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At least 19 recordsLinked to original sources
PubMed1998

Glycosuria in glomerular diseases: histopathology and clinical correlations.

There are doubts about the presence of glycosuria and the progress of glomerular disease. Some reports suggest that glycosuria could be an index of a more severe tubulointerstitial lesion. We investigated the presence of glycosuria in 60 patients with primary glomerular diseases: 17 patients (28%) had glycosuria and 43 patients (72%) were glycosuria free. The two groups were similar in age, arterial pressure and sex. Serum creatinine was higher in patients with glycosuria (2.0 +/- 1.7 vs 1.3 +/- 0.9 mg/dl, P < 0.05). The protein excretion rate was 7.5 +/- 3.7 vs 5.3 +/- 4.2 g/day (P > 0.05) in patients with and without glycosuria, respectively, while serum albumin was lower in patients with glycosuria (1.7 +/- 0.6 vs 2.7 +/- 1.0 g/dl, P < 0.05). Several histological forms were present in the group with glycosuria, with membraneous glomerulonephritis being the most frequent. Histological evidence of tubular atrophy and interstitial fibrosis prevailed in patients with glycosuria, suggesting a poor prognosis for these patients. We may conclude that the presence of glycosuria in patients with glomerular disease is associated with more pronounced tubular atrophy and interstitial fibrosis and therefore imply a poorer prognosis.

Adult↗
PubMed1969

Familial renal glycosuria: a genetic reappraisal of hexose transport by kidney and intestine.

Renal glucose titration studies were carried out in 10 members of two pedigrees with familial renal glycosuria to test the accepted hypothesis of autosomal dominant inheritance and to investigate the genetic significance of "type A" and "type B" renal glycosuria. In one family, a brother and sister each had a moderately reduced threshold and tubular maximum for glucose (type A), but both of their parents reabsorbed glucose normally. In the second family, two brothers had severe type A renal glycosuria, their mother and one brother had a mild type A defect, and another brother demonstrated a reduced threshold, an exaggerated splay, and a normal tubular maximum, indicative of type B glycosuria.Hexose transport by intestinal mucosa was also investigated in controls and in the three brothers with the most severe renal glycosuria. D-glucose-(14)C and 3-O-methylglucose-(14)C were accumulated by jejunal mucosa from controls by processes which were saturable and concentrative. No differences in hexose transport were observed in the patients with renal glycosuria. We conclude that familial renal glycosuria can be inherited as an autosomal recessive trait; that mild and severe type A renal glycosuria and type B renal glycosuria can occur in the same pedigree; and that defective reabsorption of glucose by the kidney need not be accompanied by abnormalities in intestinal glucose transport. These findings indicate that glucose transport in the gut and kidney are not mediated by identical mechanisms, and that several different mutations are responsible for the phenotypic variability in familial renal glycosuria.

Adult↗
PubMed1999

Is glycosuria a reliable indicator of adequacy of glucose infusion rate in preterm infants?

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 preferm 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 < or = 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.

Biomarkers↗
PubMed1990

Screening for glycosuria during pregnancy.

It is currently recommended that every pregnant woman have a blood glucose screening test for gestational diabetes at 24 to 28 weeks' gestation. Random urine samples are also tested for glucose at each prenatal visit. In 500 consecutive pregnant women, random urine glucose screening values from each prenatal visit were compared with a serum glucose test done at 28 weeks' gestation after ingestion of a 50 gm glucose-containing beverage. Twenty-two patients (4.4%) subsequently were identified as having gestational diabetes. Eighty-five (17%) had some degree of glycosuria, and 19 (3.8%) had severe glycosuria. Only six (27%) of the 22 women with gestational diabetes had any glycosuria. As a screening test for gestational diabetes, glycosuria had a 27% sensitivity and a positive predictive value of only 7.1%. Severe glycosuria, although increased in women with gestational diabetes (P = .0071), occurred in only 18% of cases. Detection of severe glycosuria before 24 weeks' gestation is an indication to do earlier blood glucose screening. After blood glucose screening is done, routinely screening the urine for glycosuria at each prenatal visit does not appear to be clinically useful.

