921 Renal Abnormalities in Fetal Alcohol Syndrome

Oazi, Qutub H; Masakawa, Akjko; Milman, Doris H.; Mcgann, Barbara; Chua, Ajbna; Alvi, S.

doi:10.1203/00006450-197804001-00926

Cited by 13 publications

(13 citation statements)

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“…Genitourinary malformations have been described as occurring more commonly in children with FAS than in general (Clarren and Smith 1978; Havers et al 1980; Qazi et al 1979). A few animal studies have found that fetal alcohol exposure may result in abnormalities of the genitourinary tract (Gage and Sulik 1991; Randall et al 1977).…”

Section: Discussionmentioning

confidence: 99%

Cryptorchidism and Maternal Alcohol Consumption during Pregnancy

Damgaard

Jensen

Petersen

et al. 2007

Environ Health Perspect

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BackgroundPrenatal exposure to alcohol can adversely affect the fetus. We investigated the association between maternal alcohol consumption during pregnancy and cryptorchidism (undescended testis) among newborn boys.MethodsWe examined 2,496 boys in a prospective Danish–Finnish birth cohort study for cryptorchidism at birth (cryptorchid/healthy: 128/2,368) and at 3 months of age (33/2,215). Quantitative information on alcohol consumption (average weekly consumption of wine, beer, and spirits and number of binge episodes), smoking, and caffeine intake was obtained by questionnaire and/or interview once during the third trimester of pregnancy, before the outcome of the pregnancy was known. For a subgroup (n = 465), information on alcohol consumption was obtained twice during pregnancy by interviews.ResultsWe investigated maternal alcohol consumption both as a continuous variable and categorized. The odds for cryptorchidism increased with increasing weekly alcohol consumption. After adjustment for confounders (country, smoking, caffeine intake, binge episodes, social class, maternal age, parity, maturity, and birth weight) the odds remained significant for women with a weekly consumption of five or more alcoholic drinks (odds ratio = 3.10; 95% confidence interval, 1.05–9.10).ConclusionsRegular alcohol intake during pregnancy appears to increase the risk of congenital cryptorchidism in boys. The mechanisms for this association are unknown. Counseling of pregnant women with regard to alcohol consumption should also consider this new finding.

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Section: Discussionmentioning

confidence: 99%

Cryptorchidism and Maternal Alcohol Consumption during Pregnancy

Damgaard

Jensen

Petersen

et al. 2007

Environ Health Perspect

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“…In this regard, renal hypodysplasia is caused by salt loading during embryonic development in bradykinin B2 receptordeficient, but not in wild-type, mice [88]. Exposure to cocaine or alcohol during gestation results in CAKUT in children [92,93]. Importantly, the mechanistic basis for CAKUT associated with altered intrauterine environment remains to be elucidated.…”

Section: Insights Into the Mechanisms Controlling Cakut Phenotypementioning

confidence: 94%

Genetics of congenital anomalies of the kidney and urinary tract

2010

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Congenital anomalies of the kidney and urinary tract (CAKUT) occur in 1 in 500 births and are a major cause of morbidity in children. Notably, CAKUT account for the most cases of pediatric end-stage renal disease and predispose the individual to hypertension and cardiovascular disease throughout life. Although some forms of CAKUT are a part of a syndrome or are associated with a positive family history, most cases of renal system anomalies are sporadic and isolated to the urinary tract. Broad phenotypic spectrum of CAKUT and variability in genotype-phenotype correlation indicate that pathogenesis of CAKUT is a complex process that depends on interplay of many factors. This review focuses on the genetic mechanisms (single-gene mutations, modifier genes) leading to renal system anomalies in humans and discusses emerging insights into the role of epigenetics, in utero environmental factors, and micro-RNAs (miRNAs) in the pathogenesis of CAKUT. Common gene networks that function in defined temporospatial fashion to orchestrate renal system morphogenesis are highlighted. Derangements in cellular, molecular, and morphogenetic mechanisms that direct normal renal system development are emphasized as a major cause of CAKUT. Integrated understanding of how morphogenetic process disruptions are linked to CAKUT will enable improved diagnosis, treatment, and prevention of congenital renal system anomalies and their consequences.

