment of long-term outcomes.
MeSH term(s)	Acute Kidney Injury/epidemiology ; Acute Kidney Injury/etiology ; Adolescent ; Adult ; Female ; Gestational Age ; Humans ; Infant, Low Birth Weight ; Infant, Newborn ; Morbidity ; Pregnancy ; Premature Birth/epidemiology ; Risk Factors
Language	English
Publishing date	2020-04-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645021-0
ISSN	1476-5543 ; 0743-8346
ISSN (online)	1476-5543
ISSN	0743-8346
DOI	10.1038/s41372-020-0656-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2412: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Genetic risk of APOL1 and kidney disease in children and young adults of African ancestry.

Reidy, Kimberly J / Hjorten, Rebecca / Parekh, Rulan S

Current opinion in pediatrics

2018 Volume 30, Issue 2, Page(s) 252–259

Abstract: Purpose of review: Understanding the genetic risk of APOL1 in children and young adults is important given the lifetime risk of hypertension and kidney disease among children of African descent. We review recent epidemiologic and biologic findings on ... ...

Abstract	Purpose of review: Understanding the genetic risk of APOL1 in children and young adults is important given the lifetime risk of hypertension and kidney disease among children of African descent. We review recent epidemiologic and biologic findings on the effects of APOL1 and kidney disease. Recent findings: APOL1 in children and young adults is associated with hypertension, albuminuria and more rapid decline in kidney function and progression to end-stage kidney disease, especially among those with glomerular causes of kidney disease, and those affected by sickle cell disease or HIV. There are conflicting data on the APOL1 association with cardiovascular disease in children and young adults. APOL1 functions as part of the innate immune system. Podocyte expression of APOL1 likely contributes to the development of kidney disease. In cell culture and model organisms, APOL1 expression disrupts autophagic and ion flux, leads to defects in mitochondrial respiration and induces cell death. Summary: APOL1 explains almost 70% of the excess risk of kidney disease in those of African descent, and is common in children with glomerular disease. An evolving understanding of the pathogenesis of APOL1-mediated kidney damage may aid in personalized medicine approaches to APOL1 attributable kidney disease.
MeSH term(s)	Black or African American/genetics ; Apolipoprotein L1/genetics ; Child ; Genetic Markers ; Genetic Predisposition to Disease/ethnology ; Humans ; Kidney Diseases/ethnology ; Kidney Diseases/genetics ; United States/epidemiology ; Young Adult
Chemical Substances	APOL1 protein, human ; Apolipoprotein L1 ; Genetic Markers
Language	English
Publishing date	2018-02-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1049374-8
ISSN	1531-698X ; 1040-8703
ISSN (online)	1531-698X
ISSN	1040-8703
DOI	10.1097/MOP.0000000000000603
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3049: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Genetic causes of proteinuria and nephrotic syndrome: impact on podocyte pathobiology.

Akchurin, Oleh / Reidy, Kimberly J

Pediatric nephrology (Berlin, Germany)

2014 Volume 30, Issue 2, Page(s) 221–233

Abstract: In the past 20 years, multiple genetic mutations have been identified in patients with congenital nephrotic syndrome (CNS) and both familial and sporadic focal segmental glomerulosclerosis (FSGS). Characterization of the genetic basis of CNS and FSGS has ...

Abstract	In the past 20 years, multiple genetic mutations have been identified in patients with congenital nephrotic syndrome (CNS) and both familial and sporadic focal segmental glomerulosclerosis (FSGS). Characterization of the genetic basis of CNS and FSGS has led to the recognition of the importance of podocyte injury to the development of glomerulosclerosis. Genetic mutations induce injury due to effects on the podocyte's structure, actin cytoskeleton, calcium signaling, and lysosomal and mitochondrial function. Transgenic animal studies have contributed to our understanding of podocyte pathobiology. Podocyte endoplasmic reticulum stress response, cell polarity, and autophagy play a role in maintenance of podocyte health. Further investigations related to the effects of genetic mutations on podocytes may identify new pathways for targeting therapeutics for nephrotic syndrome.
MeSH term(s)	Animals ; Humans ; Nephrotic Syndrome/genetics ; Nephrotic Syndrome/pathology ; Podocytes/pathology ; Proteinuria/genetics ; Proteinuria/pathology
Language	English
Publishing date	2014-03-02
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/s00467-014-2753-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2196: 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)

Order via subito

Details ▾

Article ; Online: Reduced kidney function and hypertension in adolescents with low birth weight, NHANES 1999-2016.

Brathwaite, Kaye E / Levy, Rebecca V / Sarathy, Harini / Agalliu, Ilir / Johns, Tanya S / Reidy, Kimberly J / Fadrowski, Jeffrey J / Schwartz, George J / Kaskel, Frederick J / Melamed, Michal L

Pediatric nephrology (Berlin, Germany)

2023 Volume 38, Issue 9, Page(s) 3071–3082

Abstract: Background: Chronic kidney disease (CKD) is a major health problem, and the risk of CKD and hypertension in children born low birth weight (LBW) is under-recognized. We hypothesized that children born with LBW would have a higher prevalence of reduced ... ...

