Regional variance in the use of urine dipstick test for outpatients in Japan.

AIM: The urine dipstick is a simple diagnostic module for detecting proteinuria, haematuria and glycosuria and is favourably accepted in East Asia despite debates regarding its accuracy and target population, claiming that quantitative tests for a high-risk cohort should be more cost-effective. However, the current status of utilizing this test in these countries is not widely known due to lack of extensive data. We aimed to clarify the current nationwide and regional status of utilization of the urine dipstick test in an outpatient care setting and to determine the regional factors associated with adoption of this method. METHODS: This cross-sectional study used openly accessible data from the national claim database that included the health insurance claims data of the Japanese population in 2017. RESULTS: In total, 67 125 386 urine dipstick tests were performed compared with 1 862 700 quantitative urine protein tests and 17 544 949 urine sediment microscopy tests. Dipstick tests were employed principally for those who are >65 years old (60.3%) and, although the male population (52.5%) is generally larger, the female population is larger in age of 15 to 39 years and >85 years. Multivariate analysis with several regional parameters revealed that the test was performed more commonly in the areas that accommodate greater elderly population (P < .01). CONCLUSION: Despite a heated dispute, the urine dipstick test is performed even more frequently than the quantitative biochemical or microscopic sediment tests, especially in regions holding the larger elderly population, which suggests that the test forms a part of geriatric medical care.

Non-diabetic glycosuria as a diagnostic clue for acute tubulointerstitial nephritis in patients with azotemia.

BACKGROUND: Glycosuria is one of the manifestations of acute tubulointerstitial nephritis (ATIN), but may also be observed in other renal diseases. In this study, we investigated the value of non-diabetic glycosuria as a diagnostic clue for ATIN. METHODS: We retrospectively reviewed the medical records of adult patients who underwent a kidney biopsy as an evaluation for serum creatinine > 1.4 mg/dL. Patients with proteinuria in the nephrotic range, diabetes mellitus, or transplanted kidney were excluded. The laboratory abnormalities suggestive of tubular injury were compared between 28 patients (14 men and 14 women, mean age 48.5 ± 14.1 years) with ATIN and 116 patients (76 men and 40 women, mean age 53.1 ± 15.0 years) with other diagnoses. RESULTS: In ATIN, glycosuria (≥ 1+ on dipstick; 68%) was more frequent than hypophosphatemia (18%), hypouricemia (18%), hypokalemia (18%), and tubular proteinuria (40%). In other diagnoses, glycosuria (≥ 1+) was detected in 7 (6%) patients; 6 of them had the histological diagnosis of antineutrophil cytoplasmic antibody-associated glomerulonephritis. The presence of glycosuria (≥ 1+) had 68% sensitivity and 94% specificity for ATIN, with the positive likelihood ratio of 11.24 and the negative likelihood ratio of 0.34. Pyuria and low total CO2 were equally and more sensitive (68% and 71%, respectively) than glycosuria (≥ 1+), but had no diagnostic value due to low specificities (58% and 60%, respectively). CONCLUSION: In non-diabetic, non-nephrotic patients undergoing a kidney biopsy for azotemia, 1+ or higher glycosuria, if present, was a good predictor of the diagnosis of ATIN.

Glycemic control by the SGLT2 inhibitor empagliflozin decreases aortic stiffness, renal resistivity index and kidney injury.

