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Journal articles on the topic 'Glycosurie'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Brochériou, I., A. Duquesne, L. Garderet, M. C. Verpon, P. Rouvier, J. P. Rougier, P. Aucouturier, J. J. Boffa, P. Callard, and P. Ronco. "Une pseudotumeur inflammatoire rétro-orbitaire révélatrice d’une glycosurie normoglycémique." Néphrologie & Thérapeutique 8, no. 1 (February 2012): 66. http://dx.doi.org/10.1016/j.nephro.2011.07.423.

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2

Neil Dalton, R., Martin J. Wiseman, Charles Turner, and Giancarlo Viberti. "Measurement of urinary para-aminohippuric acid in glycosurie diabetics." Kidney International 34, no. 1 (July 1988): 117–20. http://dx.doi.org/10.1038/ki.1988.153.

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3

RØMCKE, OLAF, and ERLING SKOUGE. "»Zur Frage der zentral bedingten Albuminurie, Glycosurie und Azetonurie»." Acta Medica Scandinavica 77, no. 1-3 (April 24, 2009): 211–23. http://dx.doi.org/10.1111/j.0954-6820.1931.tb15394.x.

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4

ECKERSTRÖM, STEN. "HyperglycÉmie de type transitoire et glycosurie consÉcutives à un infarctus du myocarde." Acta Medica Scandinavica 95, no. 5 (April 24, 2009): 528–38. http://dx.doi.org/10.1111/j.0954-6820.1938.tb16404.x.

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5

Schlienger, J. L. "Dans les coulisses de la chimie clinique : histoire de la glycémie et de la glycosurie." Médecine des Maladies Métaboliques 7, no. 1 (February 2013): 81–85. http://dx.doi.org/10.1016/s1957-2557(13)70496-6.

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6

Carpentier, C., G. Velho, K. Mohammedi, N. Belhatem, B. Duly-Bouhanick, V. Rohmer, P. Rodien, et al. "Abondance de la glycosurie pendant l’hyperglycémie et risque de néphropathie diabétique à long terme dans le diabète de type 1." Annales d'Endocrinologie 78, no. 4 (September 2017): 297. http://dx.doi.org/10.1016/j.ando.2017.07.252.

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7

Falcão, Mário Cícero, Cléa Rodrigues Leone, and José Lauro Araújo Ramos. "Is glycosuria a reliable indicator of adequacy of glucose infusion rate in preterm infants?" Sao Paulo Medical Journal 117, no. 1 (January 7, 1999): 19–24. http://dx.doi.org/10.1590/s1516-31801999000100004.

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CONTEXT: Adequacy of glucose infusion may be monitored via the glycosuria levels, as there is a relationship between glycemia and glycosuria regulated by the renal glucose threshold. In the neonatal period, however, this relationship is not so clear. OBJECTIVE: To evaluate the occurrence of glycosuria in preterm infants submitted to glucose infusion and to verify the relationship between glycosuria and blood glucose level. DESIGN: Accuracy study. SETTING: Neonatal intensive care unit of General Maternity Hospital. PATIENTS: 40 preterm newborns receiving glucose infusion. PROCEDURES: 511 concomitant determinations of glycemia and glycosuria were performed. These 511 pairs were divided into stable and unstable, according to the clinical status of the newborn at the time of data collection, and they were studied in relation to the gestational age, birth weight and glucose infusion rate. RESULTS: The results revealed a greater frequency of glycosuria in gestational age <FONT FACE="Symbol">£</font> 30 weeks, birth weight <1500 g and glucose infusion rate > 6 mg/kg/min. Eight (25.8%) episodes of positive glycosuria occurred in the absence of hyperglycemia, indicating only a moderate concordance between them. CONCLUSION: Glycosuria alone is an unreliable marker of blood glucose concentration and adequacy of glucose infusion rate. It is therefore necessary to monitor blood glucose levels in infants submitted to continuous glucose infusion.

