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Journal articles on the topic 'Renal dysplasia'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Picut, C. A., and R. M. Lewis. "Microscopic Features of Canine Renal Dysplasia." Veterinary Pathology 24, no. 2 (March 1987): 156–63. http://dx.doi.org/10.1177/030098588702400209.

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Forty-five cases of renal dysplasia in dogs are examined. Microscopic lesions of dysplasia include asynchronous differentiation of nephrons, persistent mesenchyme, persistent metanephric ducts, atypical tubular epithelium, and dysontogenic metaplasia. These may be distinguished from secondary lesions including compensatory hypertrophy and hyperplasia of the nephron and a variety of degenerative and inflammatory lesions. Although morphological features of renal dysplasia in dogs differ somewhat from those in man, microscopic criteria used in the diagnosis of human dysplasia may be useful when applied to the dog.

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12

Rao, Kakarla S. "Fibromuscular Dysplasia of Renal Artery." Hypertension Journal 2, no. 2 (2016): 103–4. http://dx.doi.org/10.5005/jp-journals-10043-0039.

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13

Civan, N. "Hypoparathyroidism, Deafness, and Renal Dysplasia." Acta Endocrinologica (Bucharest) 10, no. 4 (2014): 687–92. http://dx.doi.org/10.4183/aeb.2014.687.

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14

QUINN, CECILY M., D. G. KELLY, and S. F. CAHALANE. "Renal Dysplasia-a Clnicopathologcal Review." British Journal of Urology 61, no. 5 (May 1988): 399–401. http://dx.doi.org/10.1111/j.1464-410x.1988.tb06583.x.

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15

Kerlin, R. L., and T. J. Van Winkle. "Renal Dysplasia in Golden Retrievers." Veterinary Pathology 32, no. 3 (May 1995): 327–29. http://dx.doi.org/10.1177/030098589503200319.

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16

SUGIYAMA, Akihiko. "Porcine Focal Segmental Renal Dysplasia." Journal of the Japan Veterinary Medical Association 58, no. 5 (2005): 347–49. http://dx.doi.org/10.12935/jvma1951.58.347.

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17

CARTER, P., J. R. BURKE, and J. SEARLE. "Renal abnormalities and spondylometaphyseal dysplasia." Journal of Paediatrics and Child Health 21, no. 2 (May 1985): 115–17. http://dx.doi.org/10.1111/j.1440-1754.1985.tb00140.x.

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18

Knops, N. B. B., E. A. M. Cornelissen, and L. A. H. Monnens. "Renal Transplantation for Fibromuscular Dysplasia." American Journal of Transplantation 11, no. 4 (March 29, 2011): 852–56. http://dx.doi.org/10.1111/j.1600-6143.2011.03455.x.

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19

Gavalas, M., R. Meisner, N. Labropoulos, A. Gasparis, and A. Tassiopoulos. "Renal Infarction Complicating Fibromuscular Dysplasia." Vascular and Endovascular Surgery 48, no. 7-8 (September 15, 2014): 445–51. http://dx.doi.org/10.1177/1538574414551206.

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20

Balzer, KM, D. Grotemeyer, T. Pfeiffer, A. Voiculescu, and W. Sandmann. "Fibromuscular dysplasia and renal transplantation." Lancet 369, no. 9557 (January 2007): 187. http://dx.doi.org/10.1016/s0140-6736(07)60101-9.

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21

Kelle, S., D. C. Teller, E. Fleck, and P. Stawowy. "Renal denervation in fibromuscular dysplasia." Case Reports 2013, aug19 1 (August 19, 2013): bcr2013010204. http://dx.doi.org/10.1136/bcr-2013-010204.

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22

Young, Joseph Y., Robert K. Ryu, and David D. Casalino. "Fibromuscular Dysplasia and Renal Transplantation." Journal of Urology 186, no. 3 (September 2011): 1073–74. http://dx.doi.org/10.1016/j.juro.2011.06.013.

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23

Chan, J. K. C., D. Saw, A. Myint, and H. C. Ho. "Squamous Cysts in Renal Dysplasia." Journal of Urology 136, no. 4 (October 1986): 987. http://dx.doi.org/10.1016/s0022-5347(17)45181-0.

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24

Azmy, Amir. "Renal dysplasia—a clinicopathological review." Journal of Pediatric Surgery 24, no. 3 (March 1989): 326. http://dx.doi.org/10.1016/s0022-3468(89)80072-7.

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25

Phua, Yu L., and Jacqueline Ho. "Renal dysplasia in the neonate." Current Opinion in Pediatrics 28, no. 2 (April 2016): 209–15. http://dx.doi.org/10.1097/mop.0000000000000324.

