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Potter Syndrome

  • Author: Sushil Gupta, MD; Chief Editor: Craig B Langman, MD  more...
 
Updated: Jan 21, 2015
 

Background

Potter syndrome refers to the typical physical appearance and associated pulmonary hypoplasia of a neonate as a direct result of oligohydramnios and compression while in utero. The term was coined after the pathologist Edith Potter, who in 1946 described the facial characteristics of infants with bilateral renal agenesis.[1] From her research, she was able to deduce the sequence of events that lead to these features. Other conditions resulting in oligohydramnios, such as obstructive uropathy, cystic kidney diseases, renal hypoplasia, and premature rupture of membranes lead to the same clinical findings. Hence, the terms Potter sequence or oligohydramnios sequence emerged. Regardless of the root cause for oligohydramnios, the terms Potter syndrome, Potter sequence, and oligohydramnios sequence are used interchangeably in the published literature.

Sonogram obtained before second-trimester amnioinf Sonogram obtained before second-trimester amnioinfusion. This fetus has bilaterally absent kidneys consistent with a diagnosis of Potter syndrome. The cystic structures in the renal fossae are most likely the adrenal glands.
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Pathophysiology

Prior to 16 weeks' gestations, the amount of amniotic fluid is dependent on the transmembrane flow. After that, fetal urine production is the predominant mechanism that determines the amniotic fluid volume. The fetus continuously swallows amniotic fluid, which is reabsorbed by the GI tract and then reintroduced into the amniotic cavity by the kidneys. Oligohydramnios occurs if the volume of amniotic fluid is less than normal for the corresponding period of gestation. This may be due to decreased urine production secondary to bilateral renal agenesis, obstruction of the urinary tract, or, occasionally, prolonged rupture of membranes[2, 3] . The resulting oligohydramnios is the cause of the deformities observed in Potter syndrome. The mechanism of lung hypoplasia in this condition is not clear. It is believed that adequate space in the fetal thorax and the movement of amniotic fluid into the fetal lungs is required for the normal development of lungs.

Genetics

The genetic aspect of renal malformation has not been fully understood yet and there is a lot of current research work in this field.

During nephrogenesis, multiple genes, transcription factors, and growth factors control the essential interaction between the ureteric bud and the metanephric mesenchyme. For example, the Lim1 and Pax2 transcription factors are essential for the formation of the mesonephric duct, from which the ureteric bud develops. Lim1 -deficient mice have complete renal agenesis. If the Pax2 gene is deficient, there is deletion of the caudal portion of the mesonephric duct, which results in renal agenesis[4, 5] .

WT-1, a zinc-finger transcription factor expressed in the metanephric mesenchyme, is essential for ureteric bud outgrowth. Homozygous null-mutants for WT-1 have complete renal agenesis. Similarly, transcription factor EYA1 from the metanephric mesenchyme is required for ureteric bud outgrowth, and deficiency of this protein is shown to cause branchio-oto-renal syndrome[6] .

The glial cell line–derived neurotrophic factor (GDNF) from the metanephric mesenchyme binds to the C-ret receptor on the branching ureteric bud and is responsible for the branching and elongation of the ureteric bud. Inactivation of either GDNF or the C-ret receptor leads to renal agenesis. Heterozygotes may have a unilateral renal abnormality while the contralateral kidney has normal development[7] .

Limb deformity (ld) gene codes for 4 different spliced formin genes, which are expressed in the mesonephric duct and branching ureteric ducts. Mutation of the ld gene leads to limb deformity with renal agenesis. Mutation of the formin IV gene leads only to kidney abnormalities. Homozygous mutation of the alpha-8 integrin subunit produces abnormalities similar to ld mutation with deformities including renal aplasia, dysplasia, or hypoplasia[8] .

Transcription factors such as EMX-2, BF-2, fibroblast growth factor 7 (FGF 7), epithelial growth factor receptor (EGF-R), GDNF, retinoic acid receptor alpha, and beta 2 are involved in the branching of the ureteric bud. A heterozygous mutation defect of the growth factor bone morphogenetic protein 4 (bmp 4) leads to renal hypoplasia or dysplasia, ureterovesicular junction obstruction, hydronephrosis, or the bifid/duplex kidney. This is a defect of ureteric branching and not induction of the ureteric bud; thus, renal aplasia does not occur[9, 10, 11] .

