bluuebunny/crossref_metadata_2025_split huggingface dataset:
532-P: Effect of ABC Control of Diabetes on the Prevalence of Chronic Kidney Disease in Patients with Type 2 Diabetes from Tibet in China
Authors: CHENGHUI ZHANG , YUNHONG WU , SUYUAN WANG , MINGXIA LI 
Published: June 2019

Aim: To investigate the effect of ABC control of diabetes (A: HbA1c, B: blood pressure and C: LDL-C) on the prevalence of chronic kidney disease (CKD) in patients with type 2 diabetes (T2D) from Tibet based on electronic medical records.
Methods: Patients (aged 18-79 years) documented from 2014 to 2018 were enrolled. Control criteria were defined base on the 2017 Chinese Guidelines for the Prevention and Treatment of Type 2 Diabetes: HbA1c &lt; 7.0%, blood pressure &lt;130/80 mmHg and LDL-C &lt;1.8 mmol/L with coronary heart disease (CHD) and 2.6 mmol/L without CHD. CKD was defined as eGFR &lt;60 ml/min per 1.73 m2 and/or urinary albumin/creatine ratio ≥ 30 mg/g. Patients were divided into four groups according to ABC control.
Results: A total of 1999 patients were enrolled. The mean (SD) age was 55.2 (10.5) years. The median diabetic duration was 7.0 (range: 0.1-32) years and 43.9% patients were female. As shown in Figure 1, the prevalence of CKD has increased in parallel with the bad control of ABC (P&lt;0.001). Compared with patients achieved all three targets, patients with none of target achieved had a 2.70-fold (95% CI: 1.25-5.86, P = 0.012) higher risk for CKD after adjusted for age, gender and diabetic duration.
Conclusions: The achievement of ABC target was associated with the prevalence of CKD. More intensive T2D management is warranted to prevent the development of CKD in this population.

Disclosure
Z. Chenghui: None. W. Yunhong: None. W. Suyuan: None. L. Mingxia: None.
534-P: Serum Sclerostin, Body Composition, and Sarcopenia in Hemodialysis Patients with Diabetes
Authors: BANDEIRA FRANCISCO , MEDEIROS MARIA CAROLINA W. , JUNIOR MARIO HENRIQUES , SILVA NATALIA ROCHA , BANDEIRA FARIAS MARIA ELBA , FARIAS LEONARDO 
Published: June 2019

Sclerostin (Scl) is an osteoblast inhibiting glycoprotein secreted mainly by osteocytes which is regulated by hormonal changes and skeletal loading. Decreased physical function and high serum Scl concentrations have been reported in chronic renal failure patients but little is known about the differences among diabetic and nondiabetic patients on hemodyalisis who are susceptible to both sarcopenia and bone fragility.
Objective: To determine the prevalence of sarcopenia and its association with serum sclerostin concentrations and metabolic parameters in 92 patients on hemodyalisis. Anthropometric data and physical performance were evaluated. Blood sample were collected for sclerostin, glucose, cholesterol, triglycerides, calcium, phosphate, PTH e 25OH-vitamin D measurements. Lean mass was evaluated using multifrequency electro-bioimpedance at a “dry weight” time (after dialysis session).
Results: Mean age was 63.3±13.6 years, 63% were male and 44.6% had diabetes. Mean BMI was higher in diabetics (26.6±5.2 vs. 24.1±3.7; p=0.01) and there were no differences in gait speed and hand grip strength between diabetic and nondiabetic subjects. A low skeletal muscle mass index (SMI) was identified in 65.2% of the participants, and among them 76.7% were men and 36.7% diabetics. Mean serum sclerostin was 86.9 ± 39.0 pmol/L, which was higher in men (94.6 ± 41.7; p = 0.017), in individuals with low SMI (94.9 ± 40.7; p &lt; 0.001) and in diabetics (97.2 ± 46.6; p &lt; 0.003). After multivariate analysis and adjustments for potential confounders, high serum sclerostin was independently associated with low SMI and with the presence of diabetes. The following variables correlated positively with diabetes: blood pressure, body mass index (BMI) waist circumference, waist/hip ratio, plasma glucose, serum sclerostin and fat mass.
Conclusions: We found higher serum sclerostin concentrations in hemodialysis patients with diabetes which were inversely related to muscle mass.

