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Relevant bibliographies by topics / Renal dysplasia

Academic literature on the topic 'Renal dysplasia'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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Journal articles on the topic "Renal dysplasia"

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Menon, Santosh, Nandita Kakkar, and B. D. Radotra. "Expression of Laminin and Fibronectin in Renal Dysplasia." Pediatric and Developmental Pathology 7, no. 6 (November 2004): 568–76. http://dx.doi.org/10.1007/s10024-003-5057-3.

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The pathogenesis of renal dysplasia is a matter of debate. Recent theories have conceptualized the role of extracellular matrix proteins in the genesis of renal dysplasia. During normal nephrogenesis, collagen type I and III and fibronectins are lost and laminin and syndecan appear once proper induction has occurred. Any deviation from the normal pattern is said to lead to dysplasia. In this study, the expressions of adhesive glycoproteins, laminin, and fibronectin were studied immunohistochemically in 25 autopsy cases of renal dysplasia and normal age-matched control cases. These cases of renal dysplasia were categorized into 3 groups based on the period of gestation: 20 to 26 weeks, 27 to 33 weeks, and 34 to 40 weeks. The immunohistochemical findings were graded from 0 to 4+ based on the visual intensity. Chi-square analysis was used to calculate the difference in expressions of laminin and fibronectin in cases and controls as a whole and within and between age groups. Immunostaining for laminin in all age groups showed a significant difference in expression between dysplastic kidneys (less expression) and normal controls (greater expression). In the case of fibronectin expression, all but 1 group showed a significant difference, with dysplastic kidneys showing more and normal controls showing less expression. The inference derived is that laminin expression decreases and fibronectin expression increases in renal dysplasia compared with normal nephrogenesis.

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Shimada, Kenji, Mototsugu Kanokogi, Shinji Okamoto, Masaak Arima, Yoshinori Mori, and Fumihiko Ikoma. "RENAL DYSPLASIA." Japanese Journal of Urology 76, no. 8 (1985): 1179–86. http://dx.doi.org/10.5980/jpnjurol1928.76.8_1179.

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Shimada, Kenji, Mototsugu Kanokogi, Shinji Okamoto, Masaaki Arima, Yoshinori Mori, and Fumihiko Ikoma. "RENAL DYSPLASIA." Japanese Journal of Urology 76, no. 8 (1985): 1187–93. http://dx.doi.org/10.5980/jpnjurol1928.76.8_1187.

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Chen, Rui-Yun, and Han Chang. "Renal Dysplasia." Archives of Pathology & Laboratory Medicine 139, no. 4 (April 1, 2015): 547–51. http://dx.doi.org/10.5858/arpa.2013-0660-rs.

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Renal dysplasia is an aberrant developmental disease usually diagnosed during the perinatal and childhood years. Prevalence is estimated at 0.1% of infants (via ultrasound screening) and 4% of fetuses and infants (via autopsy study). Occurrences may be combined with abnormalities in the collecting system or associated with complex syndromes. Histopathology shows primitive tubules surrounded by a fibromuscular collar. The differential diagnosis includes renal dysplasia, hypoplasia, and renal atrophy. Immunohistochemical expression of the paired box genes 2 and 8 (PAX2/8) and Wilms tumor 1 (WT1) is increased in the primitive ducts and fibromuscular collar, respectively. Renal dysplasia pathogenesis is not well understood, but may be caused by a nephron-inductive deficit due to ampullary inactivity or abnormal budding of the ureteric bud from the mesonephric duct. Either the PAX2 mutation only or cross-talk with the p53 pathway is involved in this deficit. Nephrectomy is the treatment of choice for symptomatic renal dysplasia.

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Aresu, Luca, Renato Zanatta, Paola Pregel, Diego Caliari, Massimiliano Tursi, Federico Valenza, and Alberto Tarducci. "Bilateral juvenile renal dysplasia in a Norwegian Forest Cat." Journal of Feline Medicine and Surgery 11, no. 4 (April 2009): 326–29. http://dx.doi.org/10.1016/j.jfms.2008.08.004.

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Renal dysplasia is defined as a condition of disorganised development of renal parenchyma due to abnormal differentiation. The case of a 5-month-old intact male Norwegian Forest Cat with a history of polyuria and polydipsia is reported. Ultrasonographic examination showed a slight enlargement of kidneys. Biochemical parameters, haematological examinations and clinical signs were compatible with chronic renal failure (CRF). Histological examination was correlated with a primary tubular disorganisation and modification of glomerular compartment. The clinical history together with the histological lesions is consistent with bilateral juvenile renal dysplasia in this cat. To our knowledge, feline renal dysplasia has been reported in fetal infections with panleukopenia virus; no reports indicate the idiopathic origin in feline dysplastic lesions.

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Sisalima, Paola, Mónica Cunalata, and Mónica Juma. "Renal multicystic dysplasia." Revista Médica del Hospital José Carrasco Arteaga 5, no. 1 (March 30, 2013): 94–98. http://dx.doi.org/10.14410/2013.5.1.94.98.

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Mousa, Albeir Y., and Gurpreet Gill. "Renal fibromuscular dysplasia." Seminars in Vascular Surgery 26, no. 4 (December 2013): 213–18. http://dx.doi.org/10.1053/j.semvascsurg.2014.06.006.

