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PubMed1981

In vitro effect of penicillins and aminoglycosides on commonly used tests for glycosuria.

The effect of penicillins (ampicillin, carbenicillin, penicillin G, and penicilloic acid) and aminoglycosides (amikacin, gentamicin, streptomycin, and tobramycin) on the accuracy of Clinitest, Diastix, and TesTape determinations of glycosuria was studied. Solutions of each of the drugs were prepared in urine in a range of clinically obtainable drug concentrations. In addition, urine solutions were prepared that contained the same drug concentrations and sufficient glucose to give final concentrations of 0.5, 1, and 2%. All solutions were tested in triplicate using the five-drop Clinitest method, Diastix, and TesTape. Falsely elevated and falsely decreased Clinitest readings were obtained with the penicillins. These readings were influenced by the concentration of the penicillins and of glucose. The aminoglycosides had no effect of Clinitest determinations. Neither drug class interfered with Diastix or TesTape readings. The Clinitest-penicillin interaction is unpredictable. If Clinitest is used as a quantitative test for glycosuria in patients receiving penicillins, the results should be rechecked using a qualitative method such as the glucose oxidase tests, Diastix or TesTape. All three tests can be used to test for glycosuria in patients receiving aminoglycosides.

Adult↗
PubMed1984

In vitro effect of new penicillins and aminoglycosides on tests for glycosuria.

The effect of newer penicillins (azlocillin, mezlocillin, cyclacillin, and piperacillin) a 6 beta-amidinopenicillanic acid derivative (amdinocillin), and newer aminoglycosides (netilmicin and sisomicin) on the accuracy of tests for glycosuria was studied. Solutions of each of the drugs were prepared in urine in a range of clinically obtainable drug concentrations. In addition, urine solutions were prepared that contained the same drug concentrations and 0.5, 1, and 2% glucose. All solutions were tested in triplicate using the five-drop Clinitest method and two glucose oxidase methods (Diastix and Tes-Tape). Falsely elevated Clinitest readings of approximately 0.25% were obtained with the penicillins. These readings were influenced by the concentration of the penicillins and of glucose. Neither amdinocillin nor the aminoglycosides had an effect on Clinitest determinations. None of the drugs interfered with Diastix or Tes-Tape readings. Because the Clinitest-penicillin interaction is unpredictable, Clinitest results should be rechecked using one of the qualitative glucose oxidase tests when Clinitest is used as a quantitative test for glycosuria in patients receiving penicillins. All three tests studied can be used to test for glycosuria in patients receiving amdinocillin or one of the aminoglycosides.

Aminoglycosides↗
PubMed1992

Hypercalciuria in children with renal glycosuria: evidence of dual renal tubular reabsorptive defects.

During the past 5 years, we have identified idiopathic hypercalciuria in five of seven patients referred for evaluation of renal glycosuria between 1985 and 1991. The children, all boys, ranged in age from 6 to 12 years. Endocrine function was normal, and none of the patients had hyperparathyroidism, hypercalcemia, renal tubular acidosis, or other secondary causes of hypercalciuria. The calcium/creatinine ratio in a fasting urine specimen was elevated in all five children who had hypercalciuria, with a mean value (+/- SD) of 0.34 +/- 0.06 (normal, < 0.2). In one child who had renal colic with spontaneous passage of gravel-like material, the idiopathic hypercalciuria persisted after 1 week on a diet containing 2000 mg of sodium and 300 mg of calcium. On the basis of studies that examined the site along the nephron responsible for hypercalciuria in rats with streptozocin-induced diabetes, we speculate that in children with renal glycosuria, there is defective reabsorption of glucose and calcium in the straight portion of the proximal tubule or in the collecting duct. It is likely that a similar mechanism accounts for the idiopathic hypercalciuria in children with diabetes mellitus.

Absorption↗
PubMed1989

Natural history of incidental hyperglycemia and glycosuria of childhood.

We prospectively followed 29 children and adolescents over a 1- to 8-year period who were referred for evaluation of hyperglycemia (in the absence of diabetes) or glycosuria found on routine screening or during acute illness. On initial examination, four subjects had islet cell autoantibodies, 4 of 22 had an abnormal intravenous glucose tolerance test result, 6 of 22 had low first-phase insulin release on intravenous glucose tolerance testing, and 10 of 20 had impaired glucose tolerance on oral glucose tolerance testing. On follow-up, insulin-dependent diabetes had developed in two of the four subjects with islet cell autoantibodies. The other two subjects with islet cell antibodies have had persistently abnormal glucose tolerance on both oral and intravenous glucose tolerance testing and have low first-phase insulin responses. Diabetes has developed in none of 25 subjects without islet cell antibodies, although two have persistently abnormal glucose tolerance or insulinopenia. All five subjects with islet cell antibodies or human leukocyte antigen DR3/DR4 with initial impaired glucose tolerance have either acquired diabetes or have abnormal glucose tolerance. In contrast, only one of five subjects with initial impaired glucose tolerance but lacking these markers has persistent glucose intolerance. We conclude that in the absence of islet cell antibodies or human leukocyte antigen DR3/DR4 heterozygosity, incidental hyperglycemia or glycosuria is unlikely to be associated with progression or diabetes.