Disclosure
F. Bandeira: None. M.W. Medeiros: None. M.H. Junior: None. N.R. Silva: None. M. Bandeira Farias: None. L. Farias: None.

Funding
Arab Society for Paediatric Endocrinology and Diabetes
537-P: sCD93 Is a Potential Biomarker for Diabetic Nephropathy
Authors: LEE SANG BAE , PARK HO SEON , LEE MINYOUNG , CHOI ARIM , PARK JONG SUK , AHN CHUL WOO , LEE SEUNG-PYO , KANG SHINAE 
Published: June 2019

Objective: CD93 is a glycoprotein that is known to enhance phagocytosis. The extracellular portion of CD93 can be enzymatically cleaved and secreted to the serum as a soluble form (sCD93). Diabetic nephropathy (DN) is a well-known inflammatory disease that commonly progresses to end stage renal disease (ESRD) in diabetes. Although albuminuria and estimated glomerular filtration rate (eGFR) is currently used for the diagnosis and the prognostication of DN, the prognostic value of the two parameters is modest at best. Here, we hypothesized that sCD93 would be a new biomarker for DN.
Methods: We registered 97 human subjects with type 2 diabetes and evaluated the association between serum sCD93 and DN. The underlying mechanism of CD93 regulation was elucidated using human umbilical cord endothelial cell (HUVEC) in vitro and diabetic db/db mice in vivo.
Results: The group with higher sCD93 has lower eGFR level and higher prevalence of CKD defined by eGFR. The log(sCD93) was significantly associated with albumin-to-creatinine ratio (ACR) (r=0.229, p=0.028) and the sCD93 level was an independent determinant of ACR and eGFR. The odds ratio of having DN was higher in the high serum sCD93 group even after adjusting for other covariates (adjusted odds ratio 7.283, 95% CI 1.255-42.268, p=0.027). In vitro, CD93 was highly expressed in HUVEC and both CD93 expression and sCD93 secretion was upregulated after LPS stimulation. In db/db mice, sCD93 level was much higher in the peritoneal fluid compared to the db/m mice. The db/db mice showed significantly higher CD93 expression in the renal glomerulus compared to that of the db/m mice suggesting that the elevated sCD93 according to the degree of DN progression might be associated with upregulated expression of CD93 in glomerulus.
Conclusion: Based on these human and rodent data, we conclude that sCD93 could be a candidate molecule associated with DN.

Disclosure
S. Lee: None. H. Park: None. M. Lee: None. A. Choi: None. J. Park: None. C. Ahn: None. S. Lee: None. S. Kang: None.

Funding
Korean National Research Foundation (2014R1A1A3051221)
543-P: A Clinical, Proteomics and Artificial Intelligence-Driven Model to Predict Acute Kidney Injury in Diabetic Patients Undergoing Coronary Angiography—Results from the Catheter Sampled Blood Archive in Cardiovascular Diseases Study
Authors: IBRAHIM NASRIEN E. , MCCARTHY CIAN P. , SHRESTHA SHREYA , GAGGIN HANNA , MUKAI RENATA , MAGARET CRAIG A. , RHYNE RHONDA F. , JANUZZI JAMES 
Published: June 2019

Background: We previously developed a clinical/proteomics panel for predicting procedural acute kidney injury (AKI) and now examine its performance in those with diabetes (DM).
Methods: We measured 109 biomarkers in blood from patients undergoing coronary angiography. Procedural AKI defined as increase in serum creatinine ≥0.3 mg/dL, increase in serum creatinine of ≥50%, or documented oliguria ≤7 days after procedure. Clinical and biomarker predictors of AKI identified using least-angle regression; a final prognostic model was developed with LASSO; the model was then measured in those with DM.
Results: Besides DM, 5 predictors were in the final model: 3 (blood urea nitrogen to creatinine ratio, C-reactive protein and osteopontin) had positive association, while 2 (CD5 antigen-like and Factor VII) had negative association with AKI risk. Among 217 patients with DM, 18 (8.3%) developed AKI. The final model had an AUC of 0.87 for predicting procedural AKI (P&lt;0.001). The optimal score cut-off had 100% sensitivity and a negative predictive value (NPV) of 100% for procedural AKI.
Conclusions: We describe a clinical and proteomics-supported biomarker model with high sensitivity/NPV for AKI in patients with DM following coronary angiography.

