Perinatal nephropathies.

Abstract

The purpose of this paper is to review the development of the mammalian kidney and to assess the influence that various perinatal manipulations may have on the developmental process either morphologically or functionally. Immature kidneys in general have less functional capacity than adult kidneys and a low rate of glomerular filtration, perhaps related to renal blood flow, which appears to limit the disposition of a fluid or solute load. Tubular reabsorption is also limited leading to the urinary loss of glucose, amino acids, bicarbonate and phosphate. Although the relatively low function of the immature kidney is a normal part of development, its capacity to respond under conditions of stress may be less adequate than in adults. An additional concern is that a variety of perinatal manipulations, such as the incidental or accidental ingestion of a chemical, may lead to varying degrees of altered morphogenesis or functional development of the kidney. Chemical induced renal anomalies may be of several types, but in typical teratology experiments hydronephrosis may be the most frequent observation. The functional consequences of these renal malformations may be lethal or inconsequential or while an animal may be able to survive and develop normally in the presence of a renal malformation, it is possible that a stressful situation would unmask a functional malformation which could compromise survival. Thus, some renal abnormalities may be subtle enough to go unnoticed without experimental tests. Without such tests it is impossible to evaluate the effect of functional alterations on successful adaptation. Images FIGURE 2. A FIGURE 2. B FIGURE 2. C FIGURE 2. D

TCDD-induced cyclooxygenase-2 expression is mediated by the nongenomic pathway in mouse MMDD1 macula densa cells and kidneys

“…It is known that TCDD, a potent environmental pollutant ubiquitously present in our environment, causes inflammation of the kidney in rats [3] and mice [4] at relatively low doses. One of the well-known toxic end-points of TCDD poisoning is “hydronephrosis” occurring in fetuses and neonates of rodents [5-7]. Recently it has been reported by our research team that hydronephrosis is induced in mouse pups by exposing them to TCDD through its ingestion through mothers’ milk [8].…”

Herbicides and the Environment

“…Unlike administration of dinoseb on GDs 9-11, teratogenicity was not observed after administration of dinoseb on GDs 13-15 up to 17.7 mg/kg bw/day. In a later review study for perinatal nephropathies, Gibson (1976) stated that an incidence of 30-40% of fetuses with hydronephrosis was observed at cesarean section owing to i.p. administration of dinoseb on GDs 9-11; however, no grossly observable hydronephrosis was evident in pups at 1 or 2 weeks of age.…”

“…On the other hand, i.p. treatment of dinoseb on GDs 9-11 at 15.8 mg/kg bw/day caused a impairment in p-aminophippuric acid (PAH) uptake into renal cortical slices of offspring at one and two weeks of age, and this effect was also evident at seven weeks of age (Gibson, 1976). Effects of food deprivation, phenobarbital (an inducer of chemical metabolism) and 2diethylaminoethyl-2,2-diphenylvalerate hydrochloride (SKF-525A; an inhibitor of chemical metabolism) on the developmental toxicity of dinoseb were evaluated in Swiss-Webster mice (Preache & Gibson, 1975a).…”