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Nemcek, AA, and CE Holmburg. "Reversible renal fibromuscular dysplasia." American Journal of Roentgenology 147, no. 4 (October 1986): 737–38. http://dx.doi.org/10.2214/ajr.147.4.737.

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Sanders, R. C., A. R. Nussbaum, and K. Solez. "Renal dysplasia: sonographic findings." Radiology 167, no. 3 (June 1988): 623–26. http://dx.doi.org/10.1148/radiology.167.3.3283832.

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Lima, Samara Rosolem, Leilane Aparecida Da Silva, Geovanny Bruno Gonçalves Dias, Letícya Lerner Lopes, Raquel Aparecida Sales Da Cruz, Luciana Sonne, Caroline Argenta Pescador, and Edson Moleta Colodel. "Displasia renal em cães: estudo retrospectivo (2008-2013)." Acta Scientiae Veterinariae 45 (June 27, 2017): 5. http://dx.doi.org/10.22456/1679-9216.85334.

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Background: Renal dysplasia, which has been reported in some dogs and human patients, refers to a developmental disorder of renal parenchyma due to imperfect inductive interaction between the mesonephric duct and the metanephric blastemal. In dogs, the characteristic histological findings on which diagnosis is based include (1) persistent metanephric ducts surrounded by primitive mesenchyme, (2) fetal or immature glomeruli, (3) fetal or immature tubules, and (4) anomalous presence of interstitial fibrous tissue. The aim of this study was to report the major pathological and immunohistochemical features of nine young dogs necropsied with renal dysplasia.Cases: The necropsy files from the Laboratório de Patologia Veterinária (LPV) of the Universidade Federal do Mato Grosso (UFMT) were reviewed between the years 2008 and 2013. Dogs diagnosed with chronic kidney failure and macroscopic and histopathological renal lesions consistent with renal dysplasia were selected. Kidney fragments in paraffin blocks were cut and stained with hematoxylin and eosin and by immunohistochemistry (IHC) using anti-vimentin and anti-cytokeratin monoclonal antibodies. The staining was considered positive for the presence of at least one renal cell marked with brown cytoplasmic staining clear and unambiguous. A total of 787 necropsies of dogs were performed. Of these, 64 had a clinical diagnosis of chronic renal failure of which 9 were classified as renal dysplasia. The age of the dogs ranged from 3 months to 2 years. Clinical signs were characterized by anorexia and non-regenerative anemia in 88.9%, vomiting 66.7%, dehydration 55.6%, uremia 55.6%, convulsion 33.4%, abdominal pain 22.3% and diarrhea in 11.2% of cases. At necropsy the main macroscopic changes in the kidneys were external surface with pale staining, in 6 of 9 dogs necropsied. Additionally, 5 dogs, cystic cavities of various sizes from 0.1 to 5 cm in diameter, diffusely distributed in the renal subcapsular surface and cutting were observed. Of the 64 dogs with diagnosis of chronic renal failure, 14.06% had dysplastic kidney changes, characterized by dilatation of Bowman’s space, glomerular and tubular atrophy, immature glomeruli and tubules, lymphocytic interstitial inflammation and fibrosis. In the dogs with renal dysplasia, it was observed that the tubular structures showed marked glomerular labeling for vimentin. Moreover, the kidneys of normal dogs showed weak or absent for marking tubes and glomerular structures for vimentin, and strong staining for cytokeratin in tubular cells, glomerular cells and collecting ducts.Discussion: Renal morphological damage observed in these nine dogs less than two years old, that contained degenerative and inflammatory changes, fibrosis and glomerular atrophy, but mostly immature glomeruli and tubules were associated with atypical renal dysplasia. This condition develops when the urethral diverticulum and metanephric blastoma not properly form in the embryonic stage, resulting in abnormal metanephric differentiation and formation of structures that do not recapitulate the normal nephrogenesis. Abnormal kidney function in young animals caused chronic renal failure resulting in death. The results of immunohistochemical observed in this study can complement the diagnosis of renal dysplasia. The morphological normality can be observed in the proportion of mesenchymal and epithelial tissue in the different structures of the kidney by staining with anti-cytokeratin and anti-vimentin. In the present study, there was moderate to strong labeling of vimentin in glomerular and tubular structures being dysplastic kidney would be expected to occur in normal dogs predominant staining with cytokeratin. Based on the clinic, pathological and immunohistochemical findings it is concluded that the animals developed renal dysplasia.

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More sources

Dissertations / Theses on the topic "Renal dysplasia"

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Cale, Catherine Mary. "Inflammatory mediators in normal and abnormal renal development." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313993.

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Théolade, Anne. "Le syndrome Bor ou branchio-oto-rénal : gravité potentielle de l'atteinte rénale, à propos de trois observations." Université Louis Pasteur (Strasbourg) (1971-2008), 1990. http://www.theses.fr/1990STR1M061.

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CRUNELLE, VALERIE, and DELTEIL FLORENCE PINTON. "La dysplasie multikystique renale de l'enfant : a propos de 56 observations." Lille 2, 1992. http://www.theses.fr/1992LIL2M264.

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Ansari, Ehsanollah. "Apport de l'imagerie médicale actuelle dans le diagnostic et traitement des dysplasies fibromusculaires de l'artère rénale." Montpellier 1, 1990. http://www.theses.fr/1990MON11130.