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8

Kaufmann, R. C., F. K. Khosho, and K. S. Amankwah. "Scanning Electron Microscopy of the glomerulus in diabetic BB/S wistar rats." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 730–31. http://dx.doi.org/10.1017/s0424820100127967.

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Renal damage secondary to diabetes seems to be related to the severity and duration of the diabetes. In streptozotocin and alloxan-induced diabetic rats, renal disease is found only in those rats that have glycosuria and then only after the glycosuria has been present for many months. In these animals, the longer they have glycosuria, the more severe the renal damage. In our colony of BB/S Wistar rats, animals that are going. to become frankly diabetic demonstrate clinical diabetes before they begin spilling glucose in their urine. After glycosuria develops, the condition of the animals worsens; yet, the glucose tolerance tests(GTT) remain essentially unchanged. The purpose of this investigation was to study the animals' kidneys to discover if lesions are present at the onset of glycosuria and how severe the lesions are.Rats of our BB/S Wistar strain were used the day they developed glycosuria. Similarly aged non-diabetic animals were used as controls.

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9

Lee, Matthew A., George McMahon, Ville Karhunen, Kaitlin H. Wade, Laura J. Corbin, David A. Hughes, George Davey Smith, Debbie A. Lawlor, Marjo-Riitta Jarvelin, and Nicholas J. Timpson. "Common variation at 16p11.2 is associated with glycosuria in pregnancy: findings from a genome-wide association study in European women." Human Molecular Genetics 29, no. 12 (March 30, 2020): 2098–106. http://dx.doi.org/10.1093/hmg/ddaa054.

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Abstract Glycosuria is a condition where glucose is detected in urine at higher concentrations than normal (i.e. not detectable). Glycosuria at some point during pregnancy has an estimated prevalence of 50% and is associated with adverse outcomes in both mothers and offspring. Little is currently known about the genetic contribution to this trait or the extent to which it overlaps with other seemingly related traits, e.g. diabetes. We performed a genome-wide association study (GWAS) for self-reported glycosuria in pregnant mothers from the Avon Longitudinal Study of Parents and Children (cases/controls = 1249/5140). We identified two loci, one of which (lead SNP = rs13337037; chromosome 16; odds ratio of glycosuria per effect allele: 1.42; 95% CI: 1.30, 1.56; P = 1.97 × 10−13) was then validated using an obstetric measure of glycosuria measured in the same cohort (227/6639). We performed a secondary GWAS in the 1986 Northern Finland Birth Cohort (NFBC1986; 747/2991) using midwife-reported glycosuria and offspring genotype as a proxy for maternal genotype. The combined results revealed evidence for a consistent effect on glycosuria at the chromosome 16 locus. In follow-up analyses, we saw little evidence of shared genetic underpinnings with the exception of urinary albumin-to-creatinine ratio (Rg = 0.64; SE = 0.22; P = 0.0042), a biomarker of kidney disease. In conclusion, we identified a genetic association with self-reported glycosuria during pregnancy, with the lead SNP located 15kB upstream of SLC5A2, a target of antidiabetic drugs. The lack of strong genetic correlation with seemingly related traits such as type 2 diabetes suggests different genetic risk factors exist for glycosuria during pregnancy.

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10

G., V. "Glycosuria as a sign of pregnancy. Seit-z and Jess (Münch, ni. Woch .. 1922, no. 1)." Kazan medical journal 18, no. 2 (September 23, 2021): 108. http://dx.doi.org/10.17816/kazmj79920.

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Glycosuria as a sign of pregnancy. Seit-z and Jess (Mnch, ni. Woch .. 1922, No. 1) found that when administered to pregnant women (at II-VIII months of pregnancy) 100 grm. of grape sugar, half of them get glycosuria.

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11

Onuigbo, Macaulay, and Cynthia Washington. "Glycosuria in Alcoholics." Nephron 87, no. 3 (2001): 287–88. http://dx.doi.org/10.1159/000045930.