BACKGROUND: Arterial stiffness is emerging as an independent risk factor for the development of chronic kidney disease. The sodium glucose co-transporter 2 (SGLT2) inhibitors, which lower serum glucose by inhibiting SGLT2-mediated glucose reabsorption in renal proximal tubules, have shown promise in reducing arterial stiffness and the risk of cardiovascular and kidney disease in individuals with type 2 diabetes mellitus. Since hyperglycemia contributes to arterial stiffness, we hypothesized that the SGLT2 inhibitor empagliflozin (EMPA) would improve endothelial function, reduce aortic stiffness, and attenuate kidney disease by lowering hyperglycemia in type 2 diabetic female mice (db/db). MATERIALS/METHODS: Ten-week-old female wild-type control (C57BLKS/J) and db/db (BKS.Cg-Dock7m+/+Leprdb/J) mice were divided into three groups: lean untreated controls (CkC, n = 17), untreated db/db (DbC, n = 19) and EMPA-treated db/db mice (DbE, n = 19). EMPA was mixed with normal mouse chow at a concentration to deliver 10 mg kg-1 day-1, and fed for 5 weeks, initiated at 11 weeks of age. RESULTS: Compared to CkC, DbC showed increased glucose levels, blood pressure, aortic and endothelial cell stiffness, and impaired endothelium-dependent vasorelaxation. Furthermore, DbC exhibited impaired activation of endothelial nitric oxide synthase, increased renal resistivity and pulsatility indexes, enhanced renal expression of advanced glycation end products, and periarterial and tubulointerstitial fibrosis. EMPA promoted glycosuria and blunted these vascular and renal impairments, without affecting increases in blood pressure. In addition, expression of "reversion inducing cysteine rich protein with Kazal motifs" (RECK), an anti-fibrotic mediator, was significantly suppressed in DbC kidneys and partially restored by EMPA. Confirming the in vivo data, EMPA reversed high glucose-induced RECK suppression in human proximal tubule cells. CONCLUSIONS: Empagliflozin ameliorates kidney injury in type 2 diabetic female mice by promoting glycosuria, and possibly by reducing systemic and renal artery stiffness, and reversing RECK suppression.

Glycosuria and hyperglycemia in the neonatal period as the first clinical sign of Fanconi-Bickel syndrome.

Fanconi-Bickel syndrome is a rare inherited disease characterized by the combination of hepatorenal glycogen accumulation, proximal renal tubular dysfunction and impaired utilization of glucose and galactose. The first symptoms of the disorder are recognized in late infancy as clinical characteristics appear. Therapeutic approach is mainly conservative with supplements of calcium, phosphate and vitamin D and small frequent feedings to avoid hypoglycemia. We report 1 clinical case of very early diagnosis, a 19 days old baby girl, in which the first clinical sign of the disease was the detection of glycosuria and vomits. Serum alkaline phosphatase levels were very high without rickets. The patient presented postprandial hyperglycemia and fasting hypoglycemia. A complete 24-hour glucose profile was obtained using a continuous glucose monitoring system in real time, which was fundamental not only for the diagnosis but also for the prevention of hypoglycemia. She received frequent small meals, galactose-free milk diet, and oral intakes of calcium, phosphorum, bicarbonate and vitamin D supplements with good evolution and normal height and weight gain.

Self-monitoring of blood glucose versus self-monitoring of urine glucose in adults with newly diagnosed Type 2 diabetes receiving structured education: a cluster randomized controlled trial.

AIMS: To compare the effectiveness and acceptability of self-monitoring of blood glucose with self-monitoring of urine glucose in adults with newly diagnosed Type 2 diabetes. METHODS: We conducted a multi-site cluster randomized controlled trial with practice-level randomization. Participants attended a structured group education programme, which included a module on self-monitoring using blood glucose or urine glucose monitoring. HbA1c and other biomedical measures as well as psychosocial data were collected at 6, 12 and 18 months. A total of 292 participants with Type 2 diabetes were recruited from 75 practices. RESULTS: HbA1c levels were significantly lower at 18 months than at baseline in both the blood monitoring group [mean (se) -12 (2) mmol/mol; -1.1 (0.2) %] and the urine monitoring group [mean (se) -13 (2) mmol/mol; -1.2 (0.2)%], with no difference between groups [mean difference adjusted for cluster effect and baseline value = -1 mmol/mol (95% CI -3, 2); -0.1% (95% CI -0.3, 0.2)]. Similar improvements were observed for the other biomedical outcomes, with no differences between groups. Both groups showed improvements in total treatment satisfaction, generic well-being, and diabetes-specific well-being, and had a less threatening view of diabetes, with no differences between groups at 18 months. Approximately one in five participants in the urine monitoring arm switched to blood monitoring, while those in the blood monitoring arm rarely switched (18 vs 1% at 18 months; P < 0.001). CONCLUSIONS: Participants with newly diagnosed Type 2 diabetes who attended structured education showed similar improvements in HbA1c levels at 18 months, regardless of whether they were assigned to blood or urine self-monitoring.