The autosomal recessive mutations of genes in the renin-angiotensin pathway result in renal tubular dysgenesis due to failed development of proximal tubules. These are heterogeneous mutations of renin, angiotensin, angiotensin converting enzyme, or type 1 angiotensin II receptor.[12, 13] . Some reports have suggested that the clinical picture of renal tubular dysgenesis is similar to the infants born to mothers who had received angiotensin converting enzyme inhibitor or angiotensin II receptor blockers during pregnancy[14, 15] .

Hepatocyte nuclear factor (HNF)-1beta gene (TCF2) is normally expressed in the Wolffian duct, metanephric tubules, and Mullerian during fetal life. This gene originally described in relation to maturity-onset diabetes, has been now recognized as a cause of cystic renal dysplasis[16, 17, 4] . Uroplakins IIIa is a protein expressed on the mammalian urothelia and has been suggested to be involved in defects of early kidney development like renal hypoplasia/dysplasia.[18]

Recognized genetic disorders such as renal coloboma syndrome (PAX2 mutation) and branchio-oto-renal syndrome (EYA1 mutation) are therefore associated with renal agenesis or dysplastic kidney abnormalities[6, 19] .

Some of the other reported Mutations associated with Renal Hypodysplasia are, FREM 1 (Causes Bifid Nose, Renal Agenesis and Anorectal Malformation)[20] , FRAS 1/FREM 2 (Fraser syndrome)[21, 22] , LRP4 (Cenani-Lenz syndrome)[23] , GLI3 (Pallister-Hall syndrome)[24] , SALL1 (Townes-Brocks syndrome, which has triad of imperforate anus, dysplastic ears and thumb malformation)[25] , KAL1 (Kallman syndrome)[26] , GATA3 (Renal hypodysplasia is associated with Hypothyroidism and sensory-neural deafness)[27] .

There are case reports on families with both unilateral and bilateral renal agenesis. This condition, termed hereditary renal adysplasia (HRA), is an autosomal dominant trait with incomplete penetrance and variable expression. Associated non-urogenital anomalies have been reported in HRA[28] .

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Epidemiology

Frequency

United States

Potter syndrome is mostly associated with obstruction of the urinary tract or severe bilateral renal hypoplasia. Bilateral renal agenesis is estimated to occur in about 1 of 5000 fetuses[29] and is responsible for 20% of Potter syndrome cases. The frequency of other causes of Potter syndrome is not known. The associated maternal high-risk factors for bilateral renal agenesis are maternal body mass index greater than 30, smoking, and binge drinking.[30, 31]

International

Data from 20 registries of 12 European countries was collected on 709,030 livebirths, stillbirths, and induced abortions. Bilateral renal agenesis was seen in 95 cases and out of this prenatal diagnosis was made in 86 cases[32] . In one other study from Europe's 17 registries reported 4366 cases diagnosed with 11 severe congenital malformations, out of which 257 cases had bilateral renal agenesis[33] .

Mortality/Morbidity

Potter syndrome is usually fatal in the first few days of the patient's life; most often, the cause is pulmonary failure. Bilateral renal agenesis is incompatible with extrauterine life and 33% of fetuses die in utero. Recently, a 70% survival rate has been reported among 23 infants with antenatal oligohydramnios and pulmonary hypoplasia.[34] The primary disease in these 23 infants included obstructive uropathy, autosomal recessive polycystic kidney disease, renal tubular dysgenesis, and bilateral renal dysplasia.

Neonates with the milder form of Potter syndrome have an increased morbidity rate because of respiratory failure, pneumothorax, and acute renal failure during the neonatal period. During early childhood, patients may have chronic lung disease and chronic renal failure.

