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Kidney abnormal

Sparschu et al. reported the embryotoxicity of TCDD in rats (1970) (refs. 122a,b). Data are summarized for rats and mice in Table 5. The three major effects observed were intestinal hemorrhages (rat fetuses) and increased incidence of cleft palate and kidney abnormalities (mouse fetuses). TCDD in pg/kg doses has also been reported to cause embryotoxic effects in hamsters eye abnormalities, reduction of mean fetal weight GI hemorrhages, increased prenatal mortality- (ref. 123). [Pg.337]

TCDD appears to be an unusually specific teratogen for cleft palate and certain kidney abnormalities. It is also notable for the very low doses (1 to 10 pg/kg) of TCDD required to induce both teratogenic and fetolethal effects in rats and mice. [Pg.337]

Blood testing, which was designed to screen for liver and kidney abnormalities, leukemia and blood diseases, showed no patterns of excess abnormality."... [Pg.39]

Animals exposed via chronic inhalation developed lethargy, weight loss, kidney abnormalities, embryo-toxicity, and inflammation to the upper respiratory tract and gastric mucosa. [Pg.46]

Whether LCAT deficiency leads to an increased content of UC in all cell plasma membranes is not yet clear, but analyses of tissues obtained from the patients have revealed increased contents of UC in the liver, kidneys, spleen, and arteries [67], Meanwhile, there are granular deposits in the cornea that seem to consist of lipid, and foam cells that seem to contain CE are seen in the bone marrow, spleen, and glomerular tufts of the kidney. The kidney abnormalities may be of special significance because renal dysfunction can be a life-threatening feature of the disease. Proteinuria is detectable in childhood, and sometimes progresses to renal failure later on in life. [Pg.110]

It is often assumed that the kidney and liver represent at least 50% of the total body burden (Herber et al., 1988). With a Cd in the liver level below 40 mg/kg the Cd in the kidney level seems to increase with increasing Cd in liver. Cd levels in the kidney above 40 mg/kg Cd in the liver however, will decrease with increasing Cd in liver levels here the kidney might lose Cd and this will be excreted in urine (Ellis et al., 1981). In a later In vivo study Ellis et al. (1984) concluded that most workers with a Cd in liver concentration above 70 mg/kg were judged to have some evidence of kidney abnormalities. [Pg.325]

It is well known that uric acid is an end product of only a few mammals man, higher apes, and the Dalmatian coach hound (F5). The Dalmation is an anomaly because its excretion is due to a kidney abnormality (F5). The other mammals that do not excrete uric acid as a primary purine end product, form it as an intermediate, but they possess the enzyme uricase, which degrades vuic acid to allantoin, a more highly water-soluble substance than uric acid, and in some cases this is degraded further. [Pg.214]

Other evidence of the protective effects of selenium against heart disease consists of (1) its action as part of the enzyme which breaks down toxic peroxides that may damage the heart muscle, particularly those formed from polyunsaturated fats and (2) its counteraction of the toxicity of cadmium, a common environmental pollutant which causes kidney abnormalities leading to high blood pressure. ... [Pg.547]

The health effects of sorbic acid and sorbates have been reviewed (165—167). The extremely low toxicity of sorbic acid enhances its desirabiHty as a food preservative. The oral LD q for sorbic acid in rats is 7—10 g/kg body weight compared to 5 g/kg for sodium chloride (165—169). In subacute and chronic toxicity tests in rats, 5% sorbic acid in the diet results in no abnormal effects after 90 days or lifetime feeding studies. A level of 10% in rat diets results in a slight enlargement of the Hver, kidneys, and thyroid gland (170). This same dietary level fed to mice also resulted in an increase in Hver and kidney weight... [Pg.287]

Urinalysis. Urine is collected at various times and examined with respect to its volume, specific gravity, and the presence of abnormal constituents. The results may indicate kidney damage or suggest tissue injury at other sites (77). [Pg.236]

B2 knockout embryos subjected to salt stress in utero show suppressed renin expression and an abnormal kidney phenotype and develop early postnatal hypertension. Consistently, although basal bradykinin formation is defective tissue kallikrein-null mice have normal blood pressure however suffer from cardiovascular abnormalities. However suggesting a function of kinin signaling during development. [Pg.675]