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JACOTEY, GILLES. "Etude d'un cas de syndrome de turner associe a une dysplasie renale multikystique sur un pseudo-rein en fer a cheval." Lyon 1, 1988. http://www.theses.fr/1988LYO1M428.

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Mariani, Beatriz Marinho de Paula. "Padronização das técnicas de PNA e PCR em tempo real para detecção das mutações ativadoras no GNAS na síndrome de McCune-Albright." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-20122012-105425/.

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A síndrome de McCune Albrigth (SMA) é uma doença genética não hereditária, com incidência estimada entre 1/100.000 e 1/1.000.000 casos/ano. A SMA caracteriza-se clinicamente pela tríade: displasia óssea fibrosa (FD), manchas cutâneas café-com-leite e hiperfunção endócrina tais como: síndrome de Cushing, pseudo-puberdade precoce, hipertiroidismo, acromegalia. O diagnóstico da SMA clássica é usualmente baseado no quadro clínico associado a dosagens hormonais e exames de imagem, principalmente cintilografia do esqueleto. No entanto, quadros atípicos e formas parciais muitas vezes dificultam o diagnóstico preciso da síndrome. O objetivo deste estudo foi padronizar dentre as técnicas de PNA (peptide nucleic acid) e PCT em Tempo Real, para a detecção de polimorfismos de base única (SNPs), a técnica mais sensível para a discriminação das mutações ativadoras da subunidade da proteína G. Para este estudo foram selecionados 32 pacientes, 1 masculino e 31 femininos, com SMA, todos em seguimento no Hospital das Clínicas da Faculdade de Medicina da USP. Como resultado positivo, apresentamos nesse trabalho pela primeira vez o uso do RT-PCR genotipagem na detecção das mutações ativadoras da proteína G, em DNA extraído de tecidos afetados e em leucócitos de sangue periférico, sendo a técnica considerada sensível o suficiente para discriminar de forma simples e rápida as mutações ativadoras da PGs. Sugerimos nesse estudo o uso da técnica de discriminação alélica pelo sistema Taqman. Essa técnica possibilita a detecção destas mutações gsp no sangue periférico mesmo numa baixa porcentagem, uma vez que nem sempre o tecido afetado (gônada, osso, hipófise) é disponível.
The McCune-Albright Syndrome (MAS) is a genetic disease, with incidence estimated at 1/100.000 and 1/1000000 cases per year. MAS is clinically characterized by the triad: bone fibrous dysplasia (FD) café-au-lait skin spots and endocrine hyperfunction, such as: precocious puberty (PP), Cushing's syndrome, hyperthyroidism and acromegaly. The diagnosis of MAS is originally based on clinical characteristics associated with hormonal and imaging studies. However, atypical and partial forms often hamper the accurate diagnosis of the syndrome. For this study we selected 32 patients, 1male and 31 females, all being treated in Hospital das Clínicas, School of Medicine, University of São Paulo. As a positive result, we showed for the first time the use of Real Time PCR/genotyping for the detection of activating mutations of the stimulatory G protein, using blood leucocytes DNA. This technique was sensible and can bring fast results for the patient and the physician, making the diagnosis easier. Our study proposes the use of allelic discrimination by Taqman system, which can be used as a probe that allows the identification of specific genotypes. These techniques could help detect these mutations in peripheral blood when the affected tissue is not available.

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Morcel, Karine. "Génétique du syndrome de Mayer-Rokitansky-Küster-Hauser : étude d'un gène candidat, le gène ITIH5." Rennes 1, 2009. http://www.theses.fr/2009REN1B127.

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Le syndrome de Mayer-Rokitansky-Küster-Hauser (MRKH) est une aplasie utéro-vaginale congénitale pouvant être associée à d'autres malformations. Des cas familiaux ont été décrits. Une délétion chromosomique différente a été découverte chez 4 patientes indépendantes, au sein de loci associés au syndrome de DiGeorge (DGS) (22q11, 10p14, 8p23 et 4q34-ter). En 10p14, un gène, ITIH5, est concerné par la délétion. Il appartient à la famille des gènes ITI ayant un rôle dans la dynamique de la matrice extracellulaire. Chez la souris, l'expression d'Itih5 est forte et s'intensifie au cours du développement dans le tractus génital interne femelle. De plus, les tractus génitaux semblent synthétiser une isoforme protéique d'Itih5 spécifique. Ainsi les loci connus du DGS pourraient être aussi impliqués dans l'étiologie du syndrome MRKH, pouvant conduire à un syndrome dit "de gènes contigus". Enfin, l'haploinsuffisance du gène ITIH5 pourrait rendre compte du syndrome MRKH
The Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome is featured by a congenital utero-vaginal aplasia associated with other malformations. Familial cases were described. A different deletion was found in 4 independent patients within the four chromosomal loci affedted in DiGeorge syndrome (DGS) (22q11, 10p14, 8p23 and 4q34-ter). In 10p14-15, one gene, ITIH5, was affected by the deletion. It is a member of the ITI gene family, playing a role in extracellular matrix dynamics. In the mouse, Itih5 expresssion is strong and increases during embryonic development in the female genital tract. Moreover, the genital tracts seem to synthesize a specific isoform of the Itih5 protein. In conclusion, the loci involved in DGS deletion syndrome might as well be involved in the MRKH syndrome which would then be part of a wider and heterogeneous deletion syndrome. Furthermore our results show that ITIH5 haploinsufficiency could account for the MRKH syndrome

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Ohta, Hiroshi. "Molecular pathobiology for renal tubular dysplasia in Japanese black cattle due to claudin-16 deficiency." Doctoral thesis, 2006. http://hdl.handle.net/2115/32739.