Postprandial self-monitoring of urine glucose reflects glycaemic control in people with relatively well controlled Type 2 diabetes mellitus not treated with insulin: a retrospective cohort study.

AIM: To analyse the association of self-monitoring of urine glucose with HbA1c concentration in people with Type 2 diabetes not treated with insulin. METHODS: We studied the association of postprandial self-monitored urine glucose with HbA1c concentrations in 264 people with Type 2 diabetes (mean age 62.4 years, time since diagnosis of diabetes 6.8 years and HbA1c 50 mmol/l). All patients took part in a diabetes treatment and teaching programme. HbA1c values were adjusted according to the Diabetes Control and Complication Trial. RESULTS: The mean ( ± sd) HbA1c concentration for the patients with constant negative urine glucose tests (56.1% of patients) was 46 ( ± 6) mmol/mol [6.4 ( ± 0.6)%]. This was significantly lower than in patients with < 50% positive urine glucose tests (33.3% of patients): mean ( ± sd) HbA1c was 53 ( ± 8) mmol/mol [7.0( ± 0.7)%] and also lower than in patients with ≥50% positive tests (10.6% of patients): mean ( ± sd) HbA1c of 57 ( ± 8) mmol/mol [7.4 ( ± 0.7)%]; P < 0.001. There was a significant correlation between the urine glucose test results and HbA1c (r = 0.416; P < 0.001). CONCLUSION: HbA1c concentrations were observed to be in the near-normal range for people with Type 2 diabetes not receiving insulin treatment who were negative for postprandial glucosuria. Urine glucose self-monitoring is a cheap and effective method to determine the quality of glucose control.

Impaired decline in renal threshold for glucose during pregnancy - a possible novel mechanism for gestational diabetes mellitus.

BACKGROUND: The renal threshold for glucose (RT(G)) is determined by the nephron's reabsorptive capacity. Glucose is reabsorbed through sodium-coupled glucose cotransporters in the proximal tubules. During pregnancy, renal glucose reabsorptive capacity decreases, possibly, due to reduced glucose transporter expression. Our hypothesis is that inadequate decrease in RT(G) during pregnancy will make women more prone to develop gestational diabetes mellitus (GDM). METHODS: Pregnant women (n = 40) who were referred to our center for oral glucose tolerance test (OGTT) were included in the analysis. Plasma glucose levels and urinary glucose excretion were measured for 4 h after 100 g oral glucose load. These data were used to calculate RT(G) . The subjects were divided into two cohorts, GDM and non-GDM, according to the OGTT results. Mean RT(G) was compared between the two groups. RESULTS: Fifteen (37.5%) of the women were diagnosed with GDM. Seventeen participants had only trace amounts of urinary glucose excretion, and no value of RT(G) could be determined; RT(G) was determined in the other 23 subjects. Among these 23 women, 13 were diagnosed as GDM, and 10 had normal OGTT. RT(G) was lower in the non-GDM women (146 ± 14 mg/dL) than in the GDM women (182 ± 18 mg/dL), p < 0.001. CONCLUSIONS: Gestational diabetes mellitus is associated with higher RT(G) during pregnancy compared with non-GDM. These results support our hypothesis that inadequate decrease of the RT(G) may have a pathophysiological role in the development of GDM.

Mortality and causes of deaths of inhabitants with renal dysfunction induced by cadmium exposure of the polluted Jinzu River basin, Toyama, Japan; a 26-year follow-up.