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12

Challen, Antoinette. "Glycosuria in childhood." Practical Diabetes International 4, no. 3 (May 1987): 114–15. http://dx.doi.org/10.1002/pdi.1960040306.

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13

MELLON, J. P. "GLYCOSURIA AND PHENYLKETONURIA." Journal of Intellectual Disability Research 7, no. 2 (June 28, 2008): 122–28. http://dx.doi.org/10.1111/j.1365-2788.1963.tb00791.x.

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14

Davies, Melanie, and John Day. "Screening for Non-Insulin-Dependent Diabetes Mellitus (NIDDM): How Often Should it Be Performed?" Journal of Medical Screening 1, no. 2 (April 1994): 78–81. http://dx.doi.org/10.1177/096914139400100202.

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Objectives— To examine whether a screening programme for diabetes repeated after an interval of 30 months is worthwhile both in terms of yield of new cases and continued high response rate. Methods— Self testing for postprandial glycosuria was used as it has been shown to have a good response rate, a good yield of cases of diabetes, and a sensitivity and specificity which compares favourably with more expensive and invasive screening methods. A total of 3231 subjects aged 45–70 years in one practice were screened on two occasions 30 months apart. Eighty seven subjects known to have diabetes were excluded. This number included five new patients who had presented since the initial screen; two of whom had moved into the practice, one who screened positive at the initial screen but failed to attend for the oral glucose tolerance test (OGTT), and two subjects who had screened negative, the first presenting 24 months after screening. Results— At repeat screening the return rate was lower than at the first screening (72·5% v 79·2%, P < 0·0001). Glycosuria was detected in 52 subjects (2·3%), at the repeat screening, similar to that at the initial screen. Attendance for the OGTT after a positive screening test was 93·2%. Only six subjects of the 24 with Glycosuria but normal glucose at initial screen were found to have glycosuria again; repeat OGTTs were all normal. Of the remaining 46 subjects, 10 had non-insulin-dependent diabetes mellitus (NIDDM) and five impaired glucose tolerance (IGT). The number of subjects with diabetes was not significantly different from that at the initial screening (0·44% v 0·72%, P = 0·2). Conclusions— Repeat screening after 30 months has a high response rate, similar rate of detection of glycosuria, and a further yield of 0·44% of newly diagnosed cases of diabetes. A screening programme detecting postprandial glycosuria identifies additional diabetic subjects 30 months after a previous screening programme.

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15

DONATO, LUIGI, and GIOVANNI TURCHETTI. "Renal Glycosuria in Pregnancy." Acta Medica Scandinavica 152, no. 3 (April 24, 2009): 223–30. http://dx.doi.org/10.1111/j.0954-6820.1955.tb03481.x.

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16

Ferrannini, Ele. "Learning From Glycosuria: FIG. 1." Diabetes 60, no. 3 (February 25, 2011): 695–96. http://dx.doi.org/10.2337/db10-1667.

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17

KAYNAR, Kübra, Canan ŞEHİT, Arif Mansur COŞAR, and Gül CEBECİOĞLU HASANÇEBİ. "A Case with Renal Glycosuria." Turkiye Klinikleri Journal of Case Reports 26, no. 4 (2018): 213–15. http://dx.doi.org/10.5336/caserep.2018-61441.

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18

WATSON, WILLIAM J. "Screening for Glycosuria During Pregnancy." Southern Medical Journal 83, no. 2 (February 1990): 156–58. http://dx.doi.org/10.1097/00007611-199002000-00006.

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19

Holst, J. E. "Investigation into the adrenalin-glycosuria." Acta Medica Scandinavica 74, S34 (April 24, 2009): 270–76. http://dx.doi.org/10.1111/j.0954-6820.1930.tb14963.x.

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20

MØLLER, ELSE. "NONDIABETIC GLYCOSURIA IN CHRONIC SCHIZOPHRENIA1." Acta Psychiatrica Scandinavica 24, no. 2 (August 23, 2007): 223–50. http://dx.doi.org/10.1111/j.1600-0447.1949.tb03495.x.