Abstract	Background: Chronic kidney disease (CKD) is a major health problem, and the risk of CKD and hypertension in children born low birth weight (LBW) is under-recognized. We hypothesized that children born with LBW would have a higher prevalence of reduced kidney function and hypertension. Methods: Using the National Health and Nutrition Examination Survey (NHANES), we conducted a cross-sectional study to evaluate whether LBW (< 2500 g), very low birth weight (VLBW < 1500 g), and large birth weight (BW) (> 4000 g) were associated with kidney disease using 4 different estimating equations. We used the Counahan-Barratt, updated Schwartz, CKiD-U25, and full age spectrum creatinine-based GFR estimating equations to evaluate associations between a history of LBW/VLBW/large BW and reduced kidney function (eGFR < 90 mL/min/1.73 m Results: Our analysis included 6336 children (age 12-15 years) in NHANES representing over 13 million US individuals. Using the updated Schwartz, the prevalence of reduced kidney function was 30.1% (25.2-35.6) for children born with LBW compared to 22.4% (20.5-24.3) in children with normal BW. Equations yielded different estimates of prevalence of reduced kidney function in LBW from 21.5% for Counahan-Barratt to 35.4% for CKiD-U25. Compared to those with normal BW, participants with LBW and VLBW had a 7.2 and 10.3% higher prevalence of elevated BP and a 2.4 and 14.6% higher prevalence of hypertension, respectively. Conclusions: Children born with LBW are at higher risk of reduced kidney function and hypertension than previously described. A higher resolution version of the Graphical abstract is available as Supplementary information.
MeSH term(s)	Infant, Newborn ; Humans ; Child ; Adolescent ; Nutrition Surveys ; Cross-Sectional Studies ; Glomerular Filtration Rate/physiology ; Renal Insufficiency, Chronic/diagnosis ; Infant, Very Low Birth Weight ; Birth Weight ; Hypertension/epidemiology ; Kidney
Language	English
Publishing date	2023-04-13
Publishing country	Germany
Document type	Journal Article ; 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/s00467-023-05958-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2196: 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)

Order via subito

Details ▾

Article ; Online: Premature differentiation of nephron progenitor cell and dysregulation of gene pathways critical to kidney development in a model of preterm birth.

Cwiek, Aleksandra / Suzuki, Masako / deRonde, Kimberly / Conaway, Mark / Bennett, Kevin M / El Dahr, Samir / Reidy, Kimberly J / Charlton, Jennifer R

Scientific reports

2021 Volume 11, Issue 1, Page(s) 21667

Abstract: Preterm birth is a leading cause of neonatal morbidity. Survivors have a greater risk for kidney dysfunction and hypertension. Little is known about the molecular changes that occur in the kidney of individuals born preterm. Here, we demonstrate that ... ...

Abstract	Preterm birth is a leading cause of neonatal morbidity. Survivors have a greater risk for kidney dysfunction and hypertension. Little is known about the molecular changes that occur in the kidney of individuals born preterm. Here, we demonstrate that mice delivered two days prior to full term gestation undergo premature cessation of nephrogenesis, resulting in a lower glomerular density. Kidneys from preterm and term groups exhibited differences in gene expression profiles at 20- and 27-days post-conception, including significant differences in the expression of fat-soluble vitamin-related genes. Kidneys of the preterm mice exhibited decreased proportions of endothelial cells and a lower expression of genes promoting angiogenesis compared to the term group. Kidneys from the preterm mice also had altered nephron progenitor subpopulations, early Six2 depletion, and altered Jag1 expression in the nephrogenic zone, consistent with premature differentiation of nephron progenitor cells. In conclusion, preterm birth alone was sufficient to shorten the duration of nephrogenesis and cause premature differentiation of nephron progenitor cells. These candidate genes and pathways may provide targets to improve kidney health in preterm infants.
MeSH term(s)	Animals ; Cell Differentiation/physiology ; Endothelial Cells/metabolism ; Female ; Gene Expression/genetics ; Gene Expression Regulation, Developmental/genetics ; Gene Regulatory Networks/genetics ; Kidney/embryology ; Kidney/metabolism ; Kidney Glomerulus/embryology ; Kidney Glomerulus/metabolism ; Male ; Mice ; Models, Animal ; Morphogenesis ; Nephrons/embryology ; Nephrons/metabolism ; Organogenesis/genetics ; Pregnancy ; Premature Birth/metabolism ; Stem Cells/metabolism ; Stem Cells/physiology ; Transcription Factors/metabolism
Chemical Substances	Transcription Factors
Language	English
Publishing date	2021-11-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-00489-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: An uncommon case of arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome and review of the renal involvement: Questions.

Duong, Minh Dien / Rose, Chelsi M / Reidy, Kimberly J / Del Rio, Marcela

Pediatric nephrology (Berlin, Germany)

2019 Volume 35, Issue 2, Page(s) 247–248

Abstract: Arthrogryposis, renal dysfunction, and cholestasis syndrome is a rare autosomal recessive disorder caused by mutations in the VPS33B and VIPAR genes. Most cases are fatal within the first year of life. Here we describe one of the two oldest patients with ...

Abstract	Arthrogryposis, renal dysfunction, and cholestasis syndrome is a rare autosomal recessive disorder caused by mutations in the VPS33B and VIPAR genes. Most cases are fatal within the first year of life. Here we describe one of the two oldest patients with arthrogryposis, renal dysfunction, and cholestasis syndrome. This is a 12-year-old Hispanic female, from a non-consanguineous parents, diagnosed with an incomplete phenotype of arthrogryposis, renal dysfunction, and cholestasis syndrome with arthrogryposis and renal tubular dysfunction but without cholestasis. At 11 years of age, she was found to have impaired renal function, nephrotic-range proteinuria, Fanconi syndrome, and distal renal tubular acidosis. She also had hypercalciuria, nephrogenic diabetes insipidus, and small kidneys by renal ultrasound. Genetic analysis using whole exome sequencing showed a mutation and a partial deletion in the VPS33B gene. Further studies showed that the mother has a partial deletion in the VPS33B gene. Her medication regimen includes potassium citrate and enalapril.
Language	English
Publishing date	2019-08-28
Publishing country	Germany
Document type	Journal Article
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-019-04336-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2196: 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)

Order via subito

Details ▾

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito