epidermal-growth-factor and Hydronephrosis

This study aimed to assess the urinary concentrations of epidermal growth factor (EGF) and kidney injury molecule 1 (KIM-1) in patients with hydronephrosis.. Neonates with a history of prenatal hydronephrosis were enrolled in three groups. Group 1 included neonates with severe obstruction; group 2 included neonates with milder obstruction; and group 3 included neonates with normal findings on postnatal ultrasonography.. 59 neonates were enrolled. The EGF: Cr and KIM-1: Cr ratios were significantly higher in group 1 than in group 2 (p = 0.016 and 0.015, respectively). The cut-off values were measured as 16.855 (sensitivity 71%, specificity 77%) and 0.4765 (sensitivity 81%, specificity 71%) for EGF:Cr and KIM-1:Cr ratios, respectively. The values were significantly higher in group 1 than in group 2.. Evaluation of the urinary KIM-1:Cr ratio may help identify neonates with severe obstructive hydronephrosis.

Topics: Biomarkers; Epidermal Growth Factor; Female; Hepatitis A Virus Cellular Receptor 1; Humans; Hydronephrosis; Infant; Infant, Newborn; Male; Membrane Glycoproteins; Multicystic Dysplastic Kidney; Receptors, Virus; Severity of Illness Index; Ureteral Obstruction

To report a new case with elevation of Ca 125 and hydronephrotic kidney without neoplastic disease, having special reference to clinical aspects.. The clinical history, anatomopathological and immunohistochemical findings are described. We performed a bibliographic review. We report the case of a 27 year-old female with the diagnosis of giant hydronephrosis and Ca125 elevation (313 u/ml hydronephrotic kidney urine and 112.3 u/ml serum).. She underwent a radical nephrectomy and Ca125 levels decreased. After 9 years the patient did not have any neoplastic disease and Ca125 levels are normal.. The Ca125 rise with hydronephrotic kidney may be usual although there are not enough studies. We think that in patients with hydronephrotic kidney and malignant neoplasm the Ca125 antigen can lose sensitivity for the early diagnosis, staging and follow up of the malignant diseases.

Topics: Adult; Biomarkers, Tumor; CA-125 Antigen; Epidermal Growth Factor; Female; Humans; Hydronephrosis; Kidney Neoplasms; Nephrectomy; Urothelium

Obstructive nephropathy is the most common presentation of urothelial carcinoma. The role of the urine in the obstructed kidney namely "hydronephrotic urine" in urothelial carcinoma has not been extensively explored. This study aims to evaluate whether hydronephrotic urine in the obstructed kidney could promote urothelial carcinoma. The hydronephrotic urine was collected from the obstructed kidneys of Sprague-Dawley rats induced by different periods of unilateral ureteral obstruction (UUO). By the inhibition of LY294002 and PD184352, we confirm that hydronephrotic urine promotes urothelial carcinoma cell (T24) and immortalized normal urothelial cells (E6) proliferation, migration and invasion in a dose-dependent manner through the activation of the mTORC2-AKT and ERK signaling pathways. Hydronephrotic urine also increases the expression of cyclin-D2, cyclin-B and CDK2. It also decreases the expression of p27 and p21 in both urothelial carcinoma cells and normal urothelial cells. By the protein array study, we demonstrate that many growth factors which promote tumor cell survival and metastasis are over-expressed in a time-dependent manner in the hydronephrotic urine, including beta-FGF, IFN-γ, PDGF-BB, PIGF, TGF-β, VEGF-A, VEGF-D and EGF. These results suggest that hydronephrotic urine promotes normal and malignant urothelial cells proliferation, migration and invasion, through the activation of the mTORC2-AKT and ERK signaling pathways. Further investigation using live animal models of tumor growth may be needed to clarify aspects of these statements.

Topics: Animals; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; Epidermal Growth Factor; Extracellular Signal-Regulated MAP Kinases; Gene Expression Regulation, Neoplastic; Hydronephrosis; Male; Mechanistic Target of Rapamycin Complex 2; Multiprotein Complexes; Neoplasm Invasiveness; Neovascularization, Pathologic; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Signal Transduction; TOR Serine-Threonine Kinases; Urologic Neoplasms; Urothelium

Hydronephrosis is diagnosed in 0.5% of all newborns, and ureteropelvic junction obstruction (UPJO) is a common cause. The aim of this study was to test whether specific urinary cytokines can be used as UPJO biomarkers in children with hydronephrosis.. Twenty-eight children referred for pyeloplasty due to UPJO and 13 controls were included in this prospective study. Kidney function was assessed and urine samples collected pre-, peri-, and post-operatively. Urine levels of epidermal growth factor (EGF), monocyte chemotactic peptide-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α), interferon-γ-inducible protein-10 (IP-10), and RANTES were measured simultaneously by using a bead-based multiplex sandwich immunoassay.. In hydronephrotic children, preoperative urine levels were significantly increased for EGF (median 7.4 [1.2-60.2] vs. median 4.0 [1.2-13.8] ng/mg creatinine) and MCP-1 (median 136.9 [47.7-545.5] vs. median 80.1 [28.8-149.9] pg/mg creatinine) compared to those of controls. Urine levels of EGF and MCP-1 were identical to controls at the postoperative 1-year follow-up exam.. Urine levels of EGF and MCP-1 were preoperatively increased and postoperatively normalized. This study demonstrates that urine-excreted kidney cytokines may be potential biomarkers of obstruction in children with hydronephrosis.

Topics: Adolescent; Biomarkers; Chemokine CCL2; Chemokine CCL3; Chemokine CCL5; Chemokine CXCL10; Child; Child, Preschool; Epidermal Growth Factor; Female; Humans; Hydronephrosis; Infant; Infant, Newborn; Male; Preoperative Care; Prospective Studies; Ureteral Obstruction

Down-regulation of epidermal growth factor (EGF) in the renal parenchyma has been demonstrated in children who underwent pyeloplasty due to ureteropelvic junction obstruction (UPJO). Urine levels of EGF were confirmed to parallel this finding before and after surgery. The aim of our study was to evaluate the relationship between urinary EGF (uEGF) concentrations and Society of Fetal Urology (SFU) high-grade hydronephrosis in infants presenting unilateral antenatal hydronephrosis (ANH).. This was a prospective study involving 45 infants (33 in the observational group, 12 in the surgical group) who presented with unilateral ANH. Postnatal evaluation included a clinical examination, renal ultrasonography, and voiding cystourethrography. Diuretic renal scans were performed in infants with an initial SFU grade 3 or 4 hydronephrosis or increasing hydronephrosis during follow-up. Pyeloplasty was performed when a well-tempered renogram showed an obstructive drainage curve with a half-life of >20 min and/or an obstructive washout curve pattern during the diuretic phase. We studied the longitudinal changes in SFU hydronephrosis grade and uEGF in each group and compared concentration levels at three time points in both groups. The enzyme-linked immunosorbent assay (ELISA) method was used to measure EGF concentrations in the urine. The results were normalized with urinary creatinine (Cr).. During the first 6 months, from 6 to 12 months, and in the second year of life, median SFU hydronephrosis grade and uEGF levels were 2, 2 (p = 0.015), and 1 (p < 0.01), and 50, 59 (p = 0.015), and 69.5 ng/mg Cr (p < 0.01), respectively, in the observational group. In the first 6 months, preoperatively and at 3-12 months postoperatively, the median SFU hydronephrosis grade and uEGF levels were 4, 4, and 3 (p > 0.05), and 38, 46, (p > 0.05), and 55 ng/mg Cr (p < 0.01), respectively, in the surgical group. uEGF levels in the first 6 months of life were significantly lower in the surgical group than in the observational group (p < 0.01). Patients in the observational group with SFU grade 3-4 hydronephrosis showed higher uEGF levels than those in the surgical group with SFU grade 3-4 in (p = 0.048).. Urinary EGF changes over time are associated with inverse changes in SFU hydronephrosis grade, which suggests a role for uEGF as a predictive marker of worsening hydronephrosis grades in infants with ANH. uEGF in the first 6 months of life may predict the need for surgery in infants with ANH.