A number of abnormalities are associated with bilateral renal agenesis, such as caudal dysgenesis, VATERL ( ertebral anomalies, nal atresia, ardiac defects, racheoesophageal fistula, enal defects, imb defects)[35] , caudal dysplasia syndrome, and isolated anomalies of the cardiovascular, skeletal, and central nervous systems[36, 37, 38, 39] . These abnormalities can add to the morbidity and increased mortality in these patients.

Race

No racial predilection is known.

Sex

Males have an increased incidence of the Potter syndrome because they have a higher rate of Eagle-Barrett (prune belly) syndrome[40] and obstructive uropathy secondary to posterior urethral valves.

Age

Patients present as neonates.

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Contributor Information and Disclosures
Author

Sushil Gupta, MD Assistant Professor of Pediatric Nephrology, University of Louisville School of Medicine

Sushil Gupta, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, American Society of Pediatric Nephrology, Indian Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Carlos E Araya, MD, FAAP Assistant Professor of Pediatrics, University of Central Florida College of Medicine; Faculty, Florida Hospital; Faculty, Nemours Children's Hospital

Carlos E Araya, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Frederick J Kaskel, MD, PhD Director of the Division and Training Program in Pediatric Nephrology, Vice Chair, Department of Pediatrics, Montefiore Medical Center and Albert Einstein School of Medicine

Frederick J Kaskel, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, Eastern Society for Pediatric Research, Renal Physicians Association, American Academy of Pediatrics, American Pediatric Society, American Physiological Society, American Society of Nephrology, American Society of Pediatric Nephrology, American Society of Transplantation, Federation of American Societies for Experimental Biology, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Sigma Xi, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Additional Contributors

Laurence Finberg, MD Clinical Professor, Department of Pediatrics, University of California, San Francisco, School of Medicine and Stanford University School of Medicine

Laurence Finberg, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

References
  1. Edith L. Potter. Facial characteristics of infants with bilateral renal agenesis. American Journal of Obstetrics and Gynecology. 1946. 51:885-888.

  2. Fantel AG, Shepard TH. Potter syndrome. Nonrenal features induced by oligoamnios. Am J Dis Child. 1975 Nov. 129(11):1346-7. [Medline].

  3. Vanderheyden T, Kumar S, Fisk NM, et al. Fetal renal impairment. Semin Neonatol. 2003 Aug. 8(4):279-89. [Medline].

  4. Paces-Fessy M, Fabre M, Lesaulnier C, Cereghini S. Hnf1b and Pax2 cooperate to control different pathways in kidney and ureter morphogenesis. Hum Mol Genet. Apr/2012. 24:[Medline]. [Full Text].

  5. Guertl B, Senanayake U, Nusshold E, Leuschner I, Mannweiler S, Ebner B, et al. Lim1, an embryonal transcription factor, is absent in multicystic renal dysplasia, but reactivated in nephroblastomas. Pathobiology. 2011. 78(4):210-9. [Medline]. [Full Text].

  6. Wang SH, Wu CC, Lu YC, Lin YH, Su YN, Hwu WL, et al. Mutation screening of the EYA1, SIX1, and SIX5 genes in an east asian cohort with branchio-oto-renal syndrome. Laryngoscope. May/2012. 122(5):1130-6. [Medline]. [Full Text].

  7. Skinner MA, Safford SD, Reeves JG, Jackson ME, Freemerman AJ. Renal aplasia in humans is associated with RET mutations. Am J Hum Genet. Feb/2008. 82(2):344-51. [Medline]. [Full Text].

  8. Wynshaw-Boris A, Ryan G, Deng CX, Chan DC, Jackson-Grusby L, Larson D, et al. The role of a single formin isoform in the limb and renal phenotypes of limb deformity. Mol Med. Jun/1997. 3(6):372-84. [Medline]. [Full Text].

  9. Costantini F, Shakya R. GDNF/Ret signaling and the development of the kidney. Bioessays. Feb/2006. 28(2):117-27. [Medline]. [Full Text].

  10. Lu BC, Cebrian C, Chi X, Kuure S, Kuo R, Bates CM, et al. Etv4 and Etv5 are required downstream of GDNF and Ret for kidney branching morphogenesis. Nat Genet. Dec/2009. 41(12):1295-302. [Medline]. [Full Text].