Disclosure
N.E. Ibrahim: Other Relationship; Self; Novartis Pharmaceuticals Corporation. C.P. McCarthy: None. S. Shrestha: None. H. Gaggin: Other Relationship; Self; Dr. Gaggin has received research grant support from Roche Diagnostics, Jana Care, Ortho Clinical, Novartis; consulting income from Merck, Roche Diagnostics; research payments for clinical endpoint com. R. Mukai: None. C.A. Magaret: Consultant; Self; Prevencio. R.F. Rhyne: Board Member; Self; Prevencio. Employee; Self; Prevencio. Stock/Shareholder; Self; Prevencio. J. Januzzi: Consultant; Self; Abbott, Roche Diagnostic USA. Research Support; Self; Abbott, Prevencio, Quest Diagnostics, Roche Diagnostic USA.

Funding
Prevencio, Inc.
544-P: Efficacy and Safety of Insulin Degludec in Adults with T2D Macroalbuminuria and Chronic Kidney Disease Stage 2 and 3B
Authors: DE LUCAS MARIA DOLORES GARCIA , BUENO BEATRIZ AVILES , OLALLA JULIAN , LOPEZ-FERNANDEZ JUDITH 
Published: June 2019

This retrospective, observational study compared clinical outcomes of adults with T2D and chronic kidney disease (CKD) with macroalbuminuria switching from Gla-100/IDet/Gla-300 to IDeg. Endpoints were HbA1c change, hypoglycemia and units of insulin used (mean follow-up period, 36 months) in 90 patients. We established 2 groups: 46 patients with CKD stage 2 (CKD2) and 44 patients with CKD stage 3B (CKD3B). Hypoglycaemia was defined according to ADA criteria. The median age was significantly higher in the CKD3B (71.50±6.36 vs. 63.52±8.82 years). Average evolution of T2D was of 17 years in both. The CKD3B group had significantly more cardiovascular comorbidity (AMI, arteriopathy, hypertension, CHF) than CKD2. Initial basal insulin in both groups were detemir in 22.2%, glargine 100 in 60% and glargine 300 in 17.8% patients. A statistically significant improvement were observed in HbA1c (-1.71±0.25% in CKD2 and -1.28±1.17% in CKD3B p&lt;0,0001) and in basal glycaemia (p&lt;0.0001). Daily insulin basal dose decreased significantly in both groups at 36 months post-switch vs. pre-switch (p &lt;0.001 and p &lt;0.035 respectively). Hypoglycemia was significantly lower (81,3% to 34,2%, all p &lt;0.001) post-switch vs. pre-switch. Renal function remained stable with a decrease in albuminuria in both groups.
Conclusion: Degludec is effective, efficient and safe in renal patients with T2D and macroalbuminuria.

Disclosure
M. Garcia de Lucas: Speaker's Bureau; Spouse/Partner; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Janssen Pharmaceuticals, Inc., Lilly Diabetes, Merck Sharp & Dohme Corp., Novo Nordisk A/S, Sanofi. B. Aviles Bueno: Speaker's Bureau; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Janssen Pharmaceuticals, Inc., Novo Nordisk Inc. J. Olalla: None. J. Lopez-Fernandez: Consultant; Self; Lilly Diabetes, Sanofi. Other Relationship; Self; Almirall, S.A., Amgen Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., GEBRO, Janssen Pharmaceuticals, Inc., Lilly Diabetes, Merck Sharp & Dohme Corp., mundifarma, Novo Nordisk Inc., Sanofi.
548-P: Baicalin Attenuates Fibrosis Process in Human Renal Proximal Tubular Cells in Hyperglycemic Condition
Authors: NAM JUNGEUN , KIM JUNG HYE , PARK KAHUI , LEE SANG BAE , NAM JI SUN , PARK JONG SUK , PARK SU JEONG , KIM YU SIK , AHN CHUL WOO 
Published: June 2019