BACKGROUND: We aimed to investigate the mortality and causes of deaths of inhabitants with renal dysfunction induced by cadmium (Cd) exposure caused by heavy environmental contamination. METHODS: We conducted a 26-year follow-up survey targeting 7529 inhabitants of the Cd-polluted Jinzu River basin and 2149 controls from non-polluted areas who participated in urinary examinations for proteinuria and glucosuria conducted in 1979 to 1984. When the residents were divided into 4 groups, no finding group, glucosuria group, proteinuria group, glucoproteinuria group, mortality risk ratios for all and specific causes of these groups in the polluted area were compared with that of controls without glucosuria and/or proteinuria after adjustments for age at baseline, smoking status, and history of hypertension using Cox's proportional hazard model. RESULTS: The mortality risk ratios for all causes of proteinuria and glucoproteinuria in men and glucosuria, proteinuria, and glucoproteinuria in women of the polluted areas significantly increased compared with those of the controls with no urinary findings. Respiratory, renal, and cardiovascular diseases and diabetes in men, and all diseases except cerebrovascular diseases in women contributed toward an increased mortality of exposed glucoproteinuria groups, which involved chronic Cd toxicosis with renal tubular dysfunction. In women, the mortality risks for cancer of the colon and rectum, uterus and kidney and urinary tract were significantly higher in the exposed proteinuria and glucoproteinuria groups, suggesting associations between renal damage and cancer risk. In exposed women, the no finding group and glucoproteinuria group also showed increased mortality from ischemic heart diseases, indicating that all exposed women may be at risk for ischemic heart diseases. Although the control glucosuria and/or proteinuria group also showed high mortality for diabetes and renal diseases, the increased risk ratio for renal disease mortality was much higher in exposed subjects with urinary findings, particularly in women. CONCLUSIONS: These findings indicate that inhabitants with renal effects caused by Cd exposure had a poor life prognosis over long-term observation in both genders. Particularly in women, renal tubular dysfunction indicated by glucoproteinuria may increase mortality from cancer, ischemic heart diseases, and renal diseases.

Selective SGLT2 inhibition by tofogliflozin reduces renal glucose reabsorption under hyperglycemic but not under hypo- or euglycemic conditions in rats.

To understand the risk of hypoglycemia associated with urinary glucose excretion (UGE) induced by sodium-glucose cotransporter (SGLT) inhibitors, it is necessary to know the relationship between the ratio of contribution of SGLT2 vs. SGLT1 to renal glucose reabsorption (RGR) and the glycemic levels in vivo. To examine the contributions of SGLT2 and SGLT1 in normal rats, we compared the RGR inhibition by tofogliflozin, a highly specific SGLT2 inhibitor, and phlorizin, an SGLT1 and SGLT2 (SGLT1/2) inhibitor, at plasma concentrations sufficient to completely inhibit rat SGLT2 (rSGLT2) while inhibiting rSGLT1 to different degrees. Under hyperglycemic conditions by glucose titration, tofogliflozin and phlorizin achieved ≥50% inhibition of RGR. Under hypoglycemic conditions by hyperinsulinemic clamp, RGR was reduced by 20-50% with phlorizin and by 1-5% with tofogliflozin, suggesting the smaller contribution of rSGLT2 to RGR under hypoglycemic conditions than under hyperglycemic conditions. Next, to evaluate the hypoglycemic potentials of SGLT1/2 inhibition, we measured the plasma glucose (PG) and endogenous glucose production (EGP) simultaneously after UGE induction by SGLT inhibitors. Tofogliflozin (400 ng/ml) induced UGE of about 2 mg·kg⁻¹·min⁻¹ and increased EGP by 1-2 mg·kg⁻¹·min⁻¹, resulting in PG in the normal range. Phlorizin (1,333 ng/ml) induced UGE of about 6 mg·kg⁻¹·min⁻¹ and increased EGP by about 4 mg·kg⁻¹·min⁻¹; this was more than with tofogliflozin, but the minimum PG was lower. These results suggest that the contribution of SGLT1 to RGR is greater under lower glycemic conditions than under hyperglycemic conditions and that SGLT2-selective inhibitors pose a lower risk of hypoglycemia than SGLT1/2 inhibitors.