  11. Tabatabaeifar M, Schlingmann KP, Litwin M, Emre S, Bakkaloglu A, Mehls O, et al. Functional analysis of BMP4 mutations identified in pediatric CAKUT patients. Pediatr Nephrol. Dec/2009. 24(12):2361-8. [Medline]. [Full Text].

  12. Gribouval O, Gonzales M, Neuhaus T, Aziza J, Bieth E, Laurent N, et al. Mutations in genes in the renin-angiotensin system are associated with autosomal recessive renal tubular dysgenesis. Nat Genet. 2005 Sep. 37(9):964-8. [Medline].

  13. Uematsu, M.Sakamoto, O.Nishio, T.Ohura, T.Matsuda, T.Inagaki, et al. A case surviving for over a year of renal tubular dysgenesis with compound heterozygous angiotensinogen gene mutations. Am J Med Genet A. 2006. 140:2355-60. [Medline]. [Full Text].

  14. Kumar, D.Moss, G.Primhak, R.Coombs, R. Congenital renal tubular dysplasia and skull ossification defects similar to teratogenic effects of angiotensin converting enzyme (ACE) inhibitors. J Med Genet. 1997. 34:541-5. [Medline]. [Full Text].

  15. Lambot, M. A.Vermeylen, D.Noel, J. C. Angiotensin-II-receptor inhibitors in pregnancy. Lancet. 2001. 357:1619-20. [Medline]. [Full Text].

  16. Lindner TH, Njolstad PR, Horikawa Y, Bostad L, Bell GI, Sovik O. A novel syndrome of diabetes mellitus, renal dysfunction and genital malformation associated with a partial deletion of the pseudo-POU domain of hepatocyte nuclear factor-1beta. Hum Mol Genet. 1999 Oct. 8(11):2001-8. [Medline].

  17. Nakayama M, Nozu K, Goto Y, Kamei K, Ito S, Sato H, et al. HNF1B alterations associated with congenital anomalies of the kidney and urinary tract. Pediatr Nephrol. 2010 Jun. 25(6):1073-9. [Medline].

  18. Schönfelder EM, Knüppel T, Tasic V, Miljkovic P, Konrad M, Wühl E, et al. Mutations in Uroplakin IIIA are a rare cause of renal hypodysplasia in humans. Am J Kidney Dis. 2006 Jun. 47(6):1004-12. [Medline].

  19. Hoefele J, Gabert M, Heinrich U, Benz K, Rompel O, Rost I, et al. A novel interstitial deletion of 10q24.2q24.32 in a patient with renal coloboma syndrome. Eur J Med Genet. March/2012. 55(3):211-5. [Medline]. [Full Text].

  20. Alazami AM, Shaheen R, Alzahrani F, Snape K, Saggar A, Brinkmann B, et al. FREM1 mutations cause bifid nose, renal agenesis, and anorectal malformations syndrome. Am J Hum Genet. 2009 Sep. 85(3):414-8. [Medline]. [Full Text].

  21. Pitera JE, Scambler PJ, Woolf AS. Fras1, a basement membrane-associated protein mutated in Fraser syndrome, mediates both the initiation of the mammalian kidney and the integrity of renal glomeruli. Hum Mol Genet. 2008 Dec 15. 17(24):3953-64. [Medline].

  22. van Haelst MM, Maiburg M, Baujat G, Jadeja S, Monti E, Bland E, et al. Molecular study of 33 families with Fraser syndrome new data and mutation review. Am J Med Genet A. 2008 Sep 1. 146A(17):2252-7. [Medline].

  23. Li Y, Pawlik B, Elcioglu N, Aglan M, Kayserili H, Yigit G. LRP4 mutations alter Wnt/beta-catenin signaling and cause limb and kidney malformations in Cenani-Lenz syndrome. Am J Hum Genet. 2010 May 14. 86(5):696-706. [Medline].