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Goel, Pranay. "Characterisation of pathophysiological function of NEDD4-2 in kidney." Thesis, 2016. http://hdl.handle.net/2440/109813.

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Nedd4-2 (NEDD4L, neural precursor cell expressed, developmentally down regulated 4-like) belongs to the Nedd4 family of ubiquitin ligases. These ligases aid in maintaining cellular homeostasis by binding to, and ubiquitinating a number of membrane proteins to initiate their internalization and turnover. Previous work from our laboratory has suggested that Nedd4-2 plays an essential role in regulating ion channels, especially the epithelial sodium channel and voltage gated sodium channels. The misregulation of these channels has been implicated in multiple channelopathies, including hypertension and cystic fibrosis like disease. This study characterises a previously unknown function of Nedd4-2 in the kidney. In order to understand this significance of Nedd4-2 in renal homeostasis, the previously generated Nedd4-2⁻ʹ⁻ (Nedd4-2 knockout) mice (Boase et al., 2011) were characterised. The initial histological examination of postnatal kidneys suggested renal cyst formation in Nedd4-2⁻ʹ⁻ animals. Further analysis revealed that Nedd4-2 loss results in renal dysplasia. Nedd4-2⁻ʹ⁻ mice showed variable renal cystic index, onset of cyst formation starting from postnatal day 2 and progressing until the Nedd4-2⁻ʹ⁻ animals die due to respiratory distress around day 19-21. To investigate the prevalence of the cystic phenotype in other tissues histological analysis was performed in pancreas, liver, spleen, colon, stomach and thymus with no significant pathological differences observed in the knockout mice. The Nedd4-2⁻ʹ⁻ kidneys showed increased cell proliferation, with no apoptotic differences in the cells lining the cystic epithelia suggesting an imbalance between cell proliferation and apoptosis in cyst formation. The cyst formation and kidney development disorders are associated with malformation in the kidney tissue leading to extracellular matrix modification with enhanced accumulation of collagens causing increased interstitial fibrosis. The Nedd4-2⁻ʹ⁻ kidneys showed increased interstitial fibrosis, collagen-1 accumulation and expression during progression of the disease. The renal tissue membrane is made up of polysaccharides, glycogen and mucin, the Nedd4-2⁻ʹ⁻ kidneys were found to have decreased accumulation of polysaccharides. The cysts in the Nedd4-2⁻ʹ⁻ kidneys originated from different parts within the nephron. The larger cysts originated from loop of Henle and with the smaller cysts from collecting ducts and distal convoluted tubules. The cystic progression is dependent on cAMP flux initiated by fluid secretion within the cyst. The postnatal day 19 cystic kidneys in Nedd4-2⁻ʹ⁻ animals showed increased cAMP levels suggesting cystic disease progression. As renal cystic disorders may arise from abnormal cilia, ciliary anomalies were found in the Nedd4-2⁻ʹ⁻ around the cysts suggesting importance of cilia in kidney cyst formation. Polycystins are known to be involved in renal cyst development with polycystin-1 and polycystin-2 together known to form calcium ion channel. To investigate the role of Nedd4-2 in the regulation of these polycystins, in vitro and in vivo studies were conducted. In vitro studies suggested that depletion of Nedd4-2 results in increased expression of polycystin-1 on the cell membrane with a decrease in polycystin-2 levels. Further, polycystin-1 was found to be ubiquitinated by Nedd4-2 in vitro providing the first evidence of Nedd4-2-mediated regulation of polycystins. In vivo Polycystin-1 was up-regulated in the Nedd4-2⁻ʹ⁻ kidneys suggesting an important role of Nedd4-2 in regulation of polycystins in cyst formation. To analyse the transcriptional signature of the phenotype seen in the knockout kidneys, postnatal day 19 kidneys from wild-type and Nedd4-2⁻ʹ⁻ mice were subjected to RNA sequencing highlighting 537 genes that were differentially expressed between wild-type and knockout kidneys, with 167 genes down-regulated and 370 genes significantly up-regulated in the absence of Nedd4-2. DAVID and Ingenuity pathway analyses was used to highlight the importance of genes involved in extracellular matrix modification, cell junction formation and cell-cell communication. The work presented in this thesis thus provides new information on the pathophysiological role of Nedd4-2 in kidney and identifies polycystin-1 as a Nedd4-2 target, along with transcriptional changes which may partially explain the cystic phenotype associated with renal dysplasia.
Thesis (Ph.D.) (Research by Publication) -- University of Adelaide, School of Medicine, 2016.

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Ondič, Ondrej. "Praktická aplikace imunohistochemických a molekulárně - genetických metod v diferenciální diagnostice lézí urogenitálního a gynekologického traktu." Doctoral thesis, 2018. http://www.nusl.cz/ntk/nusl-391332.