Adolescent↗
PubMed1976

Micropuncture studies of glucose transport in the dog: mechanism of renal glycosuria.

Clearance and micropuncture studies were performed in 23 dogs without glucose loading to examine the tubule mechanism of renal glycosuria. Studies were carried out in three groups of animals before and after 10% extracellular volume expansion, and administration of maleic acid in low dose at 150 mumol/kg and in high dose at 300 mumol/kg. Specific hexokinase methods were used for the determination of glucose in tubule fluid and urine. Under control conditios, glucose reabsorption occurred predominantly in the proximal tubule. In all three groups, proximal tubule reabsorption of both sodium and glucose was inhibited in the second phase, showing a good correlation between the two. In contrast, fractional urinary glucose excretion remained unchanged after volume expansion and low-dose maleic acid, indicating reabsorption of virtually all the increased glucose load at a further "distal" site. On the other hand, significant glycosuria developed after high-dose maleic acid that was a result of reduced glucose reabsorption in the distal nephron, in addition to the proximal effect. It was concluded that distal glucose transport plays a significant role in regulating urinary glucose excretion and maintains renal thershold for glucose,

Aminohippuric Acids↗
PubMedDate not supplied

The prevalence of anorexia nervosa, bulimia, and induced glycosuria in IDDM females.

Questionnaires were sent to 550 female patients aged 13 to 45, with insulin-dependent diabetes to determine the prevalence of eating disorders in this population. Seventy percent of the questionnaires were returned and analyzed. One percent of respondents met criteria for lifetime prevalence of anorexia nervosa, 16.2% for lifetime prevalence of bulimia, and 4.9% for induced glycosuria. Contrary to previous studies, the prevalence of bulimia and anorexia was within the range identified in the general population, although at the upper end of the range. The medical risks incurred by women with diabetes who have eating disorders, however, are substantially greater and warrant attention. The incidence of induced glycosuria is a significant problem for diabetes educators and health care providers working with women who have discovered a dangerous but effective way to lose weight.

Adolescent↗
PubMed1989

[Studies of trichloroethylene-induced glycosuria: blood glucose and renal glucose reabsorption in rats exposed to trichloroethylene].

In our previous experiments, a remarkable increase in urinary excretion of glucose was found in rats exposed to 821 ppm trichloroethylene for 12 wk. This was not accompanied with proteinuria, aminoaciduria, phosphaturia and definite histological changes in renal tubular structure. In order to ascertain the mechanism of the increase in urinary glucose excretion, blood glucose level and renal glucose reabsorption were studied in 10 male rats exposed to 783 ppm trichloroethylene for more than 3 wk. Another 10 male rats were studied as control. The following results were obtained: 1. Urine glucose of the trichloroethylene group increased after exposure for 2 wk. All the rats showed glycosuria (above 250 mg/dl) by the 4th week of exposure. 2. Plasma glucose levels were depressed by trichloroethylene to as low as 77% of that of the control group. Glycohemoglobin was similarly decreased. 3. Intravenous glucose tolerance tests (0.5 g/kg load) revealed that decreasing constant of plasma glucose (K value) was elevated by trichloroethylene, suggesting that induced hyperglycemia in the exposed rats improved more rapidly than in the controls. Trichloroethylene did not modify the secretion of insulin after glucose load, regardless of the depression in plasma insulin level before load. 4. Glucose titration tests revealed that tubular transport maximum for glucose (TmG) was decreased by trichloroethylene to as low as 46% of that of the control group. The ratio of TmG to glomerular filtration rate (the theoretical renal threshold for glucose) was also depressed to as low as 55% of that of the control group. The foregoing results indicate that trichloroethylene-induced glycosuria is attributable to deteriorated tubular reabsorption of glucose, and not to hyperglycemia. However, the mechanism for the selective disturbance of renal reabsorption of glucose is yet unknown.

Animals↗
PubMedDate not supplied

Discrepancies between glycosuria and home estimates of blood glucose in insulin-treated diabetes mellitus.