Blood Glucose↗
PubMed1996

Relevance of postprandial glycosuria in survey for diabetes mellitus.

Since the oral glucose tolerance test is not applicable in large surveys for diabetes mellitus, economic tests or clinical criteria are required to select subjects needing a complete glycometabolic assessment. This study evaluated, in a selected high risk population (110 subjects; 71 males; median age: 53 years, range 30-70), the utility of glycosuria after a meal rich in carbohydrates in the detecting of diabetes, compared to other tests for glycosuria (fasting glycosuria, glycosuria after a glucose load) and clinical criteria (diabetic family history, overweight and their combination). For each test and, retrospectively, for clinical criteria, sensitivity, sensibility, predictive value positive (PVP) and predictive value negative (PVN) were calculated. Postprandial glycosuria resulted to be an effective approach (sensitivity: 100%; specificity: 44%; PVP: 23%, PVN: 100%) in people over 50 years old, in which both clinical criteria (sensitivity: 22-78%; PVN: 81-90%) and fasting glycosuria (sensitivity 11%; PVN: 86%) proved defective. In younger subjects both the presence of fasting glycosuria (sensitivity: 100%; specificity: 96%; PVP: 33%; PVN: 100%) and of relevant diabetic family history (sensitivity: 100%; specificity: 85%; PVN: 100%) proved more adequate as screening procedures.

Adult↗
PubMed1999

Is there a role for glycosuria testing in sub-Saharan Africa?

BACKGROUND: With increasing urbanization and westernization, rates of diabetes in sub-Saharan Africa (sSA) are likely to rise. Early detection and intervention plays an important role in delaying development of complications. In sSA in particular there is need for an affordable, reliable, safe, feasible test to avert human suffering and exhausting already stressed health facilities. METHODS: Data from two large community-based studies were used to assess the value of glycosuria testing in the detection of diabetes in adults in a sub-Saharan country. A first study (A) tested participants for glycosuria by dipstick; if positive, fasting capillary glucose was measured. A later study (B) measured glucose concentration in venous blood 2 h after a 75-g glucose load; if glycaemia was > or = 10 mmol/l, urine was tested for glycosuria. RESULTS: The positive predictive value of glycosuria for a diagnosis of diabetes (fasting glucose > or = 6.7 mmol/l) was 48%. Sensitivity was 64% (57% if a 2-h-value > or = 10 mmol/l was used as gold standard). Sensitivity was higher among overweight and/or hypertensive subjects, among elderly people in the urban area, and among subjects with higher blood glucose levels. Extrapolated specificity was 99.7%, and the likelihood ratio 190. CONCLUSIONS: Glycosuria testing can identify a considerable number of undiagnosed diabetic patients when specially targeted at high-risk groups (obese, hypertensive, or elderly people). Dipstick glycosuria testing is an appropriate, safe, feasible test for sSA, where the prevalence of diabetes is expected to increase considerably in the near future.

Adult↗
PubMed1989

Glycosuria and insulitis in NOD mice expressing the HLA-DQw6 molecule.