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This thesis focuses on gynecopathology. It consists of a collection of seven papers published in pathology journals with impact factor. Introduction section contains selection of examples showing scientific application of molecular genetic methods. Further on the aims of individual research projects are described. The first project comprises histomophologic study of skin endometriosis addressing "mullerian" differentiation. A case report of a rare tumor namely borderline papillary serous tumor of the fimbriated end of the fallopian tube follows with molecular genetic analysis of KRAS, BRAF and p53 gene mutation status. Prospective longitudinal study on high grade squamous dysplasia (HSIL) of the cervix in HPV vaccinated women, so called DAV (dysplasia after vaccination), aims to elucidate pathogenesis of this phenomenon. Two other studies focus on incidence of fumarate hydratase deficient leiomyomas of the uterus and hereditary leiomyomatosis and renal cell carcinoma syndrome (HLRCC). The aim of those studies is to improve our diagnostic capability and increase detection rate of the patients with HLRCC syndrome. Finally a new subtype of HSIL namely bizarre cell dysplasia is described in two separate studies. Conclusion remarks contemplate the role of molecular genetics in surgical pathology.

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Books on the topic "Renal dysplasia"

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Schreuder, Michiel F. Renal dysplasia. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0347.

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Renal dysplasia refers to abnormal and incomplete development of the kidney, which may be segmental, for instance, in the upper part of a duplex kidney, or affect the entire kidney. Dysplasia is by definition a histological diagnosis, but in most patients diagnosis is made on the basis of evaluation with ultrasound and renography. This typically shows cysts and/or a small kidney with decreased corticomedullary differentiation and a reduced split renal function. The latter can also be found in other conditions, such as hypoplasia, vascular insults, renal post-infectious damage, or polycystic kidney disease, making it difficult to establish the diagnosis and thereby estimate the incidence of renal dysplasia. The clinical consequences of renal dysplasia depend upon the residual renal function and may range from hypertension to chronic kidney disease.

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Schreuder, Michiel F. Renal hypoplasia. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0348.

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In true renal hypoplasia, normal nephrons are formed but with a deficit in total numbers. As nephron number estimation is not possible in vivo, renal size is used as a marker. A widely used definition of renal hypoplasia is kidneys with a normal appearance on ultrasound but with a size less than two standard deviations below the mean for gender, age, and body size. A distinct and severe form of renal hypoplasia is called (congenital) oligomeganephronia, which is characterized by small but normal-shaped kidneys with a marked reduction in nephron numbers (to as low as 10–20% of normal), a distinct enlargement of glomeruli, and a reduced renal function. In many cases, the small kidney also shows signs of dysplasia on ultrasound, leading to the diagnosis of renal hypodysplasia. Based on the hyperfiltration hypothesis and clinical studies, glomerular hyperfiltration can be expected, resulting in hypertension, albuminuria, and renal injury, for which long-term follow-up of all patients with renal hypoplasia is desirable.

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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Renal vascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0171.

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Renal vascular disease typically occurs with progressive narrowing of the main renal artery or smaller arterial vessels. Often, both patterns of disease coexist and result in ‘ischaemic nephropathy’ with damage to renal tissue. Much less commonly, inflammatory vasculitis can affect small or medium vessels. Ninety per cent of renal vascular disease is caused by atherosclerosis. Patients with renal vascular disease have an increased risk of cardiovascular death from associated cerebrovascular and coronary heart disease. Less than 10% of renal vascular disease is caused by fibromuscular dysplasia. The cause is unknown, but smoking is a risk factor. The disease is often bilateral and multifocal. It tends to affect the mid-portion of the renal artery, while atherosclerosis tends to occur at points of stress, especially at the junction of renal arteries with the aorta. This chapter reviews the diagnosis and management of renal vascular disease.

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Vester, Udo, and Stefanie Weber. Townes–Brocks syndrome. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0359.

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Townes–Brocks syndrome (TBS) is an autosomal dominant disease with variable expression. Classical features are imperforate anus, dysplastic ears with congenital hearing deficit, and triphalangeal thumbs in most cases. A variety of other malformations (renal, genitourinary, heart, central nervous system, eyes) or hypothyroidism has been described. Mutations in SALL1 have been identified in patients with TBS and genetic testing allows confirmation of the diagnosis. Familiar and sporadic forms (caused by de novo mutations) seem to be equally distributed. Renal involvement in TBS is not uncommon and includes renal agenesis, hypo-/dysplasia, and renal cysts and may eventually lead to chronic renal failure. As renal function may not deteriorate before adulthood, renal function should be monitored in all patients. As cases with TBS can be oligosymptomatic, TBS should be suspected in every case with unexplained renal failure, minor abnormalities, or indicative family history. Genetic counselling is mandatory in identified cases.

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Schreuder, Michiel F. Congenital solitary functioning kidney. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0351.

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The main cause for unilateral non-formation or non-functioning of a kidney can be found in renal agenesis/aplasia and multicystic dysplastic kidney. Even though kidney donation at adult age is considered safe, studies in recent years have shown that this may be different in congenital solitary functioning kidneys. Whether this is based on dysplasia in the remaining kidney or based on glomerular hyperfiltration damage, follow-up has shown renal injury, defined as hypertension and/or proteinuria, in up to 32% of children with a congenital solitary functioning kidney. Therefore, long-term infrequent follow-up of all patients with a congenital solitary functioning kidney seems to be indicated.

