Glucose urinary excretion

Urinary excretion patterns of six individuals. Gu = glucose C = creatine ... 

A number of clinical tests are available to detect kidney damage. The clinician examining a patient or the toxicologist monitoring an animal toxicity stndy collects urine and blood samples. Indications of kidney damage (which, of course, for the human patient could be related to many factors other then chemical toxicity) include urinary excretion of excessive amonnts of proteins and glucose, and excessive levels in the blood of unexcreted waste products such as urea and creatine. A number of additional kidney function tests are available to help pin down the location of kidney dysfunction. 

Relative kidney weight was increased on exposure to the individual compounds at their LONEL and, to about the same extent, on combined exposure at the NONEL or the LONEL/3. The other endpoints studied (histopathology, concentrating abihty, urinary excretion of glucose, protein and marker enzymes, and plasma creatinine and urea) were not or only scarcely affected upon combined exposure at the NONEL or LONEL/3. As assessed by the effect on kidney weight, the renal toxicity of the mixtures corresponded to the effect expected on the basis of the additivity assumption (Feron et al. 1995a, Jonker et al. 1996). 

Kumlien J, Chester MA, Lindberg BS, Pizzo P, Zopf D, Lundblad A (1988) Urinary excretion of a glucose containing tetrasaccharide. A parameter for increased degradation of glycogen. Clin Chim Acta 176 39-48... 

Heavy metals stimulate or inhibit a wide variety of enzyme systems (16, 71, 72), sometimes for protracted periods (71, 73). These effects may be so sensitive as to precede overt toxicity as in the case of lead-induced inhibition of 8 ALA dehydrase activity with consequential interference of heme and porphyrin synthesis (15, 16). Urinary excretion of 8 ALA is also a sensitive indicator of lead absorption (74). Another erythrocytic enzyme, glucose-6-phosphatase, when present in abnormally low amounts, may increase susceptibility to lead intoxication (75), and for this reason, screens to detect such affected persons in lead-related injuries have been suggested (76). Biochemical bases for trace element toxicity have been described for the heavy metals (16), selenium (77), fluoride (78), and cobalt (79). Heavy metal metabolic injury, in addition to producing primary toxicity, can adversely alter drug detoxification mechanisms (80, 81), with possible secondary consequences for that portion of the population on medication. 

Fanconi syndrome (metabolic acidosis secondary to malfunction of proximal renal tubules, resulting in urinary excretion of amino acids, glucose, phosphate, bicarbonate, uric acid, and other substances) secondary to longterm valproic acid has been described in an 8-year-old boy with severe developmental disability (1170). In a review of 10 previous reports of Fanconi syndrome secondary to long-term valproic acid therapy the authors found that all occurred at 4-14 years, all had taken valproic acid for 10 months to 10 years, and symptoms were fully reversible within 2-14 months after withdrawal of valproic acid. Most of the patients (9 of 11) were severely disabled, bedridden, or wheelchair-bound. 

Glucose Tolerance. Ingestion of carbohydrates temporarily increases serum glucose levels and, in response, serum insulin levels. Diminished insulin levels of diabetics permit an excessive blood glucose rise, with urinary excretion of glucose. 

A number of xenobiotics - such as polychlorinated biphenyls, DDT, and aminopyrine - increase the urinary excretion and tissue concentrations of ascorbate in rats, and increase the incorporation of label from [ C]glucose into ascorbate. The rate of ascorbate turnover can increase 5- to 10-fold under... 

People with untreated diabetes have high plasma concentrations of free inositol, and high urinary excretion of inositol, associated with relatively low intracellular concentrations of inositol, suggesting that elevated plasma glucose may inhihit the uptake of inositol. There is some evidence that impaired nerve conduction velocity in diahetic neuropathy is associated with low intracellular concentrations of inositol and that inositol supplements improve nerve conduction velocity. However, high intracellular concentrations of inositol also impair nerve conduction velocity, and supplements may have a deleterious effect. 

Glucose is almost completely and actively reabsorbed within the first third of the proximal tubule of the kidney (9). Because of this and the importance of glucose and its urinary excretion in the monitoring of diabetes, much... 

Renal concentrating abiUty is reduced in the elderly adult, so that creatinine clearance may decline by as much as 50% between the third and ninth decades. This decreased clearance is caused more by a decrease in urinary creatinine excretion as a result of decreased lean body mass than by altered renal function. The tubular maximum capacity for glucose is reduced. The plasma urea concentration rises with age, as does the urinary excretion of protein. The serum median IgG and IgM concentrations are reduced in the elderly although serum IgA concentrations in men increase shghtly in the elderly. 

With blindness, the normal stimulation of the hypothalamic-pituitary axis is reduced. Consequently, certain features of hypopituitarism and hypoadrenalism may be observed. In some blind individuals, the normal diurnal variation of cortisol may persist in others it does not. Urinary excretion of 17-ketosteroids and 17-hydroxycorticosteroids is reduced. Plasma sodium and chloride are often low in blind individuals, probably as a result of reduced aldosterone secretion. Plasma glucose may be reduced in blind people, and insuhn tolerance is often less. The excretion of urate is reduced. Renal function may be slightly impaired, as evidenced by slight increases in serum creatinine and urea nitrogen. 

Fever provokes many hormonal responses. Hyperglycemia occurs early and stimulates the secretion of iasuHn, which improves glucose tolerance but insulin secretion does not necessarily reduce the blood glucose concentration because increased secretion of growth hormone and glucagon also occurs. Fever appears to reduce the secretion of thyroxine, as do acute illnesses even without fever. In response to increased corticotropin secretion, the plasma cortisol concentration is increased and its normal diurnal variation may be abolished. The urinary excretion of free cortisol, 17-hydroxycorticosteroids, and 17-ketosteroids is increased. As acute fever subsides, or if it lessens but still persists for a prolonged period, the hormone responses diminish. 

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