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21

Carel, R. S., D. S. Silverberg, R. Kaminsky, and A. Aviram. "Routine urinalysis (dipstick) findings in mass screening of healthy adults." Clinical Chemistry 33, no. 11 (November 1, 1987): 2106–8. http://dx.doi.org/10.1093/clinchem/33.11.2106.

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Abstract We present results of simple urinalysis examinations (dipstick) in a large (approximately 21,000 people) working population. In about 10% of the screened individuals at least one abnormality was found. In men the most common finding was proteinuria (4.9%). Hematuria was found in 2.6% and glycosuria in 0.6%. The most prevalent finding in women was hematuria (8.1%), followed by proteinuria (3.9%) and glycosuria (0.6%). Only about 1% of the examinees had two or more abnormalities in their urine examinations. These findings attest to the utility and practicability of incorporating urine testing into various screening and clinical examinations.

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22

NIELSEN, A. LEVIN. "On the Mechanism of Glycosuria. I1." Acta Medica Scandinavica 130, no. 3 (April 24, 2009): 219–31. http://dx.doi.org/10.1111/j.0954-6820.1948.tb10060.x.

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23

FABER, KNUD, and A. NORGAARD. "Studies on the Threshold for Glycosuria." Acta Medica Scandinavica 54, no. 1 (April 24, 2009): 289–322. http://dx.doi.org/10.1111/j.0954-6820.1921.tb15181.x.

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24

HOLST, JOHAN. "Glycosuria and diabetes in exophthalmic goitre." Acta Medica Scandinavica 55, no. 1 (April 24, 2009): 302–22. http://dx.doi.org/10.1111/j.0954-6820.1921.tb15214.x.

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25

Rebelo, Joana Chaves, Felisbela Rocha, Susana Gama de Sousa, and Paulo Teixeira. "Renal glycosuria: report of two cases." Jornal Brasileiro de Nefrologia 34, no. 3 (2012): 291–92. http://dx.doi.org/10.5935/0101-2800.20120013.

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26

Nielsen, A. Levin. "ON THE MECHANISM OF GLYCOSURIA. II1)." Acta Medica Scandinavica 131, S213 (April 24, 2009): 273–83. http://dx.doi.org/10.1111/j.0954-6820.1948.tb15137.x.

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27

Milavetz, J. J. "Angiotensin-converting enzyme inhibitors and glycosuria." Archives of Internal Medicine 152, no. 5 (May 1, 1992): 1081–83. http://dx.doi.org/10.1001/archinte.152.5.1081.

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28

Milavetz, James J. "Angiotensin-Converting Enzyme Inhibitors and Glycosuria." Archives of Internal Medicine 152, no. 5 (May 1, 1992): 1081. http://dx.doi.org/10.1001/archinte.1992.00400170151027.

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29

Goto, Masakatsu, W. Patrick Zeller, and R. Morrison Hurley. "Glycosuria and maternal licking in rats." Laboratory Animals 26, no. 4 (October 1, 1992): 295–98. http://dx.doi.org/10.1258/002367792780745751.

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Maternal anogenital licking (MAGL) has been studied to understand the mechanism of maternal behaviour. The present study showed that rats had glycosuria at the concentration of 18-20 mg/dl and glucose was the preference of postpartum rats. MAGL increased on suckling rats separated for 24 h. However, wiping anogenital region attenuated the increase of MAGL. Therefore, glucose preference of postpartum rats may be involved in MAGL.

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30

Peli, A., A. Fruganti, G. Bettini, G. Aste, and A. Boari. "Emphysematous Cystitis in Two Glycosuric Dogs." Veterinary Research Communications 27 (2003): 419–23. http://dx.doi.org/10.1023/b:verc.0000014194.93010.6a.

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31

Gruzdev, V. "Floridzin glycosuria as a sign of pregnancy." Kazan medical journal 20, no. 6 (August 11, 2021): 644. http://dx.doi.org/10.17816/kazmj76805.