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Goodyer, Paul. Kidney/ear syndromes. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0170.

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Malformations of the external ear may signal renal disease, but it is actually the disorders of the inner ear which reflect molecular pathways that are also crucial for kidney development. In a number of monogenic renal diseases, renal dysplasia is associated with deafness. Disorders of the kidney and inner ear are also linked in complex syndromes such as the human ciliopathies. In some cases, the loss of specific genes affects shared transport physiology, basement membrane assembly, or energy metabolism.The kidney and cochlea have a common susceptibility to toxins that are selectively concentrated by comparable uptake mechanisms in the two tissues.This chapter provides an overview of the many ways in which pathologies of the two organs are linked.

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Thomas, David F. M. Vesicoureteric reflux. Edited by David F. M. Thomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0115.

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The term vesicoureteric reflux (VUR) describes the retrograde flow of urine from the bladder into the upper urinary tract. VUR is not a disease entity in its own right. Nevertheless, it has the potential to cause significant morbidity by preventing effective emptying of the urinary tract and by facilitating the transport of bacteria into the upper tract and renal parenchyma. Mechanisms of renal damage associated with VUR include pyelonephritic scarring and congenital dysplasia or hypoplasia. The long-term complications of pyelonephritic scarring may include hypertension, renal failure, and an increased risk of complications during pregnancy. VUR of mild or moderate severity is best managed conservatively and surgical intervention is generally reserved for failed medical management and high grade or complex VUR. Although the introduction of endoscopic correction has revolutionized surgical management, there remains a role for open surgery for the correction of higher grades of reflux.

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Schreuder, Michiel F. Posterior urethral valves. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0354.

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Posterior urethral valves is the most common congenital cause of lower urinary tract obstruction in males, and a common cause (15–17%) for end-stage renal disease in childhood. Most commonly, posterior urethral valves is suspected on basis of a screening antenatal ultrasound. Ultrasound will not detect posterior urethral valves itself, but recognizes the consequences of lower urinary tract obstruction with a dilated thick-walled bladder and dilation of the prostatic portion of the urethra. After birth, urine drainage has to be secured by placement of a bladder catheter, and imaging is needed to confirm the presence of the urethral valves and estimate the degree of damage to the kidney. Consequences of posterior urethral valves depend on the degree of renal dysplasia and bladder dysfunction. Prevention or minimization of such consequences by intrauterine urine drainage has not definitively shown a benefit of early vesico-amniotic shunting.

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Schreuder, Michiel F. Renal agenesis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0346.

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In renal agenesis, the kidney never forms due to an absence of interaction in the developing embryo between the ureteric bud and the metanephric mesenchyme. Most cases of renal agenesis are unilateral, for which the reported incidence is around 1 in 3000. The prenatal diagnosis of unilateral renal agenesis is based on the absence of a recognizable kidney, either at the normal or an ectopic site. However, such cases of an empty renal fossa can also be explained by an involuted multicystic dysplastic kidney, or by renal aplasia. Based on the hyperfiltration hypothesis and clinical studies, glomerular hyperfiltration can be expected, resulting in hypertension, albuminuria, and renal injury, for which long-term follow-up of all patients with renal agenesis is desirable.

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Lambert, Heather. Primary vesicoureteric reflux and reflux nephropathy. Edited by Adrian Woolf. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0355_update_001.

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Vesicoureteric reflux (VUR) describes the flow of urine from the bladder into the upper urinary tract when the ureterovesical junction fails to perform as a one-way valve. Most commonly, VUR is primary, though it can be secondary to bladder outflow obstruction and can occur in several multiorgan congenital disorders. There is good evidence of a genetic basis with a greatly increased risk of VUR in children with a family history of VUR. VUR is a congenital disorder, which largely shows improvement or complete resolution with age. Fetal VUR may be associated with parenchymal developmental defects (dysplasia). Postnatally non-infected, non-obstructed VUR does not appear to have a detrimental effect on the kidneys. However there is an association of VUR with urinary tract infection and acquired renal parenchymal defects (scarring). The parenchymal abnormalities detected on imaging, often termed reflux nephropathy, may be as a result of reflux-associated dysplasia or acquired renal scarring or both. It is difficult to distinguish between the two on routine imaging. Higher grades of VUR are associated with more severe reflux nephropathy. The precise role of VUR in pyelonephritis and scarring is not clear and it may be that VUR simply increases the risk of acute pyelonephritis. Whilst most VUR resolves during childhood, it is associated with an increased risk of urinary tract infection and burden of acute disease. Investigation strategies vary considerably, related to uncertainties about the natural history of the condition and the effectiveness of various interventions. The long-term prognosis is chiefly related to the morbidity of reflux nephropathy leading in some cases to impairment of glomerular filtration rate, hypertension, proteinuria, and pregnancy-related conditions including hypertension, pre-eclampsia, and recurrent urinary tract infection. Management is controversial and ranges from simple observation with or without provision of rapid access to diagnosis and treatment of urinary tract infections; to long-term prophylactic antibiotics or various antireflux surgical procedures.

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Book chapters on the topic "Renal dysplasia"

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Goodyer, Paul. "Renal Dysplasia/Hypoplasia." In Pediatric Nephrology, 107–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-76341-3_5.

