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Kidney Glucose reabsorption

The embryonic and newborn animals, however, do not spill glucose into the urine, and bladder samples taken following glucose injection indicate that the sugar is completely reabsorbed. Segal et al (85) report that a rudimentary transport system is present in the newborn, as indicated by a decrease in accumulation in the presence of phloridzin. Thus, it seems possible that some more primitive mechanism for glucose reabsorption may operate in the embryonic kidney. [Pg.293]

Proximal tubular function is immature, and bicarbonate and glucose reabsorption is reduced. This leads to a low serum bicarbonate concentration. Glycosuria and aminoaciduria may be found in the normal neonate. A baby s ability to concentrate urine is poor. A urine osmolality of 600 mmol/kg is the maximum that can be produced. In the neonatal period, the kidney s ability to excrete water and electrolytes is limited. Thus, great care must be taken in the provision of intravenous fluids. [Pg.64]

Sodium SGLTl -dependent unidirectionai transporter Small intestine and kidney Active uptake of glucose from lumen of intestine and reabsorption of glucose in proximal tubule of kidney against a concentration gradient... [Pg.160]

Kanai, Y., et al. The human kidney low affinity Na+/glucose cotransporter SGLT2. Delineation of the major renal reabsorptive mechanism for D-glucose. J. Clin. Invest. 1994, 93, 397-404. [Pg.281]

A second form of diabetes is also recognized diabetes insipidus, which is caused by a deficiency of the pituitary hormone, vasopressin. Vasopressin promotes water reabsorption from the kidney, hence a deficiency also induces S5anptoms of excessive urination and thirst. A key diagnostic difference between the common diabetes meUitus and the rare diabetes insipidus, is the absence of glucose in the urine in the latter case. Until a few decades ago, a popular way to differentiate between the two diseases was to taste the patient s urine to see if it was sweet. [Pg.305]

Phloridzin, a toxic glycoside from the bark of the pear tree, blocks the normal reabsorption of glucose from the kidney tubule, thus causing blood glucose to be almost completely excreted in the urine. In an experiment, rats fed phloridzin... [Pg.559]

Clinical inosituria was first observed in 1858, shortly after myo-inositol had been discovered.107 It is a usual concomitant of diabetes mellitus and an extended debate has been waged as to whether inosituria is associated with the glucosuria (D-glucose excretion), characteristic of this disease or with the polyuria (excessive urine volume). The debate was apparently resolved in favor of the former hypothesis by the results of careful studies by Daughaday and coworkers.108 These workers found that, in both humans and rats, the reabsorption of myo-inositol in the kidney is inhibited by high loads of D-glucose. [Pg.160]

Since the kidneys are the main depot for cadmium, they are of greatest concern for cadmium toxicity. Cadmium interferes with the proximal tubule s reabsorption function. This leads to abnormal actions of uric acid, calcium, and phosphorus. Amino aciduria (amino acids in the urine) and glucosuria (glucose in the urine) result in later stages, proteinuria (protein in the urine) results. When this happens, it is assumed that there is a marked decrease in glomerular filtration. Long-term exposure to cadmium leads to anemia, which may result from cadmium interfering with iron absorption. [Pg.376]

The proximal tubule is the most metabolically active part of the nephron, facilitating the reabsorption of 60% to 80% of the glomerular filtrate volume—including 70% of the filtered load of sodium and chloride, most of the potassium, glucose, bicarbonate, phosphate, and sulfate—and secreting 90% of the hydrogen ion excreted by the kidney (Table 45-1). [Pg.1675]

The answer is c. (Murray, pp 505—626. Scriver, pp 4029—4240. Sack, pp 121-138. Wilson, pp 287-320.) Vasopressin, which is also called antidiuretic hormone, increases the permeability of the collecting ducts and distal convoluted tubules of the kidney and thus allows passage of water. Like the mineralocorticoid aldosterone, vasopressin results in an expansion of blood volume. However, the mode of action of aldosterone is different it causes sodium reabsorption, not water reabsorption. Sodium reabsorption indirectly leads to increased plasma osmolality and thus water retention in the blood. Cortisol is a glucocorticoid that potentiates catabolic metabolism chronically. Epinephrine stimulates catabolic metabolism acutely. Insulin acutely favors anabolic metabolism, in large part by allowing glucose and amino acid transport into cells. [Pg.281]

INULIN Inulin is a polymer of D-fructose molecules (fructofuranose), which are linked to each other in fi-2.1 bonds. There is a terminal glucose molecule. Inulin occurs as a reserve food instead of starch in plants, mainly within the family Asteraceae for example Inula helenium L., Asteraceae. In the form of a 10% aqueous solution inulin is used in tests of kidney function (like mannitol). Inulin is not absorbed or metabolised. Since there is no reabsorption in the tubules, the rate of excretion is a measure of the function of the glomerulus (inulin clearance). [Pg.70]

To date, several small molecule biomarkers of renal toxicity have been described in the literature. Urine composition is considered to reflect kidney function and pathology. Thus, in the presence of proximal tubule damage, the relative concentrations of a number of metabolites (glucose, lactate, alanine, lysine, glutamine, glutamate, and valine) are markedly increased due to impaired reabsorption of those metabolites. An increase in the relative concentrations of those metabolites in urine is typically accompanied by a corresponding decrease in plasma levels [50,55],... [Pg.304]

While alcohol abuse may be associated with a variety of electrolyte and acid-base disorders, the role of the kidneys in this process has only recently been fully defined [164]. Renal functional abnormalities have now been related to chronic alcoholism in patients without liver disease and these defects have reverted to normal with abstinence from alcohol abuse. These abnor-mahties include decreases in the maximal reabsorptive abihty and threshold for glucose, a decrease in the threshold for phosphate excretion, and increases in the fractional excretion of P2-microglobulin, uric acid, calcium, magnesium, and amino acids. Defective tubular acidification and impaired renal concentrating ability... [Pg.396]


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See also in sourсe #XX -- [ Pg.545 ]




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