Cases reported "Glycosuria, Renal"

Filter by keywords:

Retrieving documents. Please wait...

11/16. Metabolic studies and glucagon gel filtration pattern before and after surgery in a case of glucagonoma syndrome.

    A case of glucagonoma syndrome with necrolytic migratory erythema, glossitis, anemia, hyperglucagonemia and a malignant, pancreatic A-cell tumour in a 68-year-old male is described. Gel filtration of the highly elevated circulating glucagon immunoreactivity (2200 pg/ml) demonstrated 60% pancreatic glucagon and 30% "proglucagon". Metabolic studies before operation demonstrated suppression of the total plasma glucagon concentration on oral glucose tolerance test, unchanged total plasma glucagon concentration during intravenous glucose tolerance test and insulin-induced hypoglycemia. Administration of arginine was followed by a rise in both the pancreatic glucagon and the "proglucagon", whereas alanine increased only the pancreatic glucagon. The plasma somatostatin level was immeasurable preoperatively. somatostatin infusion completely suppressed the release of the pancreatic glucagon but did not significantly affect the "proglucagon". After removal of the tumour the skin lesions disappeared and the total plasma glucagon values fell to normal levels (120 pg/ml). Also, other abnormal laboratory findings returned to normal, including the preoperatively observed renal glucosuria. ( info)

12/16. Juvenile nephronophthisis diagnosed from glucosuria detected by urine screening at school.

    We describe the case of an 11-year-old girl in whom glucosuria detected by urine screening at school was the first clue to the diagnosis of juvenile nephronophthisis (JN). On admission, she showed renal failure with combined proximal and distal tubular defects and progressive deterioration of renal function. JN should be considered in children with glucosuria. ( info)

13/16. Complete absence of tubular glucose reabsorption: a new type of renal glucosuria (type 0).

    Primary renal glucosuria is an inherited defect of tubular glucose reabsorption and usually classified in type A and type B. We now observed a new type in a 15-year-old boy who had a complete absence of tubular glucose reabsorption. His father had a daily glucosuria of 1.1 g/1.73 m2 and his mother of 2.7 g/1.73 m2. Two siblings excreted 0.4 g/1.73 m2 and 0.3 g/1.73 m2 glucose and one sister had no glucosuria. The proband excreted daily 136 to 160 g/1.73 m2 glucose accompanied by normal blood glucose levels between 75-105 mg/dl. The glomerular filtration rate (inulin clearance) was 148-153 ml/min/1.73 m2 and the endogenous glucose clearance was 112-160 ml/min/1.73 m2 when blood glucose levels were 72-82 mg/dl. Thus, glucose clearance was nearly identical to inulin-clearance. After intravenous glucose loading with a blood glucose concentration of 261-342 mg/dl, glucose clearance remained in the same range and tubular glucose reabsorption was virtually absent. There were no disturbances in tubular reabsorption of other substrates. This new type of primary renal glucosuria was not recognized thus far, and we propose to call it type O glucosuria. The family tree revealed consanguinity and most probably the proband is homozygous and both his parents are heterozygous for type O renal glucosuria. ( info)

14/16. hyperoxaluria with hyperglycoluria not due to alanine:glyoxylate aminotransferase defect: a novel type of primary hyperoxaluria.

    Considering the clinical heterogeneity of primary hyperoxaluria type I (PH1) and the fact that in many instances this diagnosis was made without enzymatic and immunohistochemical investigation, other disturbances of oxalate metabolism than those presently known can be expected in PH1. Using a gaschromatographic/mass spectrometric method that allows quantification of these acids, hyperoxaluria and hyperglycoluria was found repeatedly in two unrelated patients. The hyperoxaluria was unresponsive to pyridoxine. There was no nephrocalcinosis or urolithiasis. In the liver biopsy normal AGT activity and normal localization of this enzyme in the peroxisome was found. In one patient abnormal Km and maximal activity and mozaicism of AGT were excluded. hyperoxaluria and hyperglycoluria were also found in other family members, suggesting autosomal dominant transmission. Although the underlying defect leading to hyperoxaluria and hyperglycoluria could not be identified in these patients, it is probable that they represent a separate type of primary hyperoxaluria. ( info)

15/16. hypercalciuria in renal glucosuria.

    Primary renal glucosuria is a benign condition in which serum glucose level is normal. Idiopathic hypercalciuria is defined as increased urinary calcium excretion of more than 4 mg/kg/day in normocalcemic individuals in whom all known causes of hypercalciuria have been excluded. In this paper, we report on a case who has both renal glucosuria and hypercalciuria. ( info)

16/16. Renal glycosuria treated as diabetes mellitus: case report.

    A case of renal glycosuria is reported. A 55 year old female was diagnosed and treated in an upcountry hospital for diabetes mellitus. She developed symptoms of hypoglycaemia while on an oral hypoglycaemic agent, leading to her admission in Mulago Hospital. Persistent glycosuria was noted despite treatment and normal serum glucose. Oral glucose tolerance test and timed urine glucose showed a normal curve but high urine sugar. A diagnosis of renal glycosuria was made, oral hypoglycaemic therapy was stopped, patient improved and was discharged. Though renal glycosuria is a benign condition, mistaken diagnosis for diabetes mellitus puts patients at risk of hypoglycaemia due to treatment. diagnosis of the condition requires physicians' awareness of its existence in our community and the use of Marbles' criteria obviates confusion with diabetes mellitus though it does not absolutely exclude fanconi syndrome. ( info)
<- Previous |

Leave a message about 'Glycosuria, Renal'

We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.