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Goodyer, Paul, and Indra R. Gupta. "Renal Dysplasia/Hypoplasia." In Pediatric Nephrology, 115–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-43596-0_4.

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Caliò, Anna, Diego Segala, and Guido Martignoni. "Multicystic Renal Dysplasia." In Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-28845-1_4854-1.

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Goodyer, Paul, and Indra Gupta. "Renal Dysplasia/Hypoplasia." In Pediatric Nephrology, 1–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27843-3_4-1.

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Taleb, Mohammed, and Christopher J. Cooper. "Fibromuscular Dysplasia: Renal." In Endovascular Interventions, 401–5. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7312-1_35.

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Caliò, Anna, Diego Segala, and Guido Martignoni. "Multicystic Renal Dysplasia." In Encyclopedia of Pathology, 217–18. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41894-6_4854.

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Greco, Barbara Ann. "Renal Vascular Fibromuscular Dysplasia." In Renal Vascular Disease, 23–37. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2810-6_2.

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Bacharach, J. Michael. "Renal Artery Stenosis: Fibromuscular Dysplasia." In Atlas of Clinical Vascular Medicine, 12–13. Oxford, UK: Blackwell Publishing Ltd., 2013. http://dx.doi.org/10.1002/9781118618189.ch6.

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Chalmers, David. "Congenital Upper Tract Anomalies: Duplication, Cystic Renal Dysplasia, Multicystic Dysplastic Kidney." In Practical Pediatric Urology, 247–61. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-54020-3_10.

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Myers, David A., and Jordan M. Symons. "Nephronophthisis and Renal–Hepatic–Pancreatic Dysplasia of Ivemark." In Fibrocystic Diseases of the Liver, 201–20. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-524-8_9.

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Conference papers on the topic "Renal dysplasia"

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Dalrymple, RA, H. Maxwell, and C. Gardiner. "G460(P) Clinical phenotype of children and young people with renal dysplasia in scotland." In Royal College of Paediatrics and Child Health, Abstracts of the Annual Conference, 24–26 May 2017, ICC, Birmingham. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313087.453.

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Oliveira, Jefferson Borges de, Caroline Berthier Zanin, Gustavo Carreira Henriques, Maiévi Liston, Rafael Glória Zatta, Rodrigo de Faria Martins, and Tatiana Pizzolotto Bruch. "Pallister-Hall Syndrome - case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.575.

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In 1980, Hall et all described a syndrome characterized by “hamartoblastoma”, hypopituitarism, unperfurated anus, polydactyly postaxial and numerous visceral anomalies, today known as Pallister-Hall Syndrome. On the study, Hall et all reported six cases of children with that malformation syndrome - lethal on neonatal period. None of the newborns had anterior hypophysis and the hypothalamic tumor was apparent in the inferior part of the brain, going from the optic chiasm to the interpeduncular fossa. Besides, other anomalies were found, such as: laryngeal split, abnormal pulmonary lobation, renal agenesis or dysplasia, shorts fourth metacarpals, nail dysplasia, multiple mouth frenulum, hypoadrenalism, congenital cardiomyopathy and intrauterine growth retardation. Every case was sporadic, the chromosome were apparently normal, without consaguinity relations. Several similar, milder and even asymptomatic cases were described later on. Kletter and Biesecker (1992), Topf et all (1993) and Penman Splitt et all (1994), define the disease as dominant autosomal inheritance. Kettler and Biesecker (1992) stated that most cases as sporadic as a result of a gene mutation with variable expressiveness. According to Biesecker et al (1996), an international workshop determined diagnostic criteria to the Syndrome: Hypothalamic Hamartroma and Central Polydactyly; First degree relative with hypothalamic hamartroma and polydactyly; Dominant autosomal parrent inheritance or in a consistent form with germaine mosaicism. The radiological changes are important for differential diagnosis between Pallister-Hall Syndrome and other hamartroma-present diseases. The hypothalamic hamartroma isolated has phenotypical features and causes hormonal disorders such as early puberty. On the MRI (Magnetic resonance imaging) it shows hyperintese sign on attenuated fluid. On the other hand, the Pallister-Hall Syndrome the hamartroma shows itself as a isointense signs along with other deformities as polydactyly, for example. According to Kuo et al (1999), on MRI, the classic hypothalamic hamartroma isn’t calcified, is homogenous and isointense to the grey matter on weight images in T1, and isointense and often hyperintense on weight images in T2. Those findings are pretty distinctive and help distinguish the hypothalamic hamartroma from ordinary lesions, as craniopharyngioma and hypothalamic/opticalchiasmic glioma, observed in children. Case report: The patient ALDV, male, born in 30/12/1995, was referred to evaluation on the Medical Genetic Service from HCPA. At the time, aged one year and 8 months, he was the only son of a young, healthy couple with no consanguinity. The family history of similar cases or other genetic pathologies are unknown. The prenatal happened with no intercurrences, unless the smoking mother. It was a natural birth; Birth Weight: 2kg; High: 42cm; PC: 32cm. APGAR 9. At 8 months, starts an investigation for precocious puberty, and a karyotype was performed in her hometown: 46, XY (normal). He presents convulsive crises since one year old. DNPM: cephalic support when he had 8 months, sat without support at the age of one. Physical examination: Head circumference in the 97th percentile, length above the 97th percentile. Good general condition, dysmorphic, facies with fusion of eyebrows (sinofre), epicanthus, small nose, dysplastic ears with a broad shield, three café-au-lait spots on the body. Presence of pubic hair. Increase in length and diameter of the penis, as well as of the testicles, in relation to chronological age. In the hands, significant brachydactyly with bitateral hexadactyly. In the feet, bilateral hexadactyly. Proximal cutaneous syndactyly between the 2nd and 3rd bilateral arthroids, mainly on the right. Additional exams: Rx of hands and wrists for bone age: 7 years; Chronological Age: 1 year and 10 months. Normal abdominal ultrasound; Computed Tomography of Skull/Magnetic Resonance of Skull: hypothalamic expansive lesion (3 cm), compatible with hamartoma; triventricular hydrocephalus; Cavum septum pellucidum. Endocrinological Evaluation: compatible with precocious puberty of central cause. High resolution karyotype: 46, XY (normal). Computed tomography of the brain: Examination for neurological control, performed on 10/12/2014, 18-year-old patient. It was observed solid nodular formation in the hypothalamic region, hypodense, with well-defined limits, in close contact with the mesencephalon, without impregnation by contrast medium administered intravenously, measuring about 2.9 X 2.4 X 3.0 cm, in the respective laterolateral, anteroposterior and craniocaudal planes, which in correlation with the patient’s clinical history may be related to hypothalamic Hamartoma.