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Numerous observations have convinced Klaft'a (Zentr. F. Gyn., 1924, No. 17) that if after intravenous administration of 2 mg. floridzin in a woman does not get glycosuria, then pregnancy with a high probability can be excluded.

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32

HOLST, J. E. "Investigations into Benign Glycosuria and Diabetes Mellitus." Acta Medica Scandinavica 63, no. 1 (April 24, 2009): 47–98. http://dx.doi.org/10.1111/j.0954-6820.1925.tb15344.x.

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33

Limsuwat, Chok, and Sharma S. Prabhakar. "Reversible Renal Glycosuria in Acute Interstitial Nephritis." American Journal of the Medical Sciences 344, no. 3 (September 2012): 245–47. http://dx.doi.org/10.1097/maj.0b013e318254bd71.

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34

Mavrakanas, Thomas A., Constantinos Tomos, Paraskevi Pratsiou, Ioanna Seventekidou, and George Tzouvelekis. "Transient glycosuria during a urinary tract infection." La Presse Médicale 39, no. 1 (January 2010): 145–46. http://dx.doi.org/10.1016/j.lpm.2009.09.002.

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35

Seedorff, H. H. "HEREDITARY RENAL GLYCOSURIA WITH CENTRAL MACULAR DEGENERATION." Acta Ophthalmologica 40, no. 1 (May 27, 2009): 91–95. http://dx.doi.org/10.1111/j.1755-3768.1962.tb02356.x.

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36

Toka, Hakan R., Jun Yang, Chloe A. Zera, Jeremy S. Duffield, Martin R. Pollak, and David B. Mount. "Pregnancy-Associated Polyuria in Familial Renal Glycosuria." American Journal of Kidney Diseases 62, no. 6 (December 2013): 1160–64. http://dx.doi.org/10.1053/j.ajkd.2013.05.018.

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37

Murphy, Mary, and Nancy Risser. "Routine Urine Screening for Glycosuria and Proteinuria." Nurse Practitioner 22, no. 3 (March 1997): 211. http://dx.doi.org/10.1097/00006205-199703000-00024.

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38

Savit, Russ M., and David S. Udis. "“Upside-Down” Contrast-Urine Level in Glycosuria." Journal of Computer Assisted Tomography 11, no. 5 (September 1987): 911–12. http://dx.doi.org/10.1097/00004728-198709000-00036.

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39

Sahu, S., P. K. Jain, N. Mudgal, and G. Singh. "Glycosuria sensing based on nanometric plasmonic polaritons." IOP Conference Series: Materials Science and Engineering 1136, no. 1 (June 1, 2021): 012064. http://dx.doi.org/10.1088/1757-899x/1136/1/012064.

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40

Basso, Paulo José, Lucas Favaretto Tazinafo, Mauro Ferreira Silva, and Maria José Alves Rocha. "An alternative to the use of animals to teach diabetes mellitus." Advances in Physiology Education 38, no. 3 (September 2014): 235–38. http://dx.doi.org/10.1152/advan.00051.2014.

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We developed an alternative approach to teach diabetes mellitus in our practical classes, replacing laboratory animals. We used custom rats made of cloth, which have a ventral zipper that allows stuffing with glass marbles to reach different weights. Three mock rats per group were placed into metabolic cages with real food and water and with test tubes containing artificial urine, simulating a sample collection of 24 h. For each cage, we also provided other test tubes with artificial blood and urine, simulating different levels of hyperglycemia. The artificial “diabetic” urine contained different amounts of anhydrous glucose and acetone to simulate two different levels of glycosuria and ketonuria. The simulated urine of a nondiabetic rat was prepared without the addition of glucose or acetone. An Accu-Chek system is used to analyze glycemia, and glycosuria and ketonuria intensity were analyzed by means of a Urocolor bioassay. In the laboratory classroom, students were told that they would receive three rats to find out which one has type 1 or type 2 diabetes mellitus. To do so, they had to weigh the animals, quantify the water and food ingestion, and analyze the artificial blood and urine for glycemia, glycosuria, and ketonuria. Only at the end of class did we reveal that the urine and blood were artificial. Students were instructed to plot the data in a table, discuss the results within their group, and write an individual report. We have already used this practical class with 300 students, without a single student refusing to participate.

