Glucosuria

Glucosuria Occurs When the Renal Threshold for Glucose Is Exceeded... 

Renal Effects. The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, and few or no nuclear inclusion bodies, reduction in glomerular filtration rate, and azotemia. These effects are irreversible. The acute form is reported in lead-intoxicated children, whose primary exposure is via the oral route, and sometimes in lead workers. The chronic form is reported mainly in lead workers, whose primary exposure is via inhalation. Animal studies provide evidence of nephropathy similar to that which occurs in humans, particularly the acute form (see Section 2.2.3.2). 

The proteinuria and aminoaciduria, and acidosis and glucosuria where they occur, are probably caused by reversible inhibition of some functions of the renal tubule. There would appear to be no structural damage to the kidney. However, 2 children developed nephrolithiasis while being treated with a low-lactose diet (B7, C5), The time course of events, when galactose is withdrawn from and returned to the diet, suggests that some metabolite of galactose accumulates in the cells of the renal tubules and has an inhibitory effect on the reabsorption of a number of substances. 

Laboratory procedures specific to galactosemia are dealt with below, but a number of other tests are also of value. Liver function tests, though sometimes helpful, are not always informative (see above, Section 2.2). Protein is usually present in the urine in untreated cases, but this occurs in other diseases. Aminoaciduria is a very common finding in galactosemia, though Holzel (H3) states it is absent in some older children with a mild form of galactosemia aminoaciduria occurs in other diseases and is frequently accompanied by proteinuria and glucosuria. 

In those patients who survive more than a few weeks, the effects of renal tubular dysfunction become more severe. Acidosis and hypo-phosphatemic rickets are prominent features. The urine is alkaline and gives a strong Rothera reaction. However, the ability to concentrate the urine is never lost and there is neither polydipsia nor polyuria. Aminoaciduria, hydroxyphenyluria, glucosuria, fructosuria, and proteinuria continue. The liver remains large and cirrhotic. Death finally occurs in liver failure, sometimes after several years. There is evidence that some children recover with no residual signs other than a large firm liver. 

Glucosuria (which may be indicative of proximal tubular damage if the serum glucose concentration is within the normal physiological range)... 

Overdosage can occur from topically applied clobetasol propionate absorbed in sufficient amounts to produce systemic effects producing reversible adrenal suppression, manifestations of Cushi ng s syndrome, hyperglycemia, and glucosuria in some patients. 

Serious reactions of long-term therapy (greaterthan 2 weeks) and addition of occlusive dressings are reversible hypothalamic-pituitary-adrenal (HPA) axis suppression, manifestations of Cushing s syndrome, hyperglycemia, and glucosuria. 

Cushing s syndrome, hyperglycemia, glucosuria, hypothalamic-pituitary-adrenal axis suppression... 

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. 

Based on the presence of at least three of the following findings generalized aminoaciduria, glucosuria, increased Fepo4j decreased blood bicarbonate concentration. 

Glucosuria in the face of normal plasma glucose may indicate a functional deficit in the proximal tubule that may precede the appearance of actual tubular necrosis or injury (Stonard et al. 1987 Finco 1997 Loeb and Quimby 1999 Newman and Price 1999 Aleo et al. 2002). Glucosuria is normal in gerbils. 

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