To investigate HLA-linked genes controlling the susceptibility and resistance to insulin dependent diabetes mellitus (IDDM), HLA-DQ alleles of 45 Japanese patients with IDDM were analysed, using sequence specific oligonucleotide (SSO). DQA1*0301 and DQB1*04 were positively associated (R.R = 6.6, Pc less than 0.05 and R.R. = 4.7 Pc less than 0.01) and DQA1*0103 and DQB1*0104 were negatively associated (R.R. = 0.2, Pc less than 0.01) with IDDM. DQA1*0103 and DQB1*0104 were in strong linkage disequilibrium to encode for DQw6 molecule. Therefore, in a Japanese population, the DQw6 molecule seems to control the resistance to IDDM. To determine whether or not the DQw6 molecule itself can protect against glycosuria and insulitis in NOD mice, these animals were mated with HLA-DQw6 transgenic-C57BL/6 mice (DQw6-B6) and the F1 progeny expressing the DQw6 molecule were backcrossed with NOD mice. Eighty-five female backcross progenies were classified into four groups, according to the MHC classII phenotype; I-ANOD/I-ANOD DQw6(-), I-ANOD/I-ANOD DQw6(+), I-ANOD/I-Ab DQw6(-) and I-ANOD/I-Ab DQw6(+). At the age of 16 weeks, 9.1% of the DQw6(-) I-Ab(-) mice had a glycosuria whereas none of the DQw6(+) I-Ab(-) mice had a glycosuria. At the age of 30 weeks 13.6% of the DQw6(-) I-Ab(-) mice had a glycosuria and 7.7% of the DQw6(+) I-Ab(-) mice had a glycosuria. Histological examinations of the pancreas were performed in the 30 week old mice or after the development of glycosuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed2000

Glycosuria in organophosphate and carbamate poisoning.

OBJECTIVE: Puzzled by the observation of occurrence of transient glycosuria in several patients admitted with organophosphate and carbamate compound poisoning, we undertook a critical analysis of this observation. METHODS: Of the fifty-one consecutive patients admitted to the intensive care unit with organophosphate and carbamate compound poisoning, in 23 subjects the nature of the compound consumed was known; these were studied. The occurrence and duration of glycosuria, its magnitude, associated hyperglycemia if any, and correlation thereof were recorded. RESULTS: Sixteen out of the 23 subjects (69%) demonstrated transient glycosuria. There were 13 men and 10 women. 10 subjects had euglycemia associated with glycosuria; 6 subjects had transient glycosuria with hyperglycemia (defined as random glucose over 160 mg%). None of the subjects had diabetes mellitus and the pre-hospital-discharge blood sugars were in the normal range. CONCLUSION: Glycosuria (renal), albeit transient, was noted in a proportion of subjects admitted with organophosphate and carbamate poisoning. The exact etiology of this is unclear but in the light of recent literature, it is likely that oxidative stress at the renal tubular level leading to renal tubular damage may be the most likely explanation. Further, larger studies are needed to elucidate this is detail.

Adult↗
PubMed1992

Angiotensin-converting enzyme inhibitors and glycosuria.

Renal glycosuria associated with the use of angiotensin-converting enzyme inhibitors has been previously reported in two patients. A third patient was studied who developed isolated glycosuria associated with lisinopril therapy. As in the two previously described patients, this patient had a normal serum glucose level, underlying hypertension, and onset of glycosuria between 2 and 16 weeks after initiation of therapy with an angiotensin-converting enzyme inhibitor. The patient had renal artery stenosis with elevated renin levels. Age, time until resolution of glycosuria, and a rise in serum creatinine level did not have a consistent relationship with glycosuria associated with angiotensin-converting enzyme inhibitor therapy. Since glycosuria was the only defect noted, without evidence of any other urinary solutes, angiotensin-converting enzyme inhibitors may exert an effect on the glucose-specific proximal tubule transport system.

Adult↗
PubMed1984

Renal glycosuria in renal homograft recipients.

Transient renal glycosuria was observed in eight renal transplant patients during the recovery phase from initial tubular necrosis or acute rejection. In these subjects and three homograft recipients without glycosuria we performed glucose titration experiments. Three patients were found to have type A glycosuria, two had type B and three type C. The titration curve was normal in the three patients without glycosuria. In addition, most subjects presented with hypophosphataemia and hyperphosphaturia. Apart from a direct correlation between the point of splay of the glucose titration curves and the fractional clearance of phosphate, there was no clear-cut relationship between the handling of glucose and phosphorus. Mild hyperchloraemic acidosis was observed in six subjects, but this was unrelated to the type and grade of glycosuria. It is concluded that in homograft recipients the tubular alterations have a patchy and unpredictable distribution and may cause a variety of symptoms which do not necessarily occur in close association.

Absorption↗