Gotowe bibliografie tematyczne / Fetal hydronephrosis

Gotowa bibliografia na temat „Fetal hydronephrosis”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 18 lutego 2022

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Artykuły w czasopismach na temat "Fetal hydronephrosis"

King, Lowell R. "Fetal Hydronephrosis". Mayo Clinic Proceedings 70, nr 6 (czerwiec 1995): 601–2. http://dx.doi.org/10.1016/s0025-6196(11)64324-3.

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Medjebeur, A. A., L. Bussieres, B. Gasser, V. Gimonet i K. Laborde. "Experimental bilateral urinary obstruction in fetal sheep: transforming growth factor-beta 1 expression". American Journal of Physiology-Renal Physiology 273, nr 3 (1.09.1997): F372—F379. http://dx.doi.org/10.1152/ajprenal.1997.273.3.f372.

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To gain insight into the role of transforming growth factor-beta 1 (TGF-beta 1) in the development of kidney pathology following fetal obstruction, we measured TGF-beta 1 gene expression, the active peptide, and the urinary concentration in a model of fetal bilateral urinary obstruction (BUO) in sheep. Fetal lambs underwent BUO at 60 (FO-60) or 80 days (FO-80) of gestation and were studied at 120 days. Independently of the onset or duration of obstruction, all fetuses developed type IV dysplasia (IV) associated with an arrest in the nephrogenesis or hydronephrosis. Fetal glomerular filtration rate was not significantly modified, whereas sodium tubular reabsorption was significantly decreased, and urinary TGF-beta 1 concentration was elevated in hydronephrosis but not in IV. Levels of TGF-beta 1 mRNA were increased in hydronephrosis compared with normal kidneys, and active TGF-beta 1 immunoreactivity was increased in both hydronephrotic and IV kidneys. In summary, TGF-beta 1 may play a role in the development of hydronephrosis and dysplasia in kidneys following fetal BUO. Its role in the arrest of nephrogenesis observed in the IV kidneys remains to be proved.

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Venkatesan, Krishnan, Joel Green, Steven R. Shapiro i George F. Steinhardt. "Correlation of Hydronephrosis Index to Society of Fetal Urology Hydronephrosis Scale". Advances in Urology 2009 (2009): 1–4. http://dx.doi.org/10.1155/2009/960490.

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Purpose. We seek to correlate conventional hydronephrosis (HN) grade and hydronephrosis index (HI).Methods. We examined 1207 hydronephrotic kidneys by ultrasound. HN was classified by Society of Fetal Urology guidelines. HN was then gauged using HI, a reproducible, standardized, and dimensionless measurement of renal area. We then calculated average HI for each HN grade.Results. Comparing HI to standard SFU HN grade, average HI is 89.3 for grade I; average HI is 83.9 for grade II; average HI is 73.0 for grade III; average HI is 54.6 for SFU grade IV.Conclusions. HI correlates well with SFU HN grade. The HI serves as a quantitative measure of HN. HI can be used to track HN over time. Versus conventional grading, HI may be more sensitive in defining severe (grades III and IV) HN, and in indicating resolving, stable, or worsening HN, thus providing more information for clinical decision-making and HN management.

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Gonçalves, Anderson, Willy G. França, Suzana G. Moraes, Luis A. V. Pereira i Lourenço Sbragia. "Adriamycin-induced fetal hydronephrosis". International braz j urol 30, nr 6 (grudzień 2004): 508–13. http://dx.doi.org/10.1590/s1677-55382004000600012.

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Biesecker, Leslie G., i Renata Laxova. "Management of Fetal Hydronephrosis". Mayo Clinic Proceedings 70, nr 6 (czerwiec 1995): 603. http://dx.doi.org/10.1016/s0025-6196(11)64325-5.

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Sherer, D. M. "Is fetal hydronephrosis overdiagnosed?" Ultrasound in Obstetrics and Gynecology 16, nr 7 (grudzień 2000): 601–6. http://dx.doi.org/10.1046/j.1469-0705.2000.00339.x.

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Ozcan, Tulin. "Ultrasonography for Fetal Hydronephrosis". Ultrasound Clinics 8, nr 1 (styczeń 2013): 69–77. http://dx.doi.org/10.1016/j.cult.2012.08.015.

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Quan, A. "Fetal and neonatal hydronephrosis". Early Human Development 82, nr 1 (styczeń 2006): 1–2. http://dx.doi.org/10.1016/j.earlhumdev.2005.11.006.

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Yiee, Jenny, i Duncan Wilcox. "Management of fetal hydronephrosis". Pediatric Nephrology 23, nr 3 (2.08.2007): 347–53. http://dx.doi.org/10.1007/s00467-007-0542-y.