  24. Cain JE, Islam E, Haxho F, Chen L, Bridgewater D, Nieuwenhuis E. GLI3 repressor controls nephron number via regulation of Wnt11 and Ret in ureteric tip cells. PLoS One. 2009. 4(10):e7313. [Medline].

  25. Miller EM, Hopkin R, Bao L, Ware SM. Implications for genotype-phenotype predictions in Townes-Brocks syndrome: case report of a novel SALL1 deletion and review of the literature. Am J Med Genet A. 2012 Mar. 158A(3):533-40. [Medline].

  26. Albuisson J, Pêcheux C, Carel JC, Lacombe D, Leheup B, Lapuzina P, et al. Kallmann syndrome: 14 novel mutations in KAL1 and FGFR1 (KAL2). Hum Mutat. 2005 Jan. 25(1):98-9. [Medline].

  27. Van Esch H, Groenen P, Nesbit MA, Schuffenhauer S, Lichtner P, Vanderlinden G, et al. GATA3 haplo-insufficiency causes human HDR syndrome. Nature. 2000 Jul 27. 406(6794):419-22. [Medline].

  28. McPherson E, Carey J, Kramer A, Hall JG, Pauli RM, Schimke RN, et al. Dominantly inherited renal adysplasia. Am J Med Genet. Apr/1987. 26(4):863-72. [Medline].

  29. McPherson E. Renal anomalies in families of individuals with congenital solitary kidney. Genet Med. 2007 May. 9(5):298-302. [Medline].

  30. Slickers JE, Olshan AF, Siega-Riz AM, Honein MA, Aylsworth AS. Maternal body mass index and lifestyle exposures and the risk of bilateral renal agenesis or hypoplasia: the National Birth Defects Prevention Study. Am J Epidemiol. 2008 Dec 1. 168(11):1259-67. [Medline].

  31. Slickers JE, Olshan AF, Siega-Riz AM, Honein MA, Aylsworth AS. Maternal body mass index and lifestyle exposures and the risk of bilateral renal agenesis or hypoplasia: the National Birth Defects Prevention Study. Am J Epidemiol. 2008 Dec 1. 168(11):1259-67. [Medline].

  32. Wiesel A, Queisser-Luft A, Clementi M, et al. Prenatal detection of congenital renal malformations by fetal ultrasonographic examination: an analysis of 709,030 births in 12 European countries. Eur J Med Genet. 2005 Apr-Jun. 48(2):131-44. [Medline].

  33. Garne E, Loane M, Dolk H. Prenatal diagnosis of severe structural congenital malformations in Europe. Ultrasound Obstet Gynecol. 2005 Jan. 25(1):6-11. [Medline].

  34. Klaassen I, Neuhaus TJ, Mueller-Wiefel DE, Kemper MJ. Antenatal oligohydramnios of renal origin: long-term outcome. Nephrol Dial Transplant. 2007 Feb. 22(2):432-9. [Medline].

  35. Prouty LA, Myers TL. Oligohydramnios sequence (Potter's syndrome): case clustering in northeastern Tennessee. South Med J. 1987 May. 80(5):585-92. [Medline].

  36. Kadhim HJ, Lammens M, Gosseye S, et al. Brain defects in infants with Potter syndrome (oligohydramnios sequence). Pediatr Pathol. 1993 Jul-Aug. 13(4):519-36. [Medline].

  37. Preus M, Kaplan P, Kirkham TH. Renal anomalies and oligohydramnios in the cerebro-oculofacio-skeletal syndrome. Am J Dis Child. 1977 Jan. 131(1):62-4. [Medline].

  38. Greenwood RD, Rosenthal A, Nadas AS. Cardiovascular malformations associated with congenital anomalies of the urinary system. Observations in a series of 453 infants and children with urinary system malformations. Clin Pediatr (Phila). 1976 Dec. 15(12):1101-4. [Medline].

  39. Tonni G, Azzoni D, Ventura A, Ambrosetti F, De Felice C. "Multicystic dysplastic kidney (Potter type II syndrome) and agenesis of corpus callosum (ACC) in two consecutive pregnancies: a possible teratogenic effect of electromagnetic exposure in utero". Fetal Pediatr Pathol. 2008. 27(6):264-73. [Medline].

