Cases reported "Glycosuria"

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1/56. Longterm treatment of psoriasis using fumaric acid preparations can be associated with severe proximal tubular damage.

    Fumaric acid preparations are used as longterm and effective treatment of psoriasis. Apart from gastrointestinal, dermatological and hematological side-effects, transient renal damage was observed during treatment with fumaric acid. The case of a 38 year old woman who was treated with fumaric acid (420 mg bid) for 5 years before she complained of fatigue and weakness. According to clinical laboratory she had developed severe proximal tubular damage. hypophosphatemia, glycosuria and proteinuria persisted although medication was stopped immediately. ( info)

2/56. diagnosis of diabetes mellitus at the hospital of Venice in 1863.

    In 1674 Thomas Willis reported that the presence of urine 'as sweet as honey' was the pathognomonic sign of diabetes mellitus. In the 19th Century several reactions for the detection of glucose in urine were proposed and glucose measurement became common in the laboratories that were being set up in europe. A case of diabetes mellitus, diagnosed by Namias, the head of the women's Section of the medicine Department of Venice Hospital, was reported in 1863 in the 'Giornale Veneto di Scienze Mediche' which contains clinical and laboratory information. A 34-year-old woman was admitted to the hospital for polydypsia, polyuria, bulimia and fatigue. urine was weighed for 2 months (2-10 kgday(-1)) and the relative density ranged from 1.045 to 1.038. Glucose was measured in the urine using Moore, Trommer and Fehling reagents. A few days after admission a urine sample showed 7.69 parts/100 parts of urine and a blood sample showed 547 mg of glucose/100 g of serum. The assays were carried out in the Clinical Laboratory of Venice Hospital, founded in 1863, directed by Giovanni Bizio, one of the first chemists who graduated at Padua University. In 1863 chemical analyses were commonly carried out in Venice as in the other parts of Habsburg empire. ( info)

3/56. Early development of the renal lesions in infantile cystinosis.

    To identify the early renal lesions in cystinosis, including whether the "swan neck" deformity of the proximal tubule is a congenital or an acquired lesion, we performed renal function tests and kidney biopsies on two cystinotic infants, on one at 5 and 14 months and on the other at 6 and 12 months of age. The "swan neck" deformity appears to be an acquired lesion for two reasons. First, the characteristic thin neck of the proximal tubule was not demonstrated by nephron microdissection or light microscopy until after 6 months of life. Second, electron microscopy revealed that prior to the development of the lesion, the tubular cells in the neck region of the proximal tubule were undergoing degenerative changes. Renal function tests indicated that the manifestations of the fanconi syndrome correlated with the stages of development of the "swan neck" lesion. Minute crystalline spaces having some of the characteristics of lysosomal cystine crystals appeared in the early biopsies only in that portion of the proximal tubule which was undergoing atrophy to form the "swan neck" lesion observed in the later biopsies. These findings provide evidence of at least a temporal relationship between apparent cellular cystine accumulation and the development of the "swan neck" lesion and the fanconi syndrome. ( info)

4/56. Reversible tubular dysfunction that mimicked Fanconi's syndrome in a patient with anorexia nervosa.

    patients with anorexia nervosa exhibit acid-base and electrolyte disturbances. hypophosphatemia is commonly found in these patients during nutritional recovery. However, marked, possibly, life-threatening hypophosphatemia associated with proximal tubular dysfunction has not been previously described. We report a case of anorexia nervosa complicated by a nonacidotic proximal tubulopathy, which was manifested by renal glycosuria, as well as inappropriate phosphaturia and uricosuria resulting in hypophosphatemia and hypouricemia. ( info)

5/56. glycogen synthase deficiency (glycogen storage disease type 0) presenting with hyperglycemia and glucosuria: report of three new mutations.

    Although glycogen storage disease type 0 (GSD0) is included in the differential diagnosis of ketotic hypoglycemia, it usually is not considered in the evaluation of glucosuria or hyperglycemia. We describe two children with GSD0, confirmed by mutation analysis, who had glucosuria and hyperglycemia. Because of the variable presentation of this disorder and previous dependence on liver biopsy to confirm diagnosis, it is likely that GSD0 is underdiagnosed. ( info)

6/56. Renal tubular dysfunction in a patient with beta-thalassemia minor.

    beta-thalassemia minor is a hemoglobinopathy which has been known as a symptomless carrier state. Although there are many causes leading to renal tubular dysfunction, beta-thalassemia minor has not been reported among them in reviewing the literature. In a 20-year-old male patient referred to us because of glucosuria detected with dipstick, there was also anemia (hemoglobin, 11.5 g/dl; mean cell volume, 60 fl; and mean cell hemoglobin concentration, 19.5 pg). The 24-hour urinary glucose excretion rate was 5 g and, additionally, he had tubular proteinuria (albumin/beta(2)-microglobulin ratio in urine was 17.32). Based upon the detailed evaluation for both asymptomatic urinary abnormality and anemia, he was diagnosed as having renal tubular dysfunction and beta-thalassemia minor (hemoglobin a(1)was 91%, and hemoglobin a(2)was 9%). In conclusion, further reports are needed to reveal whether there is an association between these two distinct disorders. ( info)

7/56. Tenofovir-related nephrotoxicity in human immunodeficiency virus-infected patients: three cases of renal failure, fanconi syndrome, and nephrogenic diabetes insipidus.