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41

Kim, Kyeong Min, Soon Kil Kwon, and Hye-Young Kim. "A Case of Isolated Glycosuria Mediated by anSLC5A2Gene Mutation and Characterized by Postprandial Heavy Glycosuria Without Salt Wasting." Electrolytes & Blood Pressure 14, no. 2 (2016): 35. http://dx.doi.org/10.5049/ebp.2016.14.2.35.

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42

Lytvyn, Yuliya, Marko Škrtić, Gary K. Yang, Paul M. Yip, Bruce A. Perkins, and David Z. I. Cherney. "Glycosuria-mediated urinary uric acid excretion in patients with uncomplicated type 1 diabetes mellitus." American Journal of Physiology-Renal Physiology 308, no. 2 (January 15, 2015): F77—F83. http://dx.doi.org/10.1152/ajprenal.00555.2014.

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Plasma uric acid (PUA) is associated with metabolic, cardiovascular, and renal abnormalities in patients with type 2 diabetes but is less well understood in type 1 diabetes (T1D). Our aim was to compare PUA levels and fractional uric acid excretion (FEUA) in patients with T1D vs. healthy controls (HC) during euglycemia and hyperglycemia. PUA, FEUA, blood pressure (BP), glomerular filtration rate (GFR-inulin), and effective renal plasma flow (ERPF-paraaminohippurate) were evaluated in patients with T1D ( n = 66) during clamped euglycemia (glucose 4–6 mmol/l) and hyperglycemia (9–11 mmol/l), and in HC ( n = 41) during euglycemia. To separate the effects of hyperglycemia vs. increased glycosuria, parameters were evaluated during clamped euglycemia in a subset of T1D patients before and after sodium glucose cotransporter 2 (SGLT2) inhibition for 8 wk. PUA was lower in T1D vs. HC (228 ± 62 vs. 305 ± 75 μmol/l, P < 0.0001). In T1D, hyperglycemia further decreased PUA (228 ± 62 to 199 ± 65 μmol/l, P < 0.0001), which was accompanied by an increase in FEUA (7.3 ± 3.8 to 11.6 ± 6.7, P < 0.0001). In T1D, PUA levels correlated positively with SBP ( P = 0.029) and negatively with ERPF ( P = 0.031) and GFR ( P = 0.028). After induction of glycosuria with SGLT2 inhibition while maintaining clamped euglycemia, PUA decreased ( P < 0.0001) and FEUA increased ( P < 0.0001). PUA is lower in T1D vs. HC and positively correlates with SBP and negatively with GFR and ERPF in T1D. Glycosuria rather than hyperglycemia increases uricosuria in T1D. Future studies examining the effect of uric acid-lowering therapies should account for the impact of ambient glycemia, which causes an important uricosuric effect.

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43

Carpentier, Charlyne, Séverine Dubois, Kamel Mohammedi, Narimène Belhatem, Béatrice Bouhanick, Vincent Rohmer, Claire Briet, et al. "Glycosuria amount in response to hyperglycaemia and risk for diabetic kidney disease and related events in Type 1 diabetic patients." Nephrology Dialysis Transplantation 34, no. 10 (July 5, 2018): 1731–38. http://dx.doi.org/10.1093/ndt/gfy197.