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Bergholt, Mads Sylvest, Wei Zheng, Khek Yu Ho, Khay Guan Yeoh, Ming Teh, Jimmy Bok Yan So, and Zhiwei Huang. "Real-time depth-resolved Raman endoscopy forin vivodiagnosis of dysplasia in Barrett's esophagus." In SPIE BiOS, edited by Israel Gannot. SPIE, 2013. http://dx.doi.org/10.1117/12.2003995.

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Baria, Enrico, Flavio Giordano, Anna M. Buccoliero, Riccardo Cicchi, and Francesco S. Pavone. "Fast and label-free optical detection of dysplastic and tumour brain tissues." In Optical Biopsy XVIII: Toward Real-Time Spectroscopic Imaging and Diagnosis, edited by Robert R. Alfano, Stavros G. Demos, and Angela B. Seddon. SPIE, 2020. http://dx.doi.org/10.1117/12.2546019.

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Steelman, Zachary A., Derek Ho, Yang Zhao, Haoran Zhang, Evan Jelly, Ge Song, Wesley Y. Kendall, et al. "Progress in angle-resolved low-coherence interferometry for real-time detection of epithelial dysplasia (Conference Presentation)." In Biomedical Applications of Light Scattering X, edited by Adam Wax and Vadim Backman. SPIE, 2020. http://dx.doi.org/10.1117/12.2545173.

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Michopoulos, S., G. Axiaris, P. Baxevanis, M. Stoupaki, V. Gagari, A. Karlaftis, E. Zampeli, D. Theodorou, M. Sotiropoulou, and K. Petraki. "REAL LIFE DATA FOR DYSPLASTIC BARRETT'S ESOPHAGUS MANAGEMENT AND FOLLOW-UP." In ESGE Days 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1681896.

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Keyte, Georgina, Muhammad Iqbak, YKS Viswanath, and Anjan Dhar. "PTU-053 Dysplasia diagnosis at barrett’s surveillance – seattle protocol dominant strategy in real world non-expert centres." In British Society of Gastroenterology Annual Meeting, 17–20 June 2019, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-bsgabstracts.266.

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Axiaris, G., A. Ioannou, E. Papathanasiou, M. Tzakri, G. Leonidakis, E. Zampeli, P. Baxevanis, and S. Michopoulos. "DYSPLASTIC BARRETT’S OESOPHAGUS (DBO): REAL WORLD DATA REGARDING LONG TERM FOLLOW-UP." In ESGE Days 2022. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1745103.

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Abraham, Christine, John Rodriguez, Jenni Buckley, Shane Burch, and Mohammad Diab. "An Evaluation of the Accuracy of Computer Assisted Surgery in Preoperatively Three Dimensionally Planned Periacetabular Osteotomies." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206222.

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Adults with unresolved developmental dysplasia of the hip (DDH) often warrant Pelvic Periacetabular Osteotomy (PAO). Making the correct osteotomies, and then finding the “ideal” position of the acetabular fragment is difficult, even for the experienced surgeon. Due to its 3-D nature, need for precision, and limited direct visualization of the surgical site, the PAO procedure is a good candidate for Computer Assisted Surgery (CAS). Using CAS, a virtual image is created, which is then used to navigate through the procedure in real time. Improved imaging hardware, along with intra-operative navigation systems have the potential to reduce complication rates, and lessen the learning curve in the inexperienced surgeon. PAO cuts have been made using intra-operative navigation and acetabular fragments have been positioned in pre-operative computer models. As of yet, modeled PAO cuts have not been used to navigate intraoperative cuts. Furthermore, modeled acetabular positioning has not been combined with intra-operative navigation to position fragments. The aim of this study is to prove the utility of pre-operative 3D imaging, PAO osteotomy planning and acetabular fragment positioning with computer software. These modeled images can be used to complete highly accurate and effective PAO surgeries.

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