Background: Baicalin, isolated from Scutellaria baicalensis, has been reported to have anti-inflammatory effect by inhibiting expression of cell adhesion molecules and migration of leukocytes in vascular cells. However, there is a limited evidence on its anti-inflammatory effect in hyperglycemia-associated milieu in other cells. Hyperglycemia and its associated factors are known to induce diabetic nephropathy by exacerbating inflammation, especially, in proximal convoluted tubule. Herein, we investigated whether baicalin exerts anti-inflammatory and anti-fibrosis effects on human renal proximal tubular cells in hyperglycemia induced conditions.
Method: HK-2 cell was maintained in normal glycemic (5.78mM glucose) or in hyperglycemic (30mM glucose) condition with or without advanced glycation end-products (AGE) and tumor necrosis factor alpha (TNFα). In each condition, baicalin was treated at 10uM. Cell viability was determined by MTT assay. Gene and protein expression of multiple inflammatory and fibrosis markers including toll-like receptor 2 (TLR2), TLR4, fibronectin, collagen IV α1 (ColIVα1), collagen IV α2 (ColIVα2), transforming growth factor β (TGFβ), intercellular adhesion molecule 1 (ICAM1), and vascular adhesion molecule 1 (VCAM1) were evaluated by PCR and WB, respectively.
Results: Baicalin had no effect on cell viability. Baicalin significantly decreased gene expression of ColIVα2 in response to TNFα stimulation in normal glycemic condition (p=0.038). In hyperglycemic condition, baicalin decreased gene expressions of ICAM1 (p=0.049) and VCAM1 (p=0.049) significantly in AGE treated cells; and it significantly decreased gene expressions of TGFβ (p=0.038) and ICAM1 (p=0.017) in TNFα treated cells. Baicalin also decreased protein expression of ICAM1 in response to AGE (p=0.048) and TNFα (p=0.040) stimulation in hyperglycemic condition.
Conclusion: Baicalin attenuated fibrosis process by hyperglycemia associated factors in HK-2 cell.

Disclosure
J. Nam: None. J. Kim: None. K. Park: None. S. Lee: None. J. Nam: None. J. Park: None. S. Park: None. Y. Kim: None. C. Ahn: None.
550-P: Age at Diabetes Onset and Risk for Diabetic Kidney Disease
Authors: CARPENTIER CHARLYNE , DUBOIS SEVERINE , ABOULEKA YAWA , DULY-BOUHANICK BEATRICE , HADJADJ SAMY , COUTANT REGIS , ROUSSEL RONAN , VELHO GILBERTO , MARRE MICHEL 
Published: June 2019

Diabetic kidney disease drives premature mortality among patients with type 1 diabetes. The role of age at diabetes onset is controversial. We analyzed risk for diabetic kidney disease according to age at onset of type 1 diabetes using follow-up of type 1 diabetic patients attending our tertiary referral center. 340 type 1 diabetic patients attending the Angers University Hospital in France between 1989 and 2000, were followed-up to 2018 or death. They were divided in tertiles of ages at type 1 diabetes onset: T1:1-13, T2:14-23, and T3: 24-40 years. The primary endpoint was first occurrence of macroalbuminuria (&gt;300mg albumin/g creatinine), doubling of serum creatinine, estimated glomerular filtration rate (eGFR, CK-EPI formula) &lt;60ml/min/1.73m2, end stage renal disease (ESRD), or all-cause death. Multivariate analyses were done. Of 114 T1 participants, 11 (9.6%) developed macroalbuminuria, 5 (4.4%) doubling of serum creatinine, 14 (12.3%) eGFR&lt;60ml/min/1.73m2, 8 (7%) ESRD, and 14(12.3%) died. Of 119 T2 participants, 8 (.6.7%) developed macroalbuminuria, 1 (0.8%) doubling of serum creatinine, 7 (5.9%) eGFR&lt;60ml/min/1.73m2, 4(3.3%) ESRD, and 15(12.6%) died. Of 114 T3 participants, 3 (2.8%) developed macroalbuminuria, 1 (0.93%) doubling of serum creatinine, 4 (3.7%) eGFR&lt;60ml/min/1.73m2, none ESRD, and 31(29%) died. Using multivariate analysis, age&lt;14years at type 1 diabetes onset increased risk for kidney disease: T1 vs. T2 HR=2.35(95% CI1.20-4.58), T1 vs. T3 HR=3.61(1.30-9.27), p&lt;0.01.
Conclusions: Age &lt;14 at type 1 diabetes onset was an independent risk factor for kidney disease in this &gt;20-year monocentric follow-up study.