Glycosuria can be a misleading indicator of blood or plasma glucose levels. Thus glycosuria may be present when blood glucose levels are within the normal fasting or postprandial range, and it may be absent when the blood glucose is distinctly above normal. In such patients the blood glucose must be measured, preferably by the patient, as a guide to insulin and other therapy. However, urine glucose tests are valid indicators in a minority of patients and are essential in all patients for the detection of acetone.

Blood Glucose↗
PubMedDate not supplied

Glycosylated hemoglobin in diabetes mellitus: correlations with fasting plasma glucose, serum lipids, and glycosuria.

The levels of glycosylated hemoglobin (GlHb), fasting plasma glucose (FPG), urine glucose, serum triglycerides, cholesterol, and HDL-cholesterol were monitored in several hundred patients attending an adult diabetic clinic. Thirty-five percent of the patients were being treated with insulin, 30% with diet alone, and 20% with sulfonylurea. Therapy was changed during the study in the remaining 15%. The levels of GlHb and FPG were significantly lower in the patients treated with diet alone than in the other groups. The overall coefficient of correlation (r) between FPG and GlHb was 0.64, with the highest r (0.70) for the diet group and the lowest r (0.55) for the insulin group. A follow-up study showed that in about 50% of the patients GlHb and FPG levels changed in different directions from one visit to the next. The absence of glycosuria was noted in two-thirds of the patients, while in 78% of the patients GlHb values were above the normal range. A weak but positive correlation was found between GlHb and serum triglycerides and cholesterol. There was no significant correlation between GlHb and HDL-cholesterol. The HDL-cholesterol levels were significantly lower in male than in female diabetic subjects, but no significant difference was found between the diabetic and nondiabetic subjects of the same sex. The results of this study suggest that (1) although there is a positive correlation between GlHb and FPG, the two tests cannot be used interchangeably in the evaluation of diabetic control; and (2) in the majority of the patients the absence of glycosuria tends to create the false assurance of satisfactory blood glucose control.

Blood Glucose↗
PubMed2000

[Acute interstitial nephritis. A cause of inflammatory renal glycosuria].

The discovery of glycosuria with normal glycemia is generally interpreted as a consequence of a congenital tubular defect. Nevertheless it may be also the result of an acute interstitial nephritis. This conclusion is supported by the clinical and biochemical picture observed in two children, presenting with apparently unexplained fever and significant increase of inflammatory blood indices, in whom euglycemic glycosuria represented the critical finding for diagnosis of acute interstitial nephritis.

Acute Disease↗
PubMed1990

[A study of proteinuria. (12) The incidence of the patients with proteinuria, microscopic hematuria and glycosuria in Fukuoka Dental College students in 1987 and 1988].

An investigation was made on the incidence of patients with proteinuria, microscopic hematuria and glycosuria in 757 (in 1987) and in 681 (in 1988) students of Fukuoka Dental College; and the results were as follows. 1) The incidence of patients with proteinuria was 6.3% (48/757) in 1987, and 6.9% (47/681) in 1988. 2) The incidence of patients with microscopic hematuria was 4.0% (30/757) in 1987, and 5.0% (34/681) in 1988. 3) The incidence of patients with glycosuria was 0.5% (4/757) in 1987, and 0.1% (1/681) in 1988. 4) Further medical examinations were made on 33 students in 1987, and 37 students in 1988. a) 27 students in 1987 and 34 students in 1988 were diagnosed as normal respectively. b) In three cases, clinical diagnoses could not be established without long-term observation and two cases were diagnosed as urinary tract infection and a case was diagnosed as possible chronic glomerulonephritis in 1987. c) In 1988, a case was diagnosed as urinary tract infection, a case was urethritis and a case should be needed a longterm observation.

Adult↗
PubMed1987

Glucose tolerance and glycosuria in Ethiopian porphyria cutanea tarda patients.

Oral glucose tolerance test (OGTT) was performed in 50 Ethiopians with proven porphyria cutanea tarda (PCT) in 30 of whom urine sugar was also checked. The result of the OGTT, interpreted according to WHO criteria, showed that 35 (70%) patients had normal OGTT, 14 (28%) impaired glucose tolerance (IGT) and 1 diabetes mellitus. Seven patients with IGT, the diabetic and one with normal OGTT had glycosuria of variable degree during the OGTT; none had fasting glycosuria. The patient with diabetes and one other with IGT later on developed mild but nonspecific symptoms. In addition, their blood glucose deteriorated further and required the administration of oral agents to control it. The study clearly indicates the association of diabetes with PCT. Since diabetes mellitus may remain asymptomatic in some of the PCT patients, an early diagnosis of the former is likely to be missed unless looked for.

Adult↗
PubMed1978

[Renal glycosuria with loss of phosphate (author's transl)].