Urinary lipid and protein oxidation products upon halothane, isoflurane, or sevoflurane anesthesia in humans: potential biomarkers for a subclinical nephrotoxicity.

OBJECTIVE: To investigate whether lipid and protein oxidation products are elevated and correlated with routine clinical markers of hepatic and renal function in patients anesthetized with halothane, isoflurane, or sevoflurane. METHODS: Urine and blood samples were collected from patient groups. Excretion of aldehydes, acetone, and o,o'-dityrosine was measured before and after anesthesia. Blood samples were analysed for clinical markers. RESULTS: Urinary concentrations of aldehydes, acetone, o,o'-dityrosine and glucose were significantly increased after anesthesia in halothane and sevoflurane groups earlier than clinical markers. Significant correlations were found in sevoflurane group. CONCLUSION: Lipid and protein oxidation contributes to subclinical sevoflurane nephrotoxicity. Oxidation products may serve as early biomarkers.

Continuous subcutaneous hydrocortisone infusion (CSHI) in a young adolescent with congenital adrenal hyperplasia (CAH).

Congenital adrenal hyperplasia (CAH) is an autosomal recessive enzymatic defect caused by mutations or deletions of the cytochrome P450 21-hydroxylase CYP21 gene. Oral therapy with glucocorticoids and mineralcorticoids is administered to prevent adrenal crisis and to control hyperandrogenism. During puberty this type of therapy is difficult to manage owing to physiological and hormonal changes and poor compliance. We describe a case of a pubertal boy affected by CAH, in whom continuous subcutaneous infusion of hydrocortisone led to improved metabolic control and compliance.

Gluconeogenesis defect presenting with resistant hyperglycemia and acidosis mimicking diabetic ketoacidosis.

Fructose-1,6-diphosphatase (FDPase) enzyme deficiency is a rare inherited metabolic disease. Affected patients usually present with metabolic crisis including hypoglycemia, acidosis, ketonuria, and hyperuricemia. A previously healthy 8-month-old male infant presented with fever, vomiting, and hypoactivity. He had tachycardia, tachypnea, and a tendency to sleep. The patient had signs of severe dehydration and shock. Laboratory findings revealed significant lactic acidosis, hyperuricemia, hyperglycemia, elevated liver enzyme level, and hyperlipidemia. The urine analysis had evidence of glycosuria and ketonuria. Hyperuricemia, lactic acidemia, and hyperglycemia persisted despite insulin infusion, adequate hydration, and perfusion. Consequently, peritoneal dialysis was started. About 12 hours after dialysis, his metabolic derangements were normalized, and clinical status was improved dramatically. His metabolic disease workup was compatible with FDPase deficiency. Here, we described a metabolic attack of FDPase deficiency presented with hyperglycemia mimicking diabetic ketoacidosis.

A novel heterozygous mutation in the SLC5A2 gene causing severe glycosuria, mild failure to thrive, and subclinical hypoglycemia.

Highlights A novel heterozygous mutation in the SLC5A2 gene in a 2-year-old girl with severe asymptomatic glycosuria, mild failure to thrive, and subclinical hypoglycemia: Continuous glucose monitoring identified 14% hypoglycemic excursions (< 70 mg/dl), reduced at 1% with 1 g/Kg uncooked cornstarch at bed-time milk and eliminated (0%) adjusting the dose at 1.5 g/Kg, as shown by Flash technology.

Virus-induced diabetes mellitus. I. Hyperglycemia and hypoinsulinemia in mice infected with encephalomyocarditis virus.