Disclosure
C. Carpentier: None. S. Dubois: None. Y. Abouleka: None. B. Duly-Bouhanick: Research Support; Self; Novo Nordisk A/S, Sanofi, Servier. S. Hadjadj: Consultant; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Merck & Co., Inc., Novo Nordisk A/S, Sanofi, Servier. Research Support; Self; Bayer AG, Janssen Research & Development. Speaker's Bureau; Self; Abbott, Valbiotis. R. Coutant: None. R. Roussel: Advisory Panel; Self; Merck Sharp & Dohme Corp., Sanofi. Consultant; Self; Abbott, AstraZeneca, Eli Lilly and Company, Medtronic, Novo Nordisk A/S, Physiogenex. Research Support; Self; Janssen Pharmaceuticals, Inc. G. Velho: None. M. Marre: Advisory Panel; Self; Servier. Board Member; Self; Merck Sharp & Dohme Corp., Novo Nordisk A/S.
568-P: Pain Threshold of Intraepidermal Nerve Terminal Reflects Small Nerve Fiber Function and Rises in Early Phase of Diabetes
Authors: SASAKI HIDEYUKI , KISHIMOTO SHOHEI , OGAWA KENICHI , KURISU SEIGO , NANJO KISHIO 
Published: June 2019

We measured pain threshold of intra-epidermal nerve terminal (PINT) which is a simple and noninvasive method that can measure pain threshold of A delta fiber by intra-epidermal electrical stimulation. We aimed to investigate normal value, prevalence of abnormality and clinically associated factors to PINT and quantitative vibratory perception threshold (QVT). PINT and QVT were measured by a portable peripheral nerve testing device PNS-7000, and a vibration sensation meter AU 02-B in 656 Japanese regional health checkup examinees (40-75 years old; years old). Glucose tolerance; normal (N), pre-DM, newly diagnosed DM (NDM) and known DM (KDM), and neuropathic findings (pain, paresthesia, numbness in legs and reduced ATRs) were also determined. Relationship between age, glucose tolerance, neuropathic findings and PINT or QVT were investigated by simple and multivariate analyses. In 445 non-DM subjects without neuropathic findings, normal limit value of PINT (mA) was set by quantile regression method, and relationship between prevalence of PINT or QVT abnormalities and clinical factors were examined. As results, PINT was not changed under 70 years old, then somewhat elevated. QVT elevated from 50 years old. PINT was not associated with QVT. PINT was significantly elevated in NDM and KDM. QVT was elevated in diabetes and hypertension. Among the neuropathic findings, PINT was significantly associated with only pain. By multiple regression analyses, significant aggravating factors of PINT were aging and glucose intolerance. Normal values of PINT were &gt; 0.4 (&lt;69 years old) and &gt;0.5 (70&lt; years old) Prevalence of PINT abnormality were 3%, 4%, 13% and 9% in N, pre-DM, NDM and KDM, respectively. They were significantly increased with the deterioration of glucose tolerance. QVT abnormality was not significantly increased with glucose intolerance.
In conclusion, PINT reflects small nerve fiber function, and associates with DM. So, PINT may be a useful for diagnosis and evaluation of small fiber neuropathy.

Disclosure
H. Sasaki: None. S. Kishimoto: None. K. Ogawa: None. S. Kurisu: None. K. Nanjo: None.