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Abstract Background Hyperglycaemia impairs tubulo-glomerular feedback. We tested whether variable tubulo-glomerular feedback during hyperglycaemia contributes to renal risk heterogeneity seen in Type 1 diabetes. Methods During the period 1990–92, we studied the tubulo-glomerular feedback in Type 1 diabetic patients at high or low renal risk [21 of 54 with glomerular hyperfiltration and/or microalbuminuria against 11 of 55 with normal glomerular filtration rate (GFR) and urinary albumin despite uncontrolled diabetes]. The GFR, effective renal plasma flow, mean arterial pressure and fractional reabsorptions of glucose, osmols, sodium and lithium were measured sequentially during normo- and hyperglycaemia. All patients were followed up until 2016 for incident proteinuria, estimated GFR <60 mL/min/1.73 m2, doubling of serum creatinine, end-stage renal disease or all-cause death. Results Glycaemia increased from 6.1 ± 1.3 to 15.1 ± 1.9 mmol/L in both high-risk and low-risk patients. Glycosuria was lower in the high- versus low-risk patients: 0.34 ± 0.25 versus 0.64 ± 0.44 mmol/min (P = 0.03). Both groups displayed similar kidney function during normoglycaemia. Hyperglycaemia increased more importantly GFR and fractional reabsorptions, and pre-glomerular vasodilatation in the high- than in the low-risk patients (all P < 0.05). Over 21 years, 31.5% high- versus 12.7% low-risk patients developed endpoints (adjusted P = 0.006). In a multi-adjusted survival analysis of patients having undergone renal tests, each 0.10 mmol/min glycosuria during hyperglycaemia reduced the outcome risk by 0.72 (95% confidence interval 0.49–0.97, P = 0.03). Conclusions Reduced tubulo-glomerular feedback and glycosuria during hyperglycaemia indicate high renal risk for Type 1 diabetic patients. Inter-individual variability in tubulo-glomerular feedback activity determines renal risk in Type 1 diabetes.

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44

Agbozo, Faith, Abdulai Abubakari, Clement Narh, and Albrecht Jahn. "Accuracy of glycosuria, random blood glucose and risk factors as selective screening tools for gestational diabetes mellitus in comparison with universal diagnosing." BMJ Open Diabetes Research & Care 6, no. 1 (June 2018): e000493. http://dx.doi.org/10.1136/bmjdrc-2017-000493.

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ObjectiveDespite the short-term and long-term health implications of gestational diabetes mellitus (GDM), opinions are divided on selective vis-à-vis universal screening. We validated the accuracy of screening tests for GDM.Research design and methodsPregnant women (n=491) were recruited to this prospective, blind comparison with a gold standard study. We did selective screening between 13 and 20 weeks using reagent-strip glycosuria, random capillary blood glucose (RBG) and the presence of ≥1 risk factor(s). Between 20 and 34 weeks, we did universal screening following the ‘one-step’ approach using glycated hemoglobin (HbA1c), fasting venous plasma glucose (FPG), and the 1-hour and the ‘gold standard’ 2-hour oral glucose tolerance test (OGTT). Tests accuracy was estimated following the WHO and the National Institute for Health and Care Excellence (NICE) diagnostic criteria. Overall test performance was determined from the area under the receiver operating characteristic curve (AUC).ResultsGDM prevalence per 2-hour OGTT was 9.0% for the WHO criteria and 14.3% for the NICE criteria. Selective screening using glycosuria, RBG and risk factors missed 97.4%, 87.2% and 45.7% of cases, respectively. FPG threshold ≥5.1 mmol/L had the highest clinically relevant sensitivity (68%) and specificity (81%), but FPG threshold ≥5.6 mmol/L had higher positive predictive value. Although sensitivity of 1-hour OGTT was 39.5%, it had the highest accuracy and diagnostic OR. Regarding test performance, 1-hour OGTT and FPG were very good (AUC>0.8), RBG was poor (AUC≈0.60), whereas HbA1c was invaluable (AUC<0.5).ConclusionsSelective screening using glycosuria and random blood glucose is unnecessary due to its low sensitivity. Fasting glucose ≥5.1 mmol/L could be applicable for screening at the population level. Where 2-hour OGTT is not available, FPG ≥5.6 mmol/L, complemented by the presence of risk factors, could be useful in making therapeutic decision.