Infection of DBA/2N male mice with encephalomyocarditis virus resulted in a diabeteslike syndrome characterized by hyperglycemia, glycosuria, hypoinsulinemia, polydipsia, and polyphagia. Blood glucose levels were elevated within 4 days after infection and reached a maximum mean level of 320 mg/100 ml within 12 days. Approximately 60-80% of the animals developed a transient hyperglycemia while 10-15% of the animals remained hyperglycemic for well over 6 mo. The remaining animals failed to become hyperglycemic but many had abnormal glucose tolerance curves. Hyperglycemia was most pronounced when animals were allowed free access to food, and the incidence of byperglycemia was related both to the strain and sex of the animals, with few females developing hyperglycemia. The amount of immunoreactive insulin in the plasma of infected hyperglycemic mice was significantly lower than in appropriate controls, and injection of exogenous insulin resulted in a rapid drop in the blood glucose levels. Despite the fact that certain animals were hyperglycemic for many months, virus could not be recovered from the pancreas after the first 10 days of the infection.

Can we contribute to the diagnosis of diabetes and regulation of blood glucose by increasing the urologists' awareness of glucosuria?

AIMS: Diabetes mellitus is a progressive, chronic, systemic, metabolic disease that must be managed effectively. Its prevalence is increasing rapidly. We investigated whether urologists' awareness and recognition of glucosuria contributed to the diagnosis of diabetes and regulation of blood glucose. METHODS: A total of 39,053 patients were retrospectively evaluated between January 2018 and February 2019. Of them, 16,211 had undergone urinalysis for varied reasons. Glucosuria was semi-quantitatively measured as (+), (++), (+++), and (++++). Patients were assessed in terms of whether they had been referred to endocrinology or internal medicine departments within the 15 days and the presence/absence of a previous or new diagnosis of diabetes mellitus by measuring blood glucose and HgbA1c levels. RESULTS: Glucosuria was detected in 665 patients (4.1%), of whom 495 were included in the study. 417 (84.2%) had been previously diagnosed with diabetes mellitus, and 56 (11.3%) newly received a diabetes mellitus diagnosis. Blood glucose and HbA1c values were normal in 22 (4.4%) patients with glucosuria. HgbA1c value was determined as 7 or above in 381 (91.3%) of 417 cases with a previous diabetes mellitus diagnosis. CONCLUSION: Referring all patients detected to have glucosuria in the spot urine test at any time regardless of fasting/non-fasting to the relevant departments can contribute to the diagnosis and treatment of diabetes mellitus disease.

Western Diet Promotes Renal Injury, Inflammation, and Fibrosis in a Murine Model of Alström Syndrome.

INTRODUCTION: Alström syndrome is a rare recessive genetic disease caused by mutations in ALMS1, which encodes a protein that is related to cilia function and intracellular endosome trafficking. The syndrome has been linked to impaired glucose metabolism and CKD. Polymorphisms in Alms1 have likewise been linked to CKD, but little is known about the modification of the phenotype by environmental factors. METHODS: To gain further insights, the fat aussie (foz) mouse strain, a genetic murine model of Alström syndrome, was exposed to a normal chow (NC) or to a Western diet (WD, 20% fat, 34% sucrose by weight, and 0.2% cholesterol) and renal outcomes were measured. RESULTS: Body weight and albuminuria were higher in foz than in wild-type (WT) mice on both diets but WD significantly increased the difference. Measurement of plasma creatinine and cystatin C indicated that glomerular filtration rate was preserved in foz versus WT independent of diet. Renal markers of injury, inflammation, and fibrosis were similar in both genotypes on NC but significantly greater in foz than in WT mice on WD. A glucose tolerance test performed in foz and WT mice on WD revealed similar basal blood glucose levels and subsequent blood glucose profiles. CONCLUSIONS: WD sensitizes a murine model of Alström syndrome to kidney injury, inflammation, and fibrosis, an effect that may not be solely due to effects on glucose metabolism. Polymorphisms in Alms1 may induce CKD in part by modulating the deleterious effects of high dietary fat and sucrose on kidney outcome.

Nephrological disorders and neurological involvement in pediatric primary Sjogren syndrome:a case report and review of literature.

