Differentiation of the Glomerular Filtration Barrier in the Rat Fetus: Possible Role of Collagen

Bakala, Hilaire; Geloso-Meyer, A.; Cheignon, M.; Schaeverbeke, J.

doi:10.3109/03008208509152409

Cited by 18 publications

(17 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The elevation in BUN concentration of nephrectomized mothers implies the elevation in functional demand to remaining kidney. Since the fetal kidney becomes functional during the late gestation period (Bakala et al, 1985), the decrease in BUN from day 14 to 22 of gestation reflects the instigation of fetal urine production. On day 22 of gestation, the concentration of urea nitrogen (UN) in maternal blood, fetal blood, and amniotic fluid were significantly higher in 5/6 nephrectomized pregnant rats than in shamoperated ones (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, maternal renal function elevates during pregnancy in rats (Churchill et al, 1982). Throughout gestation, fetal waste products are primarily excreted by maternal kidneys through placental circulation (Liggins, 1972) and fetal kidneys start secreting urine during the final days of gestation (Bakala et al, 1985). This implies that an increase of fetal waste products in circulation, indicative of the latter gestational period, stimulates fetal kidneys to start urine production.…”

Section: Effects Of Maternal Renal Dysfunction On the Development Of mentioning

confidence: 99%

“…During the final days of gestation, fetal kidneys start secreting urine (Bakala et al, 1985). This implies that an increase of fetal waste products in circulation, indicative of the latter gestational period, stimulates fetal kidneys to start urine production.…”

Section: Aim Of Studymentioning

confidence: 99%

“…Maternal conditions affect the growth of the fetal kidney, which begins to secrete urine during late gestation (Bakala et al, 1985;Schaeverbeke & Cheignon, 1980). For example, during pregnancy, the maternal kidney undergoes various changes such as an increase in glomerular filtration rate (Baylis, 1994;Atherton & Pirie, 1981) and an alteration in tubular function (Dafnis & Sabatini, 1992).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Effects of Maternal Renal Dysfunction on Fetal Development

Okada¹,

Kitano-Amahori²,

Mino³

et al. 2012

Renal Failure - The Facts

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

Section: Effects Of Maternal Renal Dysfunction On the Development Of mentioning

confidence: 99%

Section: Aim Of Studymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effects of Maternal Renal Dysfunction on Fetal Development

Okada¹,

Kitano-Amahori²,

Mino³

et al. 2012

Renal Failure - The Facts

View full text Add to dashboard Cite

“…The GBM is progressively formed by two membranes: the lamina rara interna (LRI; formed from the endothelial cells) and the lamina rara externa (LRE; formed from the pedicels of the epithelial cells), which fuse and generate a common lamina densa (LD) in the central part (2,19,40,44). In the rat neonate, all these stages can be observed, the first differentiated (older) nephrons being in the juxta-medullary area.…”

mentioning

confidence: 99%

Gentamicin administered during gestation alters glomerular basement membrane development

Smaoui

Mallié

Schaeverbeke

et al. 1993

Antimicrob Agents Chemother

View full text Add to dashboard Cite

Gentamicin during gestation alters glomerular basement membrane development. A drug-induced nephrotoxicity was described for neonates after gentamicin was given intraperitoneally to pregnant Wistar rats; glomerular alterations and changes in permselectivity were important. We investigated the ultrastructure of the glomerular basement membrane (GBM), the arrangement of anionic sites, and the urinary proteins at two ages, with 1-day-and 12-month-old control and prenatally exposed animals. For neonates, the pattern of glomerular differentiation was similar, anionic sites were made of heparan sulfate proteoglycans, and the GBM had the same total thickness in both groups. After transplacental gentamicin exposure, the lamina densa was larger, the laminae rarae were thinner, the density of anionic sites was increased; the levels of hydroxyproline, sulfate, and hexuronic acid in the kidney were increased; and the immunoelectrophoresis of urinary proteins was abnormal. For adults, prenatal exposure to gentamicin led to altered juxta-medullary glomeruli with a larger GBM and abundant anionic sites, especially in the lamina densa, and to a protein excretion different from that of controls. Thus, gentamicin administered during pregnancy leads to permanent alterations of the GBM with modifications of both the layers and the anionic sites, possibly because of a perturbed protein metabolism. These altered glomeruli are at risk during life and could be the starting point for a kidney disease.Analysis of drugs in relation to their safety for mother and fetus is usually restricted to gross examinations of the newborn alone. The developing kidney, considered to be resistant to nephrotoxicity (17), is rarely investigated despite the fact that renal alterations in young and puppies have been described after administration of different drugs (18,37). Only recently has there begun to emerge a perception of how alterations of the developing kidney could explain a large variety of renal disorders, especially glomerular ones (3,44,50).In contrast, for adults nephrotoxicity studies have been expanding for 2 decades mainly because kidney diseases constitute an important economic burden which could be relieved in part by prevention. Following the widespread use of aminoglycoside antibiotics, gentamicin-induced nephrotoxicity became one of the most investigated drug-induced renal injuries (7,22,24,29,43).Observations of in utero aminoglycoside-induced nephrotoxicity after antibiotics had been given to pregnant rats (20,21,(31)(32)(33) showed that, contrary to what is seen with adults, glomerular modifications are very common while tubules are less altered. Also, an abnormal proteinuria was described and a marker with a high molecular weight (anionic ferritin) was found in the urine and glomerular podocytes after being injected intravenously into neonates (42), indicating an altered permselectivity of the glomerular basement membrane (GBM) of the mature glomeruli.Renal maturation, similar in all mammals, is often termi-* Corresponding author....

show abstract