Topics: Biomarkers; Case-Control Studies; Child, Preschool; Down-Regulation; Enzyme-Linked Immunosorbent Assay; Epidermal Growth Factor; Female; Humans; Hydronephrosis; Infant; Male; Treatment Outcome; Ureteral Obstruction

To study the potential role of pelviureteral junction obstruction (PUJO) in causing progressive renal damage in children through the renal expression of epidermal growth factor (EGF) and transforming growth factor-beta1 (TGF-beta1).. The expression of EGF and TGF-beta1 was evaluated in the renal tissues of 25 children with congenital hydronephrosis by immunohistochemistry, in situ hybridization, and reverse transcriptase polymerase chain reaction techniques.. Children with PUJO had a significant increase in TGF-beta1 and a marked reduction in EGF expression compared with controls. The TGF-beta1/glyceraldehyde phosphate dehydrogenase ratio in the hydronephrotic kidney and normal kidney was 0.53 +/- 0.13 and 0.24 +/- 0.10 respectively, and the difference was significant (P = 0.000). The EGF/glyceraldehyde phosphate dehydrogenase ratio in the hydronephrotic kidney and normal kidney was 0.15 +/- 0.06 and 0.55 +/- 0.13, respectively, and the difference was also significant (P = 0.0001). Positive correlations were found between the TGF-beta1 gene and the drainage clearance half-time (r = 0.47; P = 0.018), TGF-beta1 protein and drainage clearance half-time (r = 0.44; P = 0.028), TGF-beta1 gene and histologic grade (r = 0.53; P = 0.006), and TGF-beta1 protein and histologic grade (r = 0.76; P = 0.000). Negative correlations were found between the EGF gene and drainage clearance half-time (r = -0.59; P = 0.002), EGF protein and drainage clearance half-time (r = -0.61; P = 0.001), EGF gene and histologic grade (r = -0.58; P = 0.003), and EGF protein and histologic grade (r = -0.47; P = 0.019).. TGF-beta1 expression was increased and EGF expression was decreased in the renal tissue after clinical PUJO. The alterations of TGF-beta1 and EGF may play a potential role in the pathogenesis of renal damage in PUJO.

Topics: Child, Preschool; Epidermal Growth Factor; Female; Humans; Hydronephrosis; Kidney; Kidney Pelvis; Male; Transforming Growth Factor beta; Transforming Growth Factor beta1; Ureteral Obstruction

Epidermal growth factor (EGF) markedly attenuates tubular apoptosis induced by unilateral ureteral obstruction (UUO) in the neonatal rat, and reduces apoptosis induced by mechanical stretch of cultured rat tubular cells.. To investigate the role of EGF in modulating apoptosis resulting from UUO, neonatal wild type and mutant mice lacking EGF (knockout), or with diminished EGF receptor activity (waved-2 mutant) were compared to control mice for tubular apoptosis and atrophy. Rat and mouse kidneys were compared for localization of the EGF receptor. Apoptosis was also measured in cultured mouse tubular cells subjected to stretch and exposed to EGF.. UUO reduced endogenous renal EGF expression in wild-type mice. Unlike the rat, exogenous EGF did not decrease tubular apoptosis or atrophy in the obstructed kidney, and significantly increased stretch-induced apoptosis of cultured mouse tubular cells. Tubular apoptosis was 50% lower in the obstructed kidney of EGF knockout and waved-2 mice relative to wild type and heterozygous animals. Exogenous EGF increased tubular apoptosis and doubled atrophy in the obstructed kidney of waved-2 mice. Species differences in EGF receptor localization were detected in 3-day-old kidneys.. EGF acts as a survival factor in the neonatal rat, but potentiates tubular cell death in the neonatal mouse. Species differences are maintained in cultured cells, suggesting that differences in EGF receptor signaling underlie these opposing effects.

Topics: Animals; Animals, Newborn; Apoptosis; Cell Survival; Cells, Cultured; Epidermal Growth Factor; ErbB Receptors; Hydronephrosis; Mice; Mice, Inbred C57BL; Mice, Knockout; Rats; Signal Transduction; Species Specificity

The environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produces cleft palate (CP) and hydronephrosis (HN) in mice. The etiology of these defects involves hyperproliferation of epithelial cells of the secondary palatal shelf and ureter, respectively. These effects correlate with altered expression of the epidermal growth factor receptor (EGFR), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha). In this study, the developmental toxicity of TCDD was examined in EGF, TGF-alpha, and double EGF + TGF-alpha knockout (-/-) and wild type (WT) mice. The influence of background genetics in responsiveness to TCDD was examined using liver 7-ethoxyresorufin-O-deethylase (EROD) activity. Animals were dosed by gavage with 0, 0.2, 1, 5, 24, 50, 100, or 150 micro g TCDD/kg (5 ml/kg) body weight on gestation day 12. The mixed genetic background of WT, EGF (-/-), and EGF + TGF-alpha (-/-) made these mice less responsive to TCDD relative to C57BL/6J and TGF-alpha (-/-), which have a C57BL background. These results show that EGF and TGF-alpha are not required for response to TCDD; however, the specific ligand available to bind EGFR affects the responsiveness to TCDD. EGF (-/-) mice are less responsive for CP, but more sensitive to HN. TGF-alpha (-/-) mice were similar to WT in sensitivity for induction of CP and HN. The responses of EGF + TGF-alpha (-/-) mice were like the WT except at higher doses where sensitivity to CP increased, suggesting that the responses may be mediated by alternative ligands for EGFR that are not functional equivalents of EGF or TGF-alpha. In conclusion, the EGFR pathway is mechanistically important in responses of the embryo to TCDD. Specific ligands confer sensitivity or resistance that are target tissue-dependent.