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26

Bruder, Marc C., Ahmed M. Shoieb, Norimitsu Shirai, Germaine G. Boucher, and Thomas A. Brodie. "Renal Dysplasia in Beagle Dogs." Toxicologic Pathology 38, no. 7 (September 30, 2010): 1051–57. http://dx.doi.org/10.1177/0192623310382558.

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27

Schoepf, Daniel, and Philipp Eller. "Fibromuscular dysplasia of renal arteries." Wiener klinische Wochenschrift 121, no. 1-2 (January 2009): 33. http://dx.doi.org/10.1007/s00508-008-1114-2.

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28

Dinu-Florin Albu, Cristina-Crenguța Albu, and Ştefan-Dimitrie Albu. "Bilateral renal agenesis/hypoplasia associated with oligohydramnios and major intrauterine growth restriction: Prenatal ultrasound study." World Journal of Advanced Research and Reviews 16, no. 2 (November 30, 2022): 851–57. http://dx.doi.org/10.30574/wjarr.2022.16.2.1266.

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Bilateral renal agenesis/hypoplasia/dysplasia is a lethal malformation in humans with an incidence of 1.3 per 10,000 live births. In the etiology of bilateral renal agenesis/hypoplasia/dysplasia, the genetic factor plays an important role. In addition to genetic factors, the etiology of bilateral renal agenesis/hypoplasia/dysplasia also involves the teratogenic effect of hyperglycemia on the embryo in mothers with insulin-dependent maternal diabetes. The purpose of this paper is to present a special case of bilateral renal agenesis/hypoplasia/dysplasia, which was successfully diagnosed prenatally by ultrasonography, confirmed and managed appropriately, so as to limit the incidence of serious, lethal congenital malformations.

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29

Devadass, Clement Wilfred, Madhu Aramane Basavaraj, Prasanna Shetty Badila, and Mangala Gouri. "Renal Dysplasia: A 6 Year Retrospective Study with Clinicopathological Correlation." Annals of Pathology and Laboratory Medicine 5, no. 7 (July 29, 2018): A585–590. http://dx.doi.org/10.21276/apalm.1880.

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30

Antonio M, Puppo, Caro Manuel Fernández, Sastre Sara Martín, Gómez Francisco T, and Sánchez Jose Mariá López. "Fibromuscular dysplasia and aortic dissection." Journal of Cardiology and Cardiovascular Medicine 7, no. 1 (March 30, 2022): 023–25. http://dx.doi.org/10.29328/journal.jccm.1001127.

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Fibromuscular dysplasia is a rare, non-atherosclerotic, non-inflammatory vascular disease that typically affects women between the ages of 20 and 60 years. Although any artery can be affected fibromuscular dysplasia most commonly affects the renal and carotid arteries. Fibromuscular dysplasia of the renal arteries usually presents with hypertension, while carotid or vertebral artery disease causes transient ischemic attacks, strokes, or dissection. Aortic dissection is rare. We present the clinical case of a patient with fibromuscular dysplasia with type B aortic dissection.

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31

Sapin, Carolina Da Fonseca, Luisa Mariano Cerqueira da Silva, Haide Valeska Scheid, Ceres Cristina Tempel Nakasu, Marlete Brum Cleff, and Fabiane Borelli Grecco. "Urethral dysontogenic metaplasia in cat with bilateral renal dysplasia." Semina: Ciências Agrárias 38, no. 5 (October 3, 2017): 3383. http://dx.doi.org/10.5433/1679-0359.2017v38n5p3383.

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This paper to describe a case of dysontogenic urethral metaplasia in a one month old mongrel feline who also had bilateral renal dysplasia. Dysontogenic metaplasia in cats are scarce and this change may be associated with renal dysplasia and/or lower urinary tract. The animal had history of abdominal enlargement since birth and dysuria, eliminating urine only dropwise. Due to the poor prognosis we opted for euthanasia. At necropsy was observed enlarged and distended bladder, reduced kidneys and dilated and tortuous ureters. The urethra was thickened, hard to cut, and histologically, was replacing the connective tissue, cartilage and endochondral ossification areas, which features dysontogenic metaplasia. Both kidneys presented primitive appearance featuring dysplasia. Dysontogenic metaplasia in urinary tract feline with renal dysplasia, has not been described.

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32

Chan, Maren, Jonathan L. Hecht, Theonia Boyd, and Seymour Rosen. "Congenital Cytomegalovirus Infection: A Cause of Renal Dysplasia?" Pediatric and Developmental Pathology 10, no. 4 (August 2007): 300–304. http://dx.doi.org/10.2350/06-06-0099.1.

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Cytomegalovirus (CMV) infection is one of the most frequently encountered viral infections of the fetus and induces a wide range of histologic and clinical manifestations. Congenital abnormalities are typically restricted to the central nervous system despite evidence of CMV inclusions occurring in most epithelial cells. Although tissue injury and even glomerulonephritis have been observed in congenital CMV infections, renal multicystic dysplasia has not been reported. Herein, we describe a case of unilateral renal dysplasia in a 19-week fetus with concurrent CMV infection. We believe the present case to be the first description of a virus apparently inducing renal multicystic dysplasia.