MTX is potentially toxic. Therefore, the nurse observes closely for development of adverse reactions, such as thrombocytopenia (see Nursing Alert in Gold Compounds section) and leukopenia (see discussion of adverse reactions associated with hydroxychloroquine). Hematology, liver, and renal function studies are monitored every 1 to 3 months with MTX therapy. The primary care provider is notified of abnormal hematology, liver function, or kidney function finding. The nurse immediately brings all adverse reactions or suspected adverse reactions to the attention of the primary health care provider. [Pg.196]

Once essential hypertension develops, management of this disorder becomes a lifetime task. When a direct cause of the hypertension can be identified, the condition is described as secondary hypertension. Among the known causes of secondary hypertension, kidney disease ranks first, with tumors or other abnormalities of the adrenal glands following. In malignant hypertension the diastolic pressure usually exceeds 130 mm Hg. In secondary hypertension,... [Pg.393]

These studies led to the realization that proteinuria— the abnormal appearance of protein in the urine— could result not only from the enlargement of submicroscopic holes in the glomerular capillary wall, but also from the loss or neutralization of its negatively charged components. This finding has provided a new direction for research on the molecular basis for the nephrotic syndrome, a group of kidney diseases all characterized by massive proteinuria. [Pg.46]

Inherited defects in lipoprotein metabofism lead to the primary condition of either hypo- or hyperlipoproteinemia (Table 26-1). In addition, diseases such as diabetes mellitus, hypothyroidism, kidney disease (nephrotic syndrome), and atherosclerosis are associated with secondary abnormal hpoprotein patterns that are very similar to one or another of the primary inherited conditions. Virtually all of the primary conditions are due to a defect at a stage in hpoprotein formation, transport, or destruction (see Figures 25—, 26-5, and 26-6). Not all of the abnormafities are harmful. [Pg.229]

Inherited defects in hpoprotein metabofism lead to a primary condition of hypo- or hyperfipoproteinemia. Conditions such as diabetes meUitus, hypothyroidism, kidney disease, and atherosclerosis exhibit secondary abnormal hpoprotein patterns that resemble certain primary conditions. [Pg.229]

From a therapeutic point of view, it is essential to confirm the presence of bacteriuria (a condition in which there are bacteria in the urine) since symptoms alone are not a reliable method of documenting infection. This applies particularly to bladder infection where the symptoms of burning micturition (dysuria) and frequency can be associated with a variety of non-bacteriuric conditions. Patients with symptomatic bacteriuria should always be treated. However, the necessity to treat asymptomatic bacteriuric patients varies with age and the presence or absence of underlying urinary tract abnormalities. In the pre-school child it is essential to treat all urinary tract infections and maintain the urine in a sterile state so that normal kidney maturation can proceed. Likewise in pregnancy there is a risk of infection ascending from the bladder to involve the kidney. This is a serious complication and may result in premature labour. Other indications for treating asymptomatic bacteriuria include the presence of underlying renal abnormalities such as stones which may be associated with repeated infections caused by Proteus spp. [Pg.140]

Abnormal test may indicate hypertension related to kidney damage... [Pg.14]

Renal ultrasound (uses sound waves to assess size, position, and abnormalities of the kidney dilatation of the urinary tract can be seen with postrenal ARF)... [Pg.364]


See other pages where Kidney abnormal is mentioned: [Pg.419]    [Pg.419]    [Pg.419]    [Pg.419]    [Pg.1730]    [Pg.2529]    [Pg.257]    [Pg.312]    [Pg.221]    [Pg.287]    [Pg.1437]    [Pg.282]    [Pg.419]    [Pg.419]    [Pg.419]    [Pg.419]    [Pg.1730]    [Pg.2529]    [Pg.257]    [Pg.312]    [Pg.221]    [Pg.287]    [Pg.1437]    [Pg.282]    [Pg.44]    [Pg.81]    [Pg.568]    [Pg.811]    [Pg.811]    [Pg.1036]    [Pg.1274]    [Pg.765]    [Pg.46]    [Pg.100]    [Pg.210]    [Pg.139]    [Pg.140]    [Pg.315]    [Pg.156]    [Pg.13]    [Pg.49]    [Pg.374]    [Pg.377]   
See also in sourсe #XX -- [ Pg.254 ]




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