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Shimada, Kenji, Shozo Hosokawa i Akira Tohda. "HISTOLOGICAL STUDY OF FETAL HYDRONEPHROSIS". Japanese Journal of Urology 84, nr 12 (1993): 2097–102. http://dx.doi.org/10.5980/jpnjurol1989.84.2097.

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Rozprawy doktorskie na temat "Fetal hydronephrosis"

Samnakay, Naeem. "Antenatal bladder outflow obstruction : effects of morphology and apoptosis in the fetal kidney, and effects on fetal ACTH and cortisol levels in an ovine model". University of Western Australia. School of Women's and Infants' Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0151.

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Posterior urethral valves cause bladder outflow obstruction and damage to the developing fetal kidney. Posterior urethral valves affect 1 in 8000 new-born males. A third of these children develop end stage renal failure by adolescence, despite valve ablation in the early post-natal period, implying that majority of the damage to the kidneys occurs in utero. How does this damage occur, and should we intervene in utero? The answers to these questions require further research, and are the basis to this thesis. This thesis focused on the effect bladder outflow obstruction has on morphology and apoptosis in the fetal kidney in a fetal lamb model. It also looked at the effect of bladder outflow obstruction on fetal stress hormone levels. Bladder outflow obstruction was created surgically in fetal lambs at day 70 of gestation, and fetal kidneys were analysed at day 2, 5, 10, 20 and 30 after creation of obstruction. Controls undergoing sham surgery were used for comparison. Four aspects were investigated: - effects of bladder outflow obstruction on renal histology effects of bladder outflow obstruction on expression of pro-apoptosis gene Bax and anti-apoptosis gene Bcl-X - effects of bladder outflow obstruction on renal regional apoptosis effects of bladder outflow obstruction on serum fetal ACTH and cortisol levels. Bladder outflow obstruction resulted in sequential morphological change in the fetal kidney over time. By 2 days post-obstruction, cystic change was noted. In addition, patchy attenuation of the nephrogenic blastema was evident by 5 days post-obstruction, with more confluent blastemal attenuation as well as generalized renal architectural disorganization by 10 days post-obstruction. By 20 and 30 days post-obstruction, cystic renal dysplasia had developed. Bladder outflow obstruction resulted in an increase in the ratio of renal expression of pro-apoptosis gene Bax to anti-apoptosis gene Bcl-X. Regional apoptosis counts showed increased tubular apoptosis compared to controls at 2 days post-obstruction, and increased blastemal apoptosis compared to controls at 5 days post-obstruction. By 10 days post-obstruction, blastemal apoptosis counts were reduced compared to controls. There were no significant differences in fetal serum ACTH and cortisol levels between fetal lambs with bladder outflow obstruction and controls. In conclusion, the results of this thesis outline the spectrum of morphological change in the fetal kidney over 30 days of bladder outflow obstruction. They show that detectable changes in morphology occur within two days of bladder outflow obstruction. Likewise, detectable changes in gene expression occur within 2 days of bladder outflow obstruction. The increased ratio of expression of Bax to Bcl-X suggests a swing towards increased apoptosis in response to bladder outflow obstruction. Further research is required to ascertain if these changes are reversible. However, the early onset of these changes as shown in this thesis suggests that any fetal intervention to protect the fetal kidney from the effects of bladder outflow obstruction may need to be instituted very early in gestation

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Książki na temat "Fetal hydronephrosis"

Fox, Grenville, Nicholas Hoque i Timothy Watts. Endocrinology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198703952.003.0016.

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This chapter provides background information on fetal and neonatal renal development, physiology, and function. Detailed information is given on management of common, antenatally diagnosed, renal anomalies (renal pelvis dilatation/hydronephrosis); post-natal diagnoses (hypospadius, hydrocele); posterior urethral valves; polycystic kidney disease; and rarer diagnoses. There is a guideline on the management of acute renal failure in the newborn, and information on dialysis.

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Części książek na temat "Fetal hydronephrosis"

Silva, Andres, i Hiep T. Nguyen. "Fetal Hydronephrosis". W Pediatric Urology for the Primary Care Physician, 1–10. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-60327-243-8_1.

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Streszczenia konferencji na temat "Fetal hydronephrosis"

Wertaschnigg, D., C. Wohlmuth, C. Schimke i TA Kiener. "Ultrasound markers in fetal hydronephrosis to predict postnatal surgery". W Ultraschall 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1606902.

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Wilkins, J., H. Lambert i S. Robson. "G235(P) Isolated fetal hydronephrosis: sonographic predictors of adverse postnatal outcome". W Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.229.

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Hondrich, M., F. Bahlmann, K. Latta i A. Al Naimi. "Schwere fetale Hydronephrosen: pränatale Diagnose – postnatales Outcome". W 29. Deutscher Kongress für Perinatale Medizin. Deutsche Gesellschaft für Perinatale Medizin (DGPM) – „Hinterm Horizont geht's weiter, zusammen sind wir stark“. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-3401264.

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