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33

Tomboravo, Christian, Narindra Lova Hasina Rajaonarison Ny Ony, Tolojanahary Herizo Andrianjakamanana, and Ahmad Ahmad. "Tableau clinique de colique néphrétique révélant une malformation vasculaire rénale." Annales Africaines de Medecine 15, no. 1 (January 30, 2022): e4499-e4501. http://dx.doi.org/10.4314/aamed.v15i1.12.

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Renal arteriovenous malformation is a rare embryonary’s dysplasia We report the case of a 44-year-old woman, who presented left-sided renal colic Uroscanner did not show any obstructive syndrome of urinary tracts associated with either lithiasis or tumoral syndrome However, it revealed a left renal arteriovenous malformation. La malformation artério-veineuse rénale est une dysplasie d’origine embryonnaire rare Nous rapportons le cas d’une femme de 44 ans, qui a présenté un tableau clinique de colique néphrétique gauche L’uroscanner ne révélait pas de syndrome obstructif des voies urinaires ni de lithiase ni de syndrome tumoral Par contre, il a montré une malformation artério-veineuse rénale à gauche.

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34

Ostatníková, Michaela, Pavel Doležal, Martin Gábor, and Jozef Záhumenský. "Unilateral macrocystic dysplasia and contralateral agenesis in a monoamniotic twin." Česká gynekologie 87, no. 4 (August 31, 2022): 278–81. http://dx.doi.org/10.48095/cccg2022278.

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Objective: We present a case report of a congenital malformation of the uropoetic tract in one of the monoamniotic twins. Case report: A 24-year-old primigravida with male monochorionic monoamniotic twins was dia gnosed with congenital malformation in fetus A at 24 weeks of gestation. Ultrasound verified macrocystic dysplasia and contralateral renal agenesis. Planned caesarean section was performed after the observational management of the patient in the 34th gestational week. In fetus B, a physiological finding was confirmed on the postpartum ultrasonography. In fetus A, CT examination of the abdomen confirmed the finding of left kidney agenesis and polycystic degeneration of the right kidney. Exitus letalis was stated on the newborn's 5th day. Conclusion: The occurrence of the described combination of congenital malformation in monoamniotic twins is rare. When dysplasia significantly affects the function of the parenchyma, renal agenesis with multicystic dysplasia of the other kidney is a condition incompatible with life. For the intrauterine survival of the affected fetus, the normal renal function of the twin was important and thus the normal volume of amniotic fluid was maintained. As a result, the fetus did not develop extrarenal symptoms of the Potter sequence in the described case – especially pulmonary hypoplasia and the newborn was able to ventilate spontaneously. The death was caused by the consequences of renal failure associated with anuria. Key words: monoamniotic twins – macrocystic renal dysplasia – renal agenesis

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35

Chub, O. I., S. O. Reshetniak, Yu V. Dumanskiy, and A. V. Maltsev. "Clinical case of hydronephrotic form of multicystic dysplastic kidney complicated by pyelonephritis in adults." KIDNEYS 11, no. 2 (July 13, 2022): 113–20. http://dx.doi.org/10.22141/2307-1257.11.2.2022.369.

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Multicystic dysplastic kidney (MCDK) is a renal dysplasia characterized by the presence of multiple cysts that are non-communicating, varying in size, separated by dysplastic parenchyma that consume the renal cortex resulting in a non-functional kidney with the absence of a normal pelvocaliceal system. The incidence of MCDK is approximately 1 : 4300 of live births, with males being affected more often than females. Many concurrent urinary tract abnormalities have been described in patients with MCDK. The most common and potentially significant urologic defect seen is vesico-ureteral reflux to the contralateral kidney. In our clinical case, multicystic dysplastic kidney complicated by hydronephrotic transformation and septic obstructive pyelonephritis, which developed on the base of undiagnosed vasorenal conflict.

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36

Dimmick, James E., Hjalmar W. Johnson, Gerald U. Coleman, and Michael Carter. "Wilms Tumorlet, Nodular Renal Blastema and Multicystic Renal Dysplasia." Journal of Urology 142, no. 2 Part 2 (August 1989): 484–85. http://dx.doi.org/10.1016/s0022-5347(17)38790-6.

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37

Morita, T., Y. Michimae, M. Sawada, T. Uemura, Y. Araki, A. Haruna, and A. Shimada. "Renal Dysplasia with Unilateral Renal Agenesis in a Dog." Journal of Comparative Pathology 133, no. 1 (July 2005): 64–67. http://dx.doi.org/10.1016/j.jcpa.2005.01.002.