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Jadoon, Khalid, and Iskandar Idris. "Dapagliflozin: A Once-Daily Oral Therapy Sodium-Glucose Cotransporter-2 Inhibitor for the Treatment of Adult Patients with Type 2 Diabetes." Clinical Medicine Insights: Therapeutics 3 (January 2011): CMT.S6168. http://dx.doi.org/10.4137/cmt.s6168.

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The induction of glycosuria using phlorizin, a nonselective inhibitor of renal and intestinal transport was well recognised to lower glucose levels and induce calorie loss in animal models of diabetes. Phlorizin and other similar molecules however were not suitable for clinical use due to adverse effects of non selective inhibition of extra-renal glucose transport system. More recent understanding of the physiology of renal glucose transport system and increased knowledge of rare genetic syndromes of renal glycosuria has resulted in the development of drugs that selectively inhibit the Sodium Glucose Transporter-2 (SGLT2). Among the various agents currently being developed within this drug class, dapagliflozin is the most advanced in clinical development. This article discusses the basic physiology of the SGLT2 transporter system, pharmacokinetics and pharmacodynamic information of dapagliflozin, its efficacy in lowering HbA1c and weight as well as its safety and adverse effects profile. This is discussed based on evidence derived from clinical trials involving a spectrum of patients with diabetes, from drug naïve to individuals already on insulin therapy.

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Lukačínová, A., J. Mojžiš, R. Beňačka, J. Keller, T. Maguth, P. Kurila, L. Vaško, O. Rácz, and F. Ništiar. "Preventive Effects of Flavonoids on Alloxan-Induced Diabetes Mellitus in Rats." Acta Veterinaria Brno 77, no. 2 (2008): 175–82. http://dx.doi.org/10.2754/avb200877020175.

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The aim of the present study was the evaluation of possible protective effects of quercetin and chrysin in experimental alloxan-induced diabetes in rats. Alloxan was injected at a single dose of 60 mg/kg (into the tail vein) for diabetes induction. Quercetin (50 and 100 mg/kg; orally) and chrysin (50 and 100 mg/kg; orally) were administered daily for 3 days prior and 7 days after alloxan injection. Alloxan induced a significant increase of glycaemia (p < 0.001) in comparison with control animals. Quercetin at both doses prevented serum glucose elevation (p < 0.001). However, the protective effect of chrysin was weaker and surprisingly, most prominent at the lower dose (p < 0.05; p < 0.01). On the other hand, glycosuria was increased in all groups of animals receiving alloxan. We suggest that the protective effect of the used flavonoids in experimental diabetes mellitus may be related to their antioxidative/chelatory properties. Increased glycosuria indicated that inhibition of renal glucose reabsorption may also play a role in the hypoglycaemic effect of both flavonoids.

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Hwa Lee, Chang, Sua Kim, Chong Myung Kang, and Gheun-Ho Kim. "Renal Glycosuria without Hyperglycemia in Cyclosporine-Treated Rats." Kidney Research and Clinical Practice 31, no. 2 (June 2012): A49—A50. http://dx.doi.org/10.1016/j.krcp.2012.04.457.

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Dornan, Tim L. "‘Glycosuria: Please Advise’. Reflections on Undergraduate Medical Education." Diabetic Medicine 9, no. 5 (June 1992): 407–9. http://dx.doi.org/10.1111/j.1464-5491.1992.tb01808.x.

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ROCH, MAURICE, ERIC MARTIN, and FRANÇOIS SCICLOUNOFF. "Les Rapports entre la Glycémie et la Glycosurie1." Acta Medica Scandinavica 88, no. 1 (April 24, 2009): 1–38. http://dx.doi.org/10.1111/j.0954-6820.1936.tb09464.x.

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Woronik, V., I. F. Freitas, L. B. Saldanha, E. Sabbaga, and M. Marcondes. "Glycosuria in glomerular diseases: histopathology and clinical correlations." Brazilian Journal of Medical and Biological Research 31, no. 5 (May 1998): 633–37. http://dx.doi.org/10.1590/s0100-879x1998000500005.

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