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“…Human studies have demonstrated that infants exposed to cocaine in utero had an increased risk of renal tract anomalies including renal hypoplasia (84 -86). Similarly, infants with Fetal Alcohol Syndrome also have a higher incidence of renal malformations, including small kidneys (87)(88)(89), and a recent study in sheep demonstrated that repeated alcohol exposure in late gestation leads to a mild nephron deficiency (90). Several clinical medications have also proven detrimental to fetal nephron endowment.…”

Section: In Utero Environment and Renal Hypoplasiamentioning

confidence: 99%

Genetics of Renal Hypoplasia: Insights Into the Mechanisms Controlling Nephron Endowment

et al. 2010

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ABSTRACT:Renal hypoplasia, defined as abnormally small kidneys with normal morphology and reduced nephron number, is a common cause of pediatric renal failure and adult-onset disease. Genetic studies performed in humans and mutant mice have implicated a number of critical genes, in utero environmental factors and molecular mechanisms that regulate nephron endowment and kidney size. Here, we review current knowledge regarding the genetic contributions to renal hypoplasia with particular emphasis on the mechanisms that control nephron endowment in humans and mice. R enal hypoplasia is a common, yet poorly understood and misused term describing congenital renal anomalies. Renal hypoplasia is defined as abnormally small kidneys (Ͻ2 SD below the expected mean when correlated with age or parameters of somatic growth) with normal morphology and reduced nephron number. This definition predicts that ϳ2.2% of the population exhibit renal hypoplasia, whereas epidemiologic studies suggest an estimated incidence of 1 in 400 births (1). Much confusion and the misapplication of this definition have arisen because the majority of congenitally small kidneys also exhibit evidence of tissue maldifferentiation, defined as renal dysplasia. The exact incidence of pure renal hypoplasia (without dysplasia) is difficult to define as renal dysplasia has often been incorrectly described as hypoplasia. This has predominantly been due to the lack of noninvasive diagnostic tools (i.e. Ultrasound) with resolution power adequate enough to discriminate dysplasia from hypoplasia in such settings. Severe reductions in nephron number that are characteristic of renal hypoplasia/dysplasia are the leading cause of childhood end stage renal disease. Indeed, if severe enough, these conditions can lead to significant impairment of intrauterine renal function which can in turn lead to the oligohydramnios sequence, a condition not compatible with extrauterine life. This includes severe and modest bilateral renal hypoplasia. More subtle defects in nephron number, such as those at the lower end of the normal range caused by mild bilateral renal hypoplasia, have been associated with the development of adult-onset hypertension and chronic renal failure (2-6). Here, we focus on knowledge derived from the study of human syndromic forms of renal hypoplasia and mouse mutants that provide insights into the molecular mechanisms that underlie renal hypoplasia and control nephron endowment. Congenital renal abnormalities characterized by nephron number and other renal pathologies including renal dysplasia, hydroureter, cystic dysplasia, and agenesis are reviewed in detail elsewhere (7-9). OVERVIEW OF KIDNEY DEVELOPMENTDevelopment of the mammalian metanephric kidney is dependent on reciprocal inductive interactions between two distinct cell lineages, the ureteric cell lineage and the metanephric mesenchyme (MM) cell lineage (Fig. 1). At the onset of metanephric development, signals emanating from the mass of uninduced MM initiate the formation of an epithelial bud (th...

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921 Renal Abnormalities in Fetal Alcohol Syndrome

Cited by 13 publications

References 0 publications

Cryptorchidism and Maternal Alcohol Consumption during Pregnancy

Cryptorchidism and Maternal Alcohol Consumption during Pregnancy

Genetics of congenital anomalies of the kidney and urinary tract

Genetics of Renal Hypoplasia: Insights Into the Mechanisms Controlling Nephron Endowment

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