Three of six members of one family have a renal glycosuria of variable degree. In addition to this they have a mild loss of phosphate under normal conditions. In one patient the phosphate-loss becomes very high after a loading dose. After describing the different data the mechanism of renal glucose transport and its relationship to phosphate transport as well as the genetic of renal glucosuria are discussed. The combination of renal glycosuria and renal loss of phosphate is very rare. The difference in regard to gluco-phosphaturia is mentioned.

Adult↗
PubMed1983

Is renal glycosuria a benign condition?

HLA typing and a range of autoantibodies were evaluated in five families affected with type A renal glycosuria. HLA typing demonstrates that this inherited disease is controlled by an autosomal dominant gene located on chromosome six in close genetic linkage with the HLA complex. All affected family members have significant titres of autoantibodies to nuclear antigens, native DNA, smooth muscle, mitochondria, liver antigens, thyroglobulin, thyroid microsomes and renal tubule brush border with variable association. This suggests that renal glycosuria is a complex HLA-linked disease with increased susceptibility to multiple autoantibody production and this urges caution with respect to its classical definition as a benign condition.

Adolescent↗
PubMed1983

[Renal glycosuria: dominant or recessive autosome anomaly? Mode of hereditary transmission based on the analysis of a 3-generation family tree].

Assessment of the pedigree of 7 persons in 3 generations showed that interpretation of the transmission modality of renal glycosuria may be influenced by the diagnostic criteria employed. Analysis of renal glucose curves and evaluation of glycosuria after an oral glucose tolerance test made it clear that albeit slight detects could be detected in family members who would be regarded as healthy according to the criteria of Marble. Distribution of the character pointed to dominant transmission, as opposed to the recessive autosomal transmission favoured in the literature. Variations in the clinical gravity of the tubular defect may be ascribable to a difference in the expressiveness of the abnormal gene or to genetic heterogeneity. Persons homozygous and heterozygous for the gene were present in the pedigree concerned.

Adolescent↗
PubMed1984

Renal glycosuria in patients with the nephrotic syndrome.

Transient or persistent renal glycosuria may occur in patients with the nephrotic syndrome. In an attempt to elucidate its mechanism, glucose titration experiments were performed in 20 nephrotic patients. The type A titration curve was found in one and type B in four patients with severe organic changes and low glomerular filtration rate. The remaining subjects displayed a particular type of curve (type C) characterized by a low point of splay but an otherwise almost physiological tracing. In type B and C patients the maximal rate of reabsorption per ml glomerular filtrate (TmG/GFR) was significantly increased and correlated inversely with the filtration fraction. In these patients the point of splay correlated with the glomerular filtration rate and the sodium clearance, but not with the plasma albumin concentration or the rate of proteinuria. These observations suggest that type A was due to diffuse tubular atrophy, and type B to increased nephron heterogeneity resulting from chronic organic changes. Type C was presumably caused by a potentially reversible alteration of the late proximal or distal glucose transport related to the nephrotic syndrome itself.

Adolescent↗
PubMed1998

Aminoaciduria and glycosuria following severe childhood lead poisoning.

To determine the incidence of renal functional abnormalities after lead poisoning, we evaluated the parameters of renal tubular function in 134 children and young adults, 8-13 years after chelation therapy for severe lead poisoning. There was no evidence of hypertension or reduced kidney function as assessed by serum creatinine (Cr) concentrations. Urinary alpha-amino nitrogen (Uaan) concentrations were significantly increased compared with 19 healthy age-matched controls. Ninety-four children (70%) had aminoaciduria (Uaan/Cr >0.23). Urinary glucose excretion was also significantly higher than that of 2 historical controls. Thirty-two children (24%) had glycosuria (>125 mg/24 h). Fractional excretion of phosphate was normal in all children. We conclude that a partial Fanconi syndrome can persist up to 13 years after childhood lead poisoning.

Adolescent↗
PubMed1976

Renal glycosuria due to gentamicin in rabbits.

Gentamicin sulfate was given to rabbits for four weeks in two dosage regimens, either 4 or 8 mg/kg subcutaneously twice a day. Two of the seven animals in each group regained nearly normal renal function after a transient rise in the level of serum creatinine, but the remainder developed severe renal failure leading to the death of all but one of these rabbits. None of the animals showed significant hyperglycemia, buy glycosuria appeared in all and was significantly correlated with the extent of renal damage. These findings demonstrate gentamicin-induced derangement of proximal tubular function and thus amplify the previously demonstrated histologic changes due to the drug. When the drug was administered twice daily, there was marked nephrotoxicity in rabbits given dosages of gentamicin only slightly higher than those employed clinically.

Acute Kidney Injury↗