Topics: Abnormalities, Drug-Induced; Administration, Oral; Animals; Cleft Palate; Cytochrome P-450 CYP1A1; Dose-Response Relationship, Drug; Environmental Pollutants; Epidermal Growth Factor; Female; Genetic Predisposition to Disease; Hydronephrosis; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Microsomes, Liver; Polychlorinated Dibenzodioxins; Pregnancy; Teratogens; Transforming Growth Factor alpha

The aim of this study was to test the hypothesis that expression of epidermal growth factor (EGF) and transforming growth factor-beta 1 (TGF-beta 1) may be altered in stenotic tissue of patients with congenital hydronephrosis caused by pelviureteric junction (PUJ) obstruction and to evaluate the role of these 2 growth factors.. The expression of EGF and TGF-beta 1 was evaluated in tissue specimens in 25 children with PUJ obstruction and 15 controls with normal PUJs by immunohistochemistry, in situ hybridization, and reverse transcriptase polymerase chain reaction (RT-PCR) techniques. All the signals of mRNA products were normalized to the mRNA levels of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) a housekeeping gene, as a ratio.. On RT-PCR study, the amount of TGF-beta 1 mRNA in stenotic tissue was higher than in controls, in addition, EGF gene expression in the obstructed junction was significantly lower than in normal junctions. The TGF-beta 1 to GAPDH ratio was 0.57 +/- 0.26 and 0.36 +/- 0.19 in the stenotic tissue and the normal ureter, respectively (P =.012). The EGF to GAPDH ratio was 0.17 +/- 0.08 and 0.37 +/- 0.14 in the stenotic tissue and the normal ureter, respectively (P =.0001). Furthermore, the positive correlations were found between TGF-beta1 gene and protein expression (r = 0.601; P =.001), TGF-beta 1 gene and drainage clearance half-time (T1/2) (r = 0.474; P =.017), TGF-beta 1 protein expression, and T1/2 (r = 0.516; P =.008). A negative correlation was found between EGF gene and T1/2 (r = -0.448; P =.025). On immunolabeling and in situ hybridization labeling, the expression of TGF-beta 1 protein was strongly positive and confined to the muscle cells, spindle cells, and collagen fibers in the stenotic tissue; the expression of TGF-beta 1 mRNA was moderately positive and mainly distributed in the collagen of the stenotic segment, both the expression of EGF protein and mRNA were negative in the normal ureter.. There were increased TGF-beta 1 mRNA expression and decreased EGF mRNA expression in the stenotic tissue after clinical ureteropelvic junction obstruction. The alteration of EGF and TGF-beta 1 expression may be involved in the pathogenesis of congenital hydronephrosis.

Topics: Child; Child, Preschool; Constriction, Pathologic; Epidermal Growth Factor; Female; Gene Expression Regulation; Genetics; Humans; Hydronephrosis; In Situ Hybridization; Kidney; Kidney Pelvis; Male; Radionuclide Imaging; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Transforming Growth Factor beta; Transforming Growth Factor beta1; Ureter; Ureteral Obstruction

