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Renal disease chronic

Chronic renal disease Hypophosphatemic vitamin D-resistant rickets Vitamin D-dependent rickets... [Pg.137]

The anemias discussed in this chapter include iron deficiency anemia, anemia in patients witii chronic renal disease pernicious anemia, and anemia resulting from a folic acid deficiency. Table 45-1 defines these anemias. Drugp used in treatment of anemia are summarized in die Summary Drug Table Drugp Used in die Treatment of Anemia. [Pg.433]

RANicH T, BHATHENA s J and VELASQUEZ M T (2001) Protective effects of dietary ph)doestrogens in chronic renal disease. J Ren Nutr. 11 (4) 183-93. [Pg.218]

Remuzzi G, Ruggenenti P, Perico N. Chronic renal diseases renopro-tective benefits of renin-angiotensin system inhibition. Ann Intern Med 2002 136 604-615. [Pg.401]

Medical disorders (e.g., chronic renal disease, anorexia nervosa, endocrine disorders)... [Pg.854]

Chronic renal disease Aromatase inhibitors (anastrazole, exemestane, letrozole)... [Pg.854]

A cohort mortality study was conducted to compare the mortality rates due to chronic renal disease in 4,519 battery plant workers and 2,300 lead production or smelter workers from 1947 to 1980 (Cooper 1988 Cooper et al. 1985). The mortality data for these workers were compared with national mortality rates for white males. Environmental lead levels and PbB levels were available for only about 30% of all workers for varying time periods from 1947 to 1972. Statistically significant increases in mortality from "other hypertensive disease" and "chronic nephritis" were seen in both lead cohorts. Limitations of this study include the fact that various confounding factors, such as smoking, were not accounted for, and the workers were probably exposed to other toxic chemicals. [Pg.69]

Cooper WC. 1988. Deaths from chronic renal disease in US battery and lead production workers. Environ Health Perspect 78 61-63. [Pg.504]

Although the kidneys are not considered endocrine glands per se, they are involved in hormone production. Erythropoietin is a peptide hormone that stimulates red blood cell production in bone marrow. Its primary source is the kidneys. Erythropoietin is secreted in response to renal hypoxia. Chronic renal disease may impair the secretion of erythropoietin, leading to development of anemia. The kidneys also produce enzymes. The enzyme renin is part of the renin-angiotensin-aldosterone system. As will be discussed, these substances play an important role in the regulation of plasma volume and therefore blood pressure. Other renal enzymes are needed for the conversion of vitamin D into its active form, 1,25-d i hyd ro xyv itamin D3, which is involved with calcium balance. [Pg.309]

Endocrine abnormalities Hypothyroidism Adrenal insufficiency Pituitary insufficiency Chronic renal disease Chronic inflammatory disease Granulomatous diseases Collagen vascular diseases Hepatic disease... [Pg.377]

Among the disadvantages of the LMWP strategy for the treatment of chronic renal disease are the requirement for parenteral administration and the possible immunogenicity of the... [Pg.143]

Hilgers KE, Maim JEE. ACE inhibitors versus ATI receptor antagonists in patients with chronic renal disease. J Am Soc Nephrol 2002 13 1100-8. [Pg.320]

Dietary protein has long been thought to play a role in the progression of chronic renal disease, but clinical trials have not consistently shown that dietary protein restriction is beneticial. A meta-analysis including the Modification of Diet in Renal Disease (MDRD) Study, of 1413 patients from 1966 to 1994 showed that dietary protein restriction slows the progression of both diabetic and non-diabetic renal disease (see Klahr et al., 1994). It is advisable to restrict protein intake moderately to 1 g/kg daily. [Pg.611]

Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker L, Kusek HW et al. The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. Modification of diet in Renal Disease Study Group. N Engl J Med 1994 330 877-84. [Pg.618]

Parenteral therapy should be reserved for patients with documented iron deficiency who are unable to tolerate or absorb oral iron and for patients with extensive chronic anemia who cannot be maintained with oral iron alone. This includes patients with advanced chronic renal disease requiring hemodialysis and treatment with erythropoietin, various postgastrectomy conditions and previous small bowel resection, inflammatory bowel disease involving the proximal small bowel, and malabsorption syndromes. [Pg.733]

Chronic renal disease may also affect metabolism, not necessarily because of impaired metabolism in the kidney, but because of an indirect effect of renal failure on liver metabolism. For example, in animals with renal failure, it was observed that there was a decrease in hepatic cytochromes P-450 content, and consequently, zoxazolamine paralysis time and ketamine narcosis time were prolonged. [Pg.166]

Disease/pathological conditions. Disposition of chemicals is potentially altered by disease and hence toxicity. Generalization, however, is difficult as the effects are unpredictable. Thus liver disease may decrease metabolism, but this depends on type of disease and particular pathway of metabolism. Disease in one organ may affect the response of another, for example, chronic renal disease decreases hepatic cytochrome P-450. [Pg.186]

In addition to the classical symptoms of zinc deficiency mentioned above, the following unusual conditions have been reported liver and spleen enlargement, abnormal dark adaptation and abnormalities of taste. Several laboratory procedures for diagnosing zinc deficiency are available. Measurement of zinc levels in plasma is useful in certain cases. Levels of zinc in the red cells and hair may be used for assessment of body zinc status. More accurate and useful parameters are neutrophil zinc determination and quantitative assay of alkaline phosphatase activity in neutrophils. Determination of zinc in 24 h urine may help diagnose deficiency if sickle cell disease, chronic renal disease and liver cirrhosis are ruled out. A metabolic balance study may clearly distinguish zinc-deficient subjects. [Pg.765]

Salusky IB, Foley J, Nelson P, et al. 1991. Aluminum accumulation during treatment with aluminum hydroxide and dialysis in children and young adults with chronic renal disease. N Engl J Med 324 527-531. [Pg.348]

This chapter does not intend to thoroughly review and compile all studies published so far, but to discuss novel aspects in the search for novel markers related to CVD, risk, and progression markers, in and out of the renal disease context. Note that separate consideration is given to these two different scenarios CV risk in the healthy population and in the chronic renal disease patients as explained in the following sections. [Pg.281]


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See also in sourсe #XX -- [ Pg.305 ]




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Renal disease

Renal disease chronic parenchymal

Uremia Chronic renal disease

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