    We report 3 cases of renal toxicity associated with use of the antiviral agent tenofovir. Renal failure, proximal tubular dysfunction, and nephrogenic diabetes insipidus were observed, and, in 2 cases, renal biopsy revealed severe tubular necrosis with characteristic nuclear changes. patients receiving tenofovir must be monitored closely for early signs of tubulopathy (glycosuria, acidosis, mild increase in the plasma creatinine level, and proteinuria). ( info)

8/56. urine glucose testing: reliable backup for whole blood glucose monitoring.

    urine glucose testing has been deemed by some to be nonessential in the management of diabetes mellitus since the technique and equipment for self-monitoring of blood glucose has become available. However, most physicians have experienced pitfalls in the management of diabetes mellitus when insulin dosage is adjusted daily based solely on the patient's monitoring of blood glucose. There have also been recent reports suggesting the use of urine glucose testing as a reliable and a reasonable alternative to monitoring of blood glucose in the management of diabetic subjects, including those using insulin as the mode of therapy. In this report, we describe a patient in whom diabetic ketoacidosis occurred during hospitalization as a result of inadequate insulin administration due to inaccurate capillary blood glucose test results. Furthermore, urine glucose and ketone values obtained simultaneously had been disregarded. If insulin therapy had been adjusted according to urine glucose results rather than blood glucose readings, diabetic ketoacidosis could have been averted in this patient. urine glucose testing may provide a reliable backup for suspect whole blood glucose values and may prevent catastrophic events requiring expensive hospitalization. This report also delineates several potential procedural problems that exist in the technique of whole blood glucose monitoring and provides recommendations to overcome these deficiencies. ( info)

9/56. Latent autoimmune diabetes mellitus in children (LADC) with autoimmune thyroiditis and celiac disease.

    Latent autoimmune diabetes mellitus in adults (LADA) is characterized by clinical presentation as type 2 diabetes mellitus after 25 years of age, initial control achieved with oral hypoglycemic agents for at least 6 months, presence of autoantibodies and some immunogenetic features of type 1 diabetes mellitus. An 8.3 year-old girl was referred to our pediatric endocrinology department because of incidental glucosuria. She did not complain of polyuria, polydipsia, or weight loss. Her body mass index (BMI) was at the 80th percentile. fasting glucose was 126 mg/dl, and OGTT glucose level at 120 min was 307 mg/dl. Although c-peptide levels were normal, her first phase insulin response (FIR) was lower than the 1st percentile. Anti-insulin antibody (AIA), islet cell antibody (ICA), and anti-glutamic acid decarboxylase (antiGAD) were negative. According to the clinical and laboratory findings, she was diagnosed as having type 2 diabetes mellitus. She was started with oral anti-diabetic treatment for a period of 1 year. insulin had to be initiated for worsening of HbA1c levels. In the fourth year of follow-up, she was admitted to our hospital with diabetic ketoacidosis although she was on an intensive insulin regimen. At this time, c-peptide levels were low, antiGAD and AIA were positive with HLA DR3/DQ2 haplotype. In addition, her thyroid peroxidase antibody and endomysium antibody were found to be high at follow-up. Small intestinal biopsy revealed celiac disease. This patient may represent the first case of latent autoimmune diabetes mellitus in children (LADC) with autoimmune thyroiditis and celiac disease. ( info)

10/56. Deletion of exon 8 causes glycosylasparaginase deficiency in an African American aspartylglucosaminuria (AGU) patient.

    We have indentified a GT-to-TT transversion at the splice donor site of intron 8 in the glycosylasparaginase gene from an African American aspartylglucosaminuria (AGU) patient. This mutation causes abnormal splicing of glycosylasparaginase pre-mRNA by joining exon 7 to 9 and excluding 134 bp exon 8. The effect of the mutation is compounded by a frame shift that occurs after the deletion site resulting in premature translational termination. The truncated AGU protein was neither catalytically active nor processed into mature alpha and beta subunits. Both this and a previously characterized Finnish AGU mutation appear to affect folding of the single-chain precursor of glycosylasparaginase and thereby prevent transport of the enzyme to lysosomes. ( info)
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