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure produces hydronephrosis and cleft palate in mice. These responses are correlated with disruption of expression of epidermal growth factor (EGF) receptor ligands, primarily EGF and transforming growth factor-alpha (TGF-alpha), and altered epithelial cell proliferation and differentiation. This research examined the role of these growth factors in TCDD-induced teratogenicity by using wild type (WT) and knockout (-/-) mice that do not express EGF, TGF-alpha, or both EGF and TGF-alpha. Pregnant females were weighed on GD 12 and dosed by gavage with either corn oil or TCDD at 24 microg/kg, 5 ml/kg. On GD 17.5, the maternal parameters evaluated included body weight, body weight gain, liver weight (absolute and adjusted for body weight). The number of implantations, live and dead fetuses, early or late resorptions, the proportion of males, fetal body weight, fetal absolute and relative liver weight, placenta weight, incidence of cleft palate, and the severity and incidence of hydronephrosis were recorded. TCDD did not affect maternal weight gain, fetal weight, or survival, but maternal and fetal liver weights and liver-to-body weight ratios were increased in all genotypes. The WT and TGF-alpha (-/-), but not the EGF (-/-) and EGF + TGF-alpha (-/-) fetuses, developed cleft palate after exposure to 24 microg TCDD/kg. Hydronephrosis was induced by TCDD in all genotypes, with the incidence in EGF + TGF-alpha (-/-) fetuses comparable to that of the WT. The incidence and severity of this defect was substantially increased in EGF (-/-) and TGF-alpha (-/-). In conclusion, this study demonstrated that expression of EGF influences the induction of cleft palate by TCDD. Also, EGF and TGF-alpha are not required for the induction of hydronephrosis, but when either is absent the response of the fetal urinary tract to TCDD is enhanced.

Topics: Abnormalities, Drug-Induced; Administration, Oral; Animals; Body Weight; Cleft Palate; Environmental Pollutants; Epidermal Growth Factor; Female; Hydronephrosis; Liver; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Organ Size; Polychlorinated Dibenzodioxins; Pregnancy; Reproduction; Teratogens; Toxicity Tests; Transforming Growth Factor alpha

To assess apoptosis in congenital hydronephrosis and discuss its clinical significance.. Apoptosis was detected in 15 kidneys from children with congenital hydronephrosis (5 mild hydronephrosis, 5 moderate hydronephrosis and 5 severe hydronephrosis) using the electronmicroscope, in situ gap labeling of fragmented nuclear DNA and DNA fragmentation analysis.. Apoptosis was seen in kidneys from children with congenital hydronephrosis. Margination of nuclear chromatin was identified and rounded apoptotic bodies were seen. The mean apoptotic index was 0.0941 +/- 0.017 in severe hydronephrosis, 0.0325 +/- 0.0169 in moderate hydronephrosis, and 0.0021 +/- 0.0031 in mild hydronephrosis. There was a significant difference between severe and moderate hydronephrosis (P = 0.0005), as well as between moderate and mild hydronephrosis (P = 0.0154). Moreover, with an increasing degree of hydronephrosis, the number of apoptotic cells also increased. Five kidneys with severe hydronephrosis and one kidney with moderate hydronephrosis showed typical apoptotic bands.. Apoptosis might participate in damaging kidneys in children with congenital hydronephrosis.

Topics: Apoptosis; Child; Child, Preschool; DNA Fragmentation; Epidermal Growth Factor; Female; Humans; Hydronephrosis; Infant; Kidney Tubules; Male; Transforming Growth Factor beta

The authors studied the potential role of ureteropelvic junction obstruction (UPJ-O) in causing progressive renal damage in children through the renal expression of epidermal growth factor (EGF) and monocyte chemotactic protein-1 (MCP-1) mRNA.. Renal tissues were harvested from 11 children with UPJ-O and from 10 normal kidneys to study the renal expression of EGF and MCP-1 detected by means of in situ hybridization. Five of the patients were found to have a history of urinary tract infection (UTI).. Children with UPJ-O had marked reduction of EGF gene expression when compared with controls. Interstitial expression of MCP-1 mRNA was present in all UPJ-O cases. Both EGF and MCP-1 expression did not correlate with age, with differential renal function, and with renal thickness measured through MAG3 renal scan. Children with a history of UTI had a more severe reduction of the renal thickness of the affected kidney compared with those without UTI. MCP-1 expression was higher and EGF more reduced in children with a history of UTI.. Our results suggest a potential role of EGF and MCP-1 in the pathogenesis of renal damage and growth failure in UPJ-O, especially in children with UTI. These important functional changes begin early in life, possibly during fetal life.