  40. Woods AG, Brandon DH. Prune belly syndrome. A focused physical assessment. Adv Neonatal Care. 2007 Jun. 7(3):132-43; quiz 144-5. [Medline].

  41. Pramanik AK, Altshuler G, Light IJ, Sutherland JM. Prune-belly syndrome associated with Potter (renal nonfunction) syndrome. Am J Dis Child. 1977 Jun. 131(6):672-4. [Medline].

  42. Ginsberg J, Buchino JJ, Menefee M, et al. Multiple congenital ocular anomalies with bilateral agenesis of the urinary tract. Ann Ophthalmol. 1979 Jul. 11(7):1021-9. [Medline].

  43. Hall JG. Oligohydramnios sequence revisited in relationship to arthrogryposis, with distinctive skin changes. Am J Med Genet A. 2014 Nov. 164A(11):2775-92. [Medline].

  44. Curry CJ, Jensen K, Holland J, Miller L, Hall BD. The Potter sequence: a clinical analysis of 80 cases. Am J Med Genet. 1984 Dec. 19(4):679-702. [Medline].

  45. Schmidt W, Kubli F. Early diagnosis of severe congenital malformations by ultrasonography. J Perinat Med. 1982. 10(5):233-41. [Medline].

  46. Strauss A, Hasbargen U, Paek B, et al. [Prenatal diagnosis of kidney parenchyma diseases]. Z Geburtshilfe Neonatol. 2001 Mar-Apr. 205(2):71-5. [Medline].

  47. Yoshimura S, Masuzaki H, Miura K, et al. Diagnosis of fetal pulmonary hypoplasia by measurement of blood flow velocity waveforms of pulmonary arteries with Doppler ultrasonography. Am J Obstet Gynecol. 1999 Feb. 180(2 Pt 1):441-6. [Medline].

  48. Hawkins JS, Dashe JS, Twickler DM. Magnetic resonance imaging diagnosis of severe fetal renal anomalies. Am J Obstet Gynecol. 2008 Mar. 198(3):328.e1-5. [Medline].

  49. Fisk NM, Ronderos-Dumit D, Soliani A, Nicolini U, Vaughan J, Rodeck CH. Diagnostic and therapeutic transabdominal amnioinfusion in oligohydramnios. Obstet Gynecol. Aug/1991. 78(2):270-8. [Medline]. [Full Text].

  50. Raboei EH. The role of the pediatric surgeon in the perinatal multidisciplinary team. Eur J Pediatr Surg. 2008 Oct. 18(5):313-7. [Medline].

  51. Rani R, Cameron A, Munro F. Prenatal diagnosis and management of urethral obstruction. J Obstet Gynaecol Res. 1997 Feb. 23(1):59-62. [Medline].

  52. Chow JS, Benson CB, Lebowitz RL. The clinical significance of an empty renal fossa on prenatal sonography. J Ultrasound Med. 2005 Aug. 24(8):1049-54; quiz 1055-7. [Medline].

  53. Colquhoun-Kerr JS, Gu WX, Jameson JL, Withers S, Bode HH. X-linked Kallmann syndrome and renal agenesis occurring together and independently in a large Australian family. Am J Med Genet. Mar/1999. 83(1):23-7. [Medline]. [Full Text].

  54. Hahn H, Park SY, Eom JH, Park SW. Quiz page. Congenital intrathoracic kidney after regression of an adrenal mass. Am J Kidney Dis. 2009 Jan. 53(1):A27-8. [Medline].

  55. Palmer RE, Kotsianti A, Cadman B, Boyd T, Gerald W, Haber DA. WT1 regulates the expression of the major glomerular podocyte membrane protein Podocalyxin. Curr Biol. Nov/2001. 11(22):1805-9. [Medline]. [Full Text].

 
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Sonogram obtained before second-trimester amnioinfusion. This fetus has bilaterally absent kidneys consistent with a diagnosis of Potter syndrome. The cystic structures in the renal fossae are most likely the adrenal glands.
 
 
 
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