Kidney Renal glucosuria

A term which implies the excretion of glucose (sugar) in the urine while blood glucose remains within the limits of normal concentrations. It is caused by a disorder in kidney (renal) function and is sometimes called renal diabetes. Glucosuria or the excretion of sugar in the urine is often, but not always, associated with diabetes mellitus. However, in diabetes mellitus the blood sugar is elevated far beyond normal concentrations. 

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nephrolithiasis while being treated with a low-lactose diet (B7, C5), The time course of events, when galactose is withdrawn from and returned to the diet, suggests that some metabolite of galactose accumulates in the cells of the renal tubules and has an inhibitory effect on the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. 

Kidneys Dysfunction of the proximal tubule may occur as a late manifestation of Wilson s disease. Epithelial flattening, a loss of the brush-border membrane, mitochondrial anomalies and fatty cellular changes can be observed. These findings are, in turn, responsible for proteinuria with a predominance of hyperaminoaciduria (L. UzMAN et al., 1948). Enhanced calciuria and phosphat-uria may cause osteomalacia as well as hypoparathyroidism. (329, 344) Glucosuria and uricosuria, if present, are without clinical relevance. Due to decreased bicarbonate resorption, tubular acidosis may occur, with a tendency towards osteomalacia as well as the development of nephrocalcinosis and renal stones (in some 15% of cases). (344, 356, 392) The intensity of the copper deposits in the kidneys correlates closely with the cellular changes and functional disorders. The glomerular function is not compromised, with the result that substances normally excreted in the urine are not retained. 

Compound A is nephrotoxic in rats at thresholds estimated at 180 ppm/hour [67]. Renal toxicity is characterized histologically by proximal tubular cell degeneration and necrosis in the corticomedullar region of die kidney and biochemically by proteinuria, glucosuria, and enzymuria (NAG and a-GST) with increased serum creatinine and BUN concentrations occurring with severe toxicity [67-70]. 

Streptozotocin and alloxan are well-known diabetogenic agents which produce hyperglycaemia, glucosuria, increased food and water consumption and depressed growth in rats and mice [426]. Injection of streptozotocin is known to cause a time-related increase in renal cortex levels of metallothionein-bond-ed copper [427-430]. This increase has been suggested to be due to increased absorption [430] resulting in nephropathy associated with chronic diabetes, however, there was no evidence for either an increase in absorption or nephropathy in these animals and the possibility that this accumulation of copper in the kidney was due to a copper conservation role of the kidney was not excluded. 

Disturbed renal function, with proteinuria, glucosuria, and aminoaciduria, has been observed in woricers exposed to cadmium. The proteinuria in chronic cadmium poisoning is of the tubular type and is caused by decreased reabsorption of proteins. " " As mentioned previously, when the kidneys have been damaged by cadmium, the excretion of the metal increases and the kidney concentration of cadmium will diminish considerably. ... 

Many potential agents of chemical warfare have little to no direct injurious effect on the kidney or urinary system, but instead may cause indirect renal injury and/ or urinary dysfunction. Nitrate esters used as explosives can cause profound hypotension with the potential to result in renal ischemia secondary to decreased renal perfusion (Gahagan and Wismer, 2012). Metabolic acidosis, proteinuria, glucosuria, and myoglobinuria were reported in a survey of five human cases of cydonite... 

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