BACKGROUND: Sjögren syndrome (SS) is a rare disease in pediatrics, and little attention has been paid to the clinical feature in these patients. To date, there are few cases concern about neurological and nephrological disorders in childhood Sjögren syndrome. We describe a case of Sjögren syndrome in a 12-year-old girl who developed neurological disorders and interstitial nephritis and review the literature currently available on this topic. CASE PRESENTATION: A 12-year-old girl was admitted to our hospital for arthritis and glucosuria. She was required to do labial gland and renal biopsy, because the positive for anti-nuclear antibody and anti-Sjögren syndrome B (anti-SSB) antibody. Then the biopsy was performed revealing the lymphocytic infiltrate in the small area and renal tubular interstitial damage,thus the diagnosis of Sjögren syndrome with tubular interstitial damage was made. Three months later, she presented again with headache, fever, nausea, vomiting and was recovered without drug therapy. Based on the patient's medical history, laboratory and imaging examination, and treatment, we speculate that the disorders of the nervous system were caused by the Sjögren syndrome. The girl has stable renal function and no residual nervous system damage in the next 1.5 years, but she underwent low dose prednisone therapy because of persistent renal glucosuria. CONCLUSIONS: Nephrological disorders and neurological involvement are rare manifestations of Sjögren syndrome in children, and rarely presented as the initial symptoms. It should be suspected in children presenting with unexplained renal diseases, neurological abnormalities, or unexplained fever. Although there is no guidelines on the diagnosis and treatment of children Sjögren syndrome are currently available, early recognition and the appropriate treatment of renal damage and neurologic involvement would improve prognosis and prevent complications.

Glucose control by the kidney: an emerging target in diabetes.

The full significance of the kidney's role in glucose homeostasis is now well recognized. For example, it is now known that renal gluconeogenesis contributes substantially to total-body glucose release in the postabsorptive state. The kidney contributes to glucose homeostasis by filtering and reabsorbing glucose. Under normal circumstances, glucose filtered by glomeruli is completely reabsorbed, but glucosuria may occur under conditions of hyperglycemia or reduced reabsorptive capacity. The sodium-glucose cotransporter SGLT2 (encoded by the SLC5A2 gene), which is expressed almost exclusively in proximal tubules, mediates approximately 90% of active renal glucose reabsorption. This transporter can be blocked by SGLT2 inhibitors, a class of compound that may prove effective in managing type 2 diabetes. The glucosuria induced by these compounds has a naturally occurring parallel in familial renal glucosuria (FRG), a condition in which SGLT2 mutations reduce renal reabsorptive capacity. Interestingly, the chronic glucosuria of patients with FRG does not appear to be associated with other pathological changes, and patients with FRG are mostly asymptomatic. This suggests that glucosuria is not intrinsically detrimental. Selective SGLT2 inhibitors are currently in clinical trials.

The glycosylation of hemoglobin: relevance to diabetes mellitus.

Glucose reacts nonenzymatically with the NH2-terminal amino acid of the beta chain of human hemoglobin by way of a ketoamine linkage, resulting in the formation of hemoglobin AIc. Other minor components appear to be adducts of glucose 6-phosphate and fructose 1,6-diphosphate. These hemoglobins are formed slowly and continuously throughout the 120-day life-span of the red cell. There is a two- to threefold increase in hemoglobin AIc in the red cells of patients with diabetes mellitus. By providing an integrated measurement of blood glucose, hemoglobin AIc is useful in assessing the degree of diabetic control. Furthermore, this hemoglobin is a useful model of nonenzymatic glycosylation of other proteins that may be involved in the long-term complications of the disease.

[Pheochromocytoma--a disease which is worth to keep in mind]. / Guz chromochlonny nadnercza--choroba, o której warto pamietac.

The case of 25 years old male patient with symptoms of hypertensive storm in the course of pheochromocytoma was presented. For some years he had been suffering from moderate increase in arterial blood pressure whose secondary cause was not suspected by physicians examining this patient. In presented case the course of pheochromocytoma has special characteristics, such as: clinical presentation in young age, the course alternate between periods of hypertension and phases of normal blood pressure, physical signs of Marfan's syndrome, increase of troponin level within hypertensive storm, and attributes of malignant hypertension presented as transient proteinuria and glycosuria within normoglycemia.