Topics: Adolescent; Biopsy; Chemokine CCL2; Child; Child, Preschool; Epidermal Growth Factor; Humans; Hydronephrosis; In Situ Hybridization; Infant; Infant, Newborn; Kidney; RNA, Messenger

Partial ureteral obstruction in the weanling rat leads to hydronephrosis of the ipsilateral kidney and renal cell deletion through the process of programmed cell death known as apoptosis. The apoptotic response following partial ureteral obstruction in weanling Sprague-Dawley rats was studied using the traditional markers of apoptosis, including deoxyribonucleic acid (DNA) laddering pattern on agarose gel electrophoresis, in situ gap labeling of fragmented DNA for quantitative apoptotic body determination, polyadenylated messenger ribonucleic acid (mRNA) expression of sulfated glycoprotein-2, and polyadenylated mRNA expression of epidermal growth factor and transforming growth factor-beta. Partial ureteral obstruction resulted in a progressive increase in the intensity of DNA fragmentation associated with apoptosis during the initial 3 weeks. Quantitative apoptotic body counting revealed a 3-fold increase by week 3 of partial obstruction. This increase represented a level of apoptosis, which is 65% of that observed in complete ureteral obstruction. By week 2 of partial obstruction there was a 13-fold increase in the expression of sulfated glycoprotein-2 mRNA, as well as changes in the growth factor environment characterized by a decline in the constitutive expression of epidermal growth factor mRNA and an increase in the expression of transforming growth factor-beta mRNA. These altered levels represent changes in expression comparable to those observed during the apoptotic response following complete ureteral obstruction, although the time course is delayed by 2 to 3 weeks.

Topics: Animals; Apoptosis; Blotting, Northern; Clusterin; DNA; Electrophoresis, Agar Gel; Epidermal Growth Factor; Glycoproteins; Hydronephrosis; Kidney Tubules; Molecular Chaperones; Rats; Rats, Sprague-Dawley; RNA, Messenger; Transforming Growth Factor beta; Ureteral Obstruction

Unilateral ureteral obstruction in the rat leads to hydronephrosis of the affected kidney and renal cell deletion through the process of apoptosis. We studied this experimental model to determine whether acute alterations in renal growth factor expression might be involved in the initiation of the apoptotic response. Northern blot analysis of hydronephrotic, contralateral and sham operated kidney polyadenylated messenger ribonucleic acid (mRNA) was performed to quantitate the expression of mRNA encoding the growth factors epidermal growth factor, transforming growth factor-beta and insulin-like growth factor II during the first 48 hours following ureteral obstruction. Although the expression of the insulin-like growth factor II mRNA was unchanged by ureteral obstruction, the expression of epidermal growth factor mRNA rapidly declined in the obstructed kidney during this period. The loss of epidermal growth factor expression was further confirmed by an immunocytochemical staining procedure that demonstrated high concentrations of epidermal growth factor in control renal tubules and a drastic loss of this staining in obstructed renal tubules. In contrast, expression of transforming growth factor-beta mRNA increased in the obstructed kidney. We believe that the altered growth factor environment of the hydronephrotic kidney might be an initiating factor in the onset of renal apoptosis associated with this condition.

Topics: Animals; Blotting, Northern; Epidermal Growth Factor; Growth Substances; Hydronephrosis; Immunohistochemistry; Insulin-Like Growth Factor II; Kidney; Rats; Rats, Inbred Strains; RNA, Messenger; Transforming Growth Factor beta; Ureteral Obstruction

Topics: Epidermal Growth Factor; Humans; Hydronephrosis; Iodine Radioisotopes; Lymph Nodes; Radionuclide Imaging

We have previously demonstrated that changes in urinary epidermal growth factor/creatinine ratios relate to gestational age and gender. It is unclear what controls this developmental pattern although chronic renal disease and thyroid aberrations have significant effects on epidermal growth factor and creatinine excretion in childhood and in adults. Therefore, we chose to explore the effects of these disease states on epidermal growth factor excretion during the perinatal time period. We collected urine samples from 8 infants with congenital renal disease and 45 infants with low T4 and normal TSH values who 'failed' the newborn screen. In addition, 2 infants with hypothyroidism and 2 infants with neonatal Grave's disease had urine samples examined. Values were compared with the epidermal growth factor and creatinine excretion from 190 infants. We demonstrated that epidermal growth factor excretion increased earlier in gestation than does creatinine excretion. In infants with renal disease or hypothyroidism, epidermal growth factor excretion was decreased while hyperthyroidism enhanced excretion. Epidermal growth factor excretion increased with relief of an obstruction but still remained low and creatinine excretion was unchanged. We confirm that in preterm infants as in childhood there are similar effects of thyroid and renal diseases on epidermal growth factor excretion.

Topics: Congenital Hypothyroidism; Creatinine; Epidermal Growth Factor; Female; Humans; Hydronephrosis; Hyperthyroidism; Hypothyroidism; Infant; Infant, Newborn; Kidney; Kidney Diseases; Male