Renal disease, and metabolism

Clearly, the determination of such compounds is crucial for diagnosis and monitoring of renal disease and metabolic disorders. The concentration of oxypurines in blood serum is among the most important parameters in biochemistry and clinical chemistry. Determination of uric acid is performed by enzymatic methods or colori-metrically by reduction of phosphotungstate. [Pg.1682]

Disorders of lipoprotein metabolism involve perturbations which cause elevation of triglycerides and/or cholesterol, reduction of HDL-C, or alteration of properties of lipoproteins, such as their size or composition. These perturbations can be genetic (primary) or occur as a result of other diseases, conditions, or drugs (secondary). Some of the most important secondary disorders include hypothyroidism, diabetes mellitus, renal disease, and alcohol use. Hypothyroidism causes elevated LDL-C levels due primarily to downregulation of the LDL receptor. Insulin-resistance and type 2 diabetes mellitus result in impaired capacity to catabolize chylomicrons and VLDL, as well as excess hepatic triglyceride and VLDL production. Chronic kidney disease, including but not limited to end-stage... [Pg.697]

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. [Pg.638]

Modified amino acid solutions are designed for patients with altered protein requirements associated with hepatic encephalopathy, renal failure, and metabolic stress or trauma. However, these solutions are expensive and their role in disease-specific PN regimens is controversial. [Pg.685]

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]

Depression and Metabolic Syndrome. Abnormal serum albumin levels and lipid profiles have both been observed in patients with major depression, as well as cardiovascular disease, diabetes mellitus, and end-stage renal disease. Depressive symptoms are very common in patients with these chronic illnesses. Recent clinical data have shown that cardiovascular disease, diabetes mellitus, end-stage renal disease, and obesity are all related to metabolic syndromes [68-74], and especially insulin resistance [75, 76]. However, the data examining major depression without physical illness and insulin resistance are still scarce. In the future, the biological relationship between depression and physical illness needs to be more fully explored. [Pg.88]

Absorption of the synthetic steroids given orally is rapid. The tY in plasma of most is 1-3 h but the maximum biological effect occurs after 2-8 h. Administration is usually 2 or 3 times a day. They are metabolised principally in the liver (some undergoing hepatic first-pass metabolism, see above) and some are excreted unchanged by the kidney. The t/ is prolonged in hepatic and renal disease and is shortened by enzyme induction to an extent that can be clinically important. [Pg.667]

Lock EA. Renal drug-metabolizing enzymes in experimental animals and humans. In Mechanisms of injury in renal disease and toxicity. Goldstein R S (editor). CRC Press Inc, Boca Raton, Florida 1994 p. 173-206. [Pg.317]

Zinc is an essential trace element and is commonly ingested as a nutritional supplement. Divalent zinc is one of the most important of the micronutrients. More than 100 enzymes are zinc dependent for example, carboxypeptidase, carbonic anhydrase (which is responsible for the exchange of carbonic acid in the blood and the exhalation of carbon dioxide), and the alcohol dehydrogenase (which metabolizes alcohol). Deficiency of zinc, especially in newborns, results in impaired growth, loss of hair, skin eruptions, and often impaired or delayed sexual maturation. Many medical problems are also associated with zinc deficiencies (e.g., ulcerative colitis, chronic renal disease, and anemia). [Pg.2870]

Kraut and Kurtz, Metabolic Acidosis of CKD Klahr and Morrissey, Progression of Chronic Renal Disease Bailey, Metabolic Acidosis. ... [Pg.186]

Hyperkalemia may occur in renal disease and adrenal insufficiency owing to impairment of normal secretory mechanisms. Metabolic acidosis, in particular diabetic acidosis, and catabolism of cellular protein in starvation or fever cause K+ release from cells. Treatment consists of correction of the acidosis and promotion of cellular uptake of K+ by administration of insulin, which enhances glucose intake. In severe cases, ion exchange resins given orally bind K+ in intestinal secretions. [Pg.934]

Although the data are not conclusive, hyperlipidemia has been associated as a susceptibility factor for CKD in both animal and human studies. The use of lipid-lowering agents in some animal models has been found to decrease the extent of glomerular injury when both underlying renal disease and hyperlipidemia are present. Therefore the correction of lipid abnormalities in patients with CKD was proposed to have a beneficial effect on the rate of progression of the disease. CKD with or without nephrotic syndrome is frequently accompanied by abnormalities in fipoprotem metabolism. The prevalence of hyperlipidemia appears to increase as kidney function declines and with the presence of the nephrotic syndrome. ... [Pg.803]

Gibson TP. Renal disease and drug metabolism an overview. Am J Kidney Dis 1986 8 7-17. [Pg.665]

Diabetes mellitus is a systemic disorder of metabolism tiiat stems from a deficiency of insulin, the hormone needed to stimulate die influx of fatty acids, amino acids, and glucose into cells. In recent years, the incidence of diabetes has reached epidemic proportions and is associated with long-term damage, dysfunction, and failure of a number of organ systems. In addition to being a leading cause of heart attacks, strokes, end-stage renal disease, and blindness, diabetes also has detrimental effects on die peripheral vasculature and die peripheral nervous system. ... [Pg.206]

High serum levels of chloride (hyperchloremia), that is levels of 109 mEq/L (109 mmol/L) or higher, can result from dehydration and other conditions, including renal disease and excess parathyroid hormone (PTH). Hyperchloremia also results from metabolic acidosis owing to the loss of base and respiratory alkalosis that occurs with hyperventilation. [Pg.70]

The primary conditions that result in decreased renal excretion of acids and a buildup of metabolic acids are renal disease and renal failure. Additionally, renal disease can result in excessive excretion of bicarbonate. The loss of bicarbonate through diarrhea or overuse of laxative, decreased production of bicarbonate, or ingestion of excessive acid such as acidic poisons, iron, or aspirin could cause metabolic acidosis. [Pg.171]

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