Re: A pitfall in the diagnosis of supernumerary kidney.
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Biomedical subjects
Publications and source records attributed to L H Zondek.
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Human fetal lung homogenates contain an inactive form of renin which may be revealed by trypsin treatment. When activated, this form of renin has some biochemical similarities with fetal kidney renin: the pH optimum of fetal lung renin is approximately 6.5; it is bound by Affigel Blue affinity chromatography resin; and is inhibited by a monoclonal antibody (R-3-36-16) raised to human kidney renin. Inactive renin, partially-purified from both fetal kidney and lung, differs from this in that the renal form is of low-molecular weight (LMW, 45,000 daltons), whereas that from fetal lung is of high molecular weight (HMW, 58,000 daltons). Using a sensitive alkaline phosphatase-anti-alkaline phosphatase (APAAP) procedure with a polyclonal anti-renin antibody (R-15), immunoreactive renin in fetal lung was found in vessels in mesenchyme between airways. The pattern of staining was distributed similarly to Factor VIII-related antigen, suggesting localization in endothelial cells.
A survey has been made of the reproductive organs of anencephalic fetuses with special reference to the uterus and the vagina. The uteri and the vaginae of 15 anencephalic fetuses were examined and compared with 29 controls. The uterus showed normal development and reacted normally to hormonal stimulation by showing vascular, stromal and glandular proliferation and glandular diastase-resistant mucin secretion in varying degrees. All these processes were fully developed during the last month of pregnancy, offering the same picture as the controls. Cervix and vagina showed good maturation of squamous epithelium with already a fair amount of diastase-resistant mucin at 27 weeks of gestation, increasing steadily towards full term. A review of 32 postmortem records from various hospitals did not reveal any external developmental abnormalities of the uterus and its appendages in the anencephalic fetus with the exception of 2 cases. These findings are in marked contrast to the gross developmental abnormalities observed in the reproductive organs of male anencephalic fetuses.
In a study of 38 fetuses total kidney renin was significantly correlated with gestational age (r = 0.63). Although whole fetal kidney renin specific activity was found to decrease with gestational age (r = -0.65), the mean value of the specific activity was about 20 times greater than in normal adult cortex and double that in tissue from patients with renal artery stenosis, suggesting renin-angiotensin system hyperactivity. In approximately 40% of fetal kidneys examined, evidence for an inactive (trypsin-activatable) renin precursor was found. The molecular weight of this form was indistinguishable from active renin (45 000 daltons) by Sephadex chromatography. Amniotic fluid from nine cases (100%) contained angiotensin (ANG) 1, angiotensin converting enzyme (ACE), renin substrate, active and inactive renin (both 45 000 daltons). Five of the 38 (13%) fetal adrenal glands contained renin, but no evidence for trypsin-activatable forms. Aldosterone was present in low concentration in the earliest adrenals examined, and a positive correlation existed between total tissue aldosterone and gestational age (r = 0.73). These findings suggest that the fetal renin-angiotensin system has an important role to play in the maintenance of extracellular fluid volume and blood pressure in the developing fetus.
The prostates of 41 foetuses and neonates have been assayed for testosterone, 5 alpha-dihydrotestosterone (DHT), oestradiol and oestriol and the presence of these hormones has been demonstrated in all cases. Oestriol was found to be present in the highest concentration. A highly significant correlation was found between testosterone and DHT as well as between DHT and oestradiol. The correlation between oestriol and oestradiol was also significant. It has been pointed out that the presence of these hormones is essential for the growth and development of the prostate gland.
The presence of ovarian hilar cells in fetuses and neonates whose mothers suffered from complications of pregnancy such as toxaemia of pregnancy, diabetes mellitus, accidental haemorrhage, hydrops foetalis and multiple pregnancy, has been investigated and compared with the presence of testicular Leydig cells in similar conditions. The examination of ovaries from 62 cases with complications of pregnancy and of 113 controls showed that such conditions did not have an influence on the presence of hilar cells in the fetal and neonatal ovary. These findings are in marked contrast to our previous observations in the fetal and neonatal testis where the mean number of Leydig cells was found to be significantly raised in cases associated with complications of pregnancy as compared with controls. This further confirms our view, already expressed in a previous publication on the ovaries and testes of anencephalic monsters, that fetal and neonatal ovarian hilar cells and testicular Leydig cells are not strictly comparable, at least in their response to hormonal stimuli.
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The presence of ovarian hilar cells in anencephaly has been investigated and compared with the presence of testicular Leydig cells in the same condition. The examination of 29 anencephalic ovaries and 49 controls showed that up to 36 weeks of gestation there was a preponderance of ovarian hilar cells in anencephalic monsters as compared with controls. Similar observations were made with regard to ovarian follicles which showed more pronounced maturational changes than controls. However, during the last month of gestation both these processes were more marked in the controls. These findings are in marked contrast to our previous observations on the testes in anencephalic monsters which showed significantly less Leydig cells than controls throughout the third trimester of pregnancy. It is assumed that these appearances are due to the fact that testes and ovaries are not strictly comparable structures and may, therefore, react in a different way to hormonal stimulation. This is of particular interest as the placental chorionic gonadotrophin levels which stimulate the development of testicular Leydig cells and, supposedly, the development of ovarian hilar cells are normal in anencephaly.
The fetal epididymis shows a weak periodic acid Schiff (PAS)-positive secretion by the 25th week of gestation which gradually increases during the following weeks and reaches its peak in the later weeks of pregnancy. It decreases again after the 3rd month of life. The organ continues to secrete throughout childhood, although in a much reduced degree. It can be assumed that androgens, produced by the fetus in response to stimulation by maternal and placental hormones, are responsible for the secretion of the organ during fetal life. The normal development and function of the epididymis in the fetus and infant can be impaired in the presence of various congenital malformations. Hormonal therapy to the mother during pregnancy may also affect the organ. However, it is possible that in the absence of any serious structural damage to the organ, the purely functional changes may only be of a temporary nature and not detrimental to fertility in later life.
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The concentration of freely extractable testosterone in amniotic fluid was measured in 54 patients whose gestational ages ranged from 10 to 20 weeks; 31 of the fetuses were male and 23 were female. The mean amniotic fluid testosterone concentration was significantly higher with a male fetus than with a female fetus. On only 7 out of 31 occasions was the presence of a male fetus associated with amniotic fluid testosterone values below 100 pg/ml, whereas the values associated with a female fetus were never higher than 90 pg/ml. After 14 weeks gestation no amniotic fluid testosterone level was lower than 120 pg/ml in the presence of a male fetus.
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