Funding
Japan Society for the Promotion of Science
581-P: Impacts of Glucose Fluctuation Management on Nerve Function in Type 2 Diabetes Patients with the First Episode of Cerebral Infarction
Authors: LI JIANING 
Published: June 2019

Objective: The purpose of this study was to assess the effects of glucose fluctuation management on nerve function (The National Institute of Health Stroke Scale, NIHSS), life ability (Modified Ranking Scale, MRS), and quality of life (Stroke Impact Scale, SIS) in type 2 diabetes patients with the first episode of cerebral infarction.
Methods: This was a randomized control trial. 75 type 2 diabetes patients with the first episode of cerebral infarction were randomized into 2 groups: control group (n=37) with usual care, focused on A1c control, targeting A1C &lt;7%, and intervention group (n=38), targeting both A1c &lt;7% and daily glucose fluctuation (LAGE &lt;80mg/dl).
Results: After 6 months, the data of 63 patients were finally analyzed (30 in the control group, 33 in the intervention group). There was no difference (P&gt;0.05) in the reduction of A1c between 2 groups, but the reductions of LAGE (P=0.030), 1,5-AG (P=0.023), 2hPG (p=0.041), and LDL(p=0.046) were significantly different between two groups. The NIHSS score in intervention group was better than in the control (2.35±0.81 vs. 3.50 ±2.24, p=0.047 group. In terms of quality of life, there was no significant difference in total score of SIS between the two groups, but in the intervention group, the scores in the strength, hand function, and participation dimensions were higher than those in the control group (P=0.041, P=0.049, P=0.048, respectively). No significant difference was identified between two groups in scores of MRS and SDSCA.
Conclusions: Blood glucose fluctuation management can add values to A1c management in improving nerve function for type 2 diabetes patients with first episode of cerebral infarction.

Disclosure
J. Li: None.
588-P: Diabetes Leads to Sodium-Glucose Cotransporter 2 (SGLT2) Increase in the Retina
Authors: LELEY SAMEER P. , LUO QIANYI , ALEX ALPHA L. , BHATWADEKAR ASHAY D. 
Published: June 2019

Introduction: Diabetes is the leading cause of microvascular disorders such as diabetic retinopathy (DR). There are no treatments for DR and finding new drug targets is of considerable interest. SGLT2 inhibitors, a newer class of antidiabetics are promising in the management of diabetes, however, the potential role of SGLT2 in diabetic retinal microvasculature remains unknown. We hypothesized that diabetes will lead to an increase in SGLT2 in the retina and that its inhibition will be beneficial in protecting retinal vasculature from the insult of diabetes milieu.
Methods: The retinal sections of diabetic (db/db; an animal model of type 2 diabetes) and control (db/m) mice were analyzed for SGLT2 expression using confocal microscopy. In parallel, the mRNA levels of SGLT2 were determined using qRT-PCR. Human retinal endothelial cells (HRECs) were treated with the SGLT2 inhibitor dapagliflozin (0.1, 1, 10 nM) to perform a glucose uptake assay and to determine its effects on mRNA levels of SGLT2.
Results: The mRNA levels of SGLT2 were significantly higher (p&lt;0.05) in the retina of db/db mice, 1.1 ± 0.46, n=5, when compared to db/m retinas, 0.06 ± 0.02, n=4. The confocal microscopy revealed SGLT2 expression throughout the retina and around the retinal blood vessels, brighter fluorescence was observed in the db/db retina. Treatment of HRECs with 10 nM dapagliflozin led to a significant decrease in SGLT2 mRNA (p&lt;0.05); dapagliflozin: 7.95 ± 4.7, n=4; vehicle: 26 ± 3.6, n=8. The dapagliflozin inhibition demonstrated a profound decrease in glucose uptake in HRECs at all concentrations. Untreated: 2012 ± 388, n=3; 0.1 nM: 545.7 ± 296, 1 nM: 358.2 ± 241.5, 10 nM: 70.67 ± 138.9; p&lt;0.01 as compared to untreated; n=6.
Conclusion: Our studies suggest that SGLT2 is significantly upregulated in the retina during diabetes and that SGLT2 potentially plays a critical role in retinal glucose transport. In future, SGLT2 inhibition could be a useful treatment option to slow down or prevent the onset of diabetic retinopathy.

Disclosure
S.P. Leley: None. Q. Luo: None. A.L. Alex: None. A.D. Bhatwadekar: None.

Funding
National Eye Institute; Indiana University Center for Diabetes and Metabolic Diseases