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38

Woods, Demi Jordan, Zakary John Woods, Kevin Alter, and Adnan Z. Choudhury. "Fibromuscular dysplasia with unilateral renal agenesis." BMJ Case Reports 14, no. 4 (April 2021): e240311. http://dx.doi.org/10.1136/bcr-2020-240311.

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Fibromuscular dysplasia (FMD) is predominantly diagnosed in women and is a congenital malformation damaging the arterial cell walls of numerous arteries, most prominently impacting the renal arteries. Although previously believed to be a disease of young women, older patients have been shown to make up a large percentage of this patient population as well. FMD is underdiagnosed, and the misdiagnosis of this disease has life-threatening consequences. Here, we present the case of a 24-year-old woman with hypertension who did not receive adequate workup until her symptoms were unrelenting. Her hypertension was presumed to be a result of her generalised anxiety disorder. However, once she began to experience vision changes and significant headaches, further workup ensued. This case exemplifies the importance of performing a thorough evaluation of all patients that present with hypertension of unknown origin, especially young women. To decrease the risk of permanent consequences such as strokes, renal failure and even death, the correct diagnosis of FMD is vital.

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39

Samal, SunilKumar, Seetesh Ghose, and Setu Rathod. "Renal dysplasia-limb reduction defect syndrome." Journal of Clinical Neonatology 4, no. 1 (2015): 38. http://dx.doi.org/10.4103/2249-4847.151166.

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40

Castro, M. B., M. P. J. Szabó, W. L. Ferreira, and A. A. Pereira. "Renal dysplasia in a Limousin calf." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 59, no. 2 (April 2007): 517–19. http://dx.doi.org/10.1590/s0102-09352007000200037.

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41

Kessler, O. J., N. Ziv, P. M. Livne, and P. Merlob. "Involution Rate of Multicystic Renal Dysplasia." PEDIATRICS 102, no. 6 (December 1, 1998): e73-e73. http://dx.doi.org/10.1542/peds.102.6.e73.

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42

Nussbaum, AR, DS Hartman, N. Whitley, RG McCauley, and RC Sanders. "Multicystic dysplasia and crossed renal ectopia." American Journal of Roentgenology 149, no. 2 (August 1987): 407–10. http://dx.doi.org/10.2214/ajr.149.2.407.

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43

LUSTMAN, FRANCOIS. "Oncogenic Osteomalacia and Renal Adenomatoid Dysplasia." Annals of Internal Medicine 102, no. 6 (June 1, 1985): 869. http://dx.doi.org/10.7326/0003-4819-102-6-869_2.

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44

Caliezi, Christoph, and Peter Reber. "Fibromuscular Dysplasia of the Renal Artery." New England Journal of Medicine 355, no. 20 (November 16, 2006): 2131. http://dx.doi.org/10.1056/nejmicm053293.

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45

Pascual, Amaryllis, Howard S. Bush, and John B. Copley. "Renal fibromuscular dysplasia in elderly persons." American Journal of Kidney Diseases 45, no. 4 (April 2005): e63-e66. http://dx.doi.org/10.1053/j.ajkd.2005.01.039.

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46

Meuse, Michael A., Ulku C. Turba, Saher S. Sabri, Auh-Whan Park, Wael E. A. Saad, J. Fritz Angle, and Alan H. Matsumoto. "Treatment of Renal Artery Fibromuscular Dysplasia." Techniques in Vascular and Interventional Radiology 13, no. 2 (June 2010): 126–33. http://dx.doi.org/10.1053/j.tvir.2010.02.007.

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Sinnamon, K., D. McNally, and J. Harty. "Fibromuscular dysplasia presenting as renal infarction." Kidney International 72, no. 10 (November 2007): 1295–96. http://dx.doi.org/10.1038/sj.ki.5002479.

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Font, A., L. Ferrer, J. M. Closa, and J. Mascort. "Renal dysplasia in a Brie sheepdog." Journal of Small Animal Practice 32, no. 12 (December 1991): 640–42. http://dx.doi.org/10.1111/j.1748-5827.1991.tb00909.x.

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Cale, Catherine M., Nigel J. Klein, Paul J. D. Winyard, and Adrian S. Woolf. "Inflammatory mediators in human renal dysplasia." Nephrology Dialysis Transplantation 15, no. 2 (February 1, 2000): 173–83. http://dx.doi.org/10.1093/ndt/15.2.173.

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Philbey, A. W., A. Mateus, R. Bexiga, D. C. Barrett, H. A. Haining, I. A. P. McCandlish, and H. Thompson. "Renal dysplasia and nephrosclerosis in calves." Veterinary Record 165, no. 21 (November 21, 2009): 626–31. http://dx.doi.org/10.1136/vr.165.21.626.

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