scholarly journals XOR - Possible Correlations with Oxidative Stress and Inflammation Markers in the Context of Diabetic Kidney Disease

2019 ◽  
Vol 70 (4) ◽  
pp. 1396-1398 ◽  
Author(s):  
Alexandra Totan ◽  
Andra-Elena Balcangiu-Stroescu ◽  
Marina Melescanu Imre ◽  
Daniela Miricescu ◽  
Daniela Balan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Microvascular Complications ◽  
Serum Levels ◽  
Control Group ◽  
Diabetic Patients ◽  
Inflammation Markers ◽  
Diabetic Kidney ◽  
Diabetic Microvascular Complications

Xanthine oxidoreductase (XOR) activity plays an important role as a pivotal source of reactive oxygen species. The aim of our study was to investigate possible correlations of XOR serum levels with oxidative stress (total antioxidant capacity - TAC, anti-oxidative stress responsive 1 antibody - OXSR1) and inflammation markers (interleukin 6 - IL-6), in 20 hemodialysis diabetic patients. The present study included the hemodialysis diabetic patients group (10 males and 10 females) and the control group (20 healthy volunteers). For serum XOR (ng/mL), TAC (U/mL) and OXSR1 (ng/ml) measurements we have used the ELISA technique. Serum IL6 (pg/mL) was performed using an automatic immunoassay system (Immulite 1000, Siemens- Germany). Comparing the two groups, our results revealed significantly increased serum levels for XOR (6.2�1.5 / 3.9�1.1); OXSR1 (11.3�2.9 / 6.2�2.1) and IL6 (7.0�1.2 / 5.0�0.4). Patients� serum levels of TAC were significantly decreased compared with the control group values (25.2�3.9 / 33.5�2.8). It becomes more and more obvious that oxidative stress is an important element initiating diabetic microvascular complications, including diabetic kidney disease. Our results suggested that XOR should be regarded as an important target in the attempt to reduce oxidative stress in the context of diabetic kidney disease.

MO580HYPOPROTEIC DIET SUPPLEMENTED WITH KETOANALOGUES IN PATIENTS WITH ADVANCED DIABETIC KIDNEY DISEASE – EFFECTS ON MINERAL BONE DISORDERS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Liliana Garneata ◽  
Carmen-Antonia Mocanu ◽  
Tudor Petrisor Simionescu ◽  
Andreea Elena Mocanu ◽  
Gabriel Mircescu
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Serum Levels ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Diabetic Patients ◽  
Bone Disorders ◽  
Diabetic Kidney ◽  
Low Protein ◽  
Ckd Stage

Abstract Background and Aims Dietary protein restriction is rediscussed as mainstay approach in advanced Chronic Kidney Disease (CKD), both in diabetics and non-diabetics to defer renal replacement therapy (RRT), mainly by better metabolic control; improvements in mineral bone disorders (MBD) were also suggested, but less studied in Diabetic Kidney Disease (DKD). An unicentric prospective interventional trial aimed to assess the effects of ketoanalogue-supplemented low protein diet (sLPD) on proteinuria and CKD progression (data already presented). The parameters of MBD were also evaluated. Method Adult diabetic patients (452) with stable CKD stage 4+, proteinuria>3g/g creatininuria and SGA A were enrolled in a run-in phase (3 mo), with LPD (0.6g/kg dry ideal bw). Those who proved adherent (92, 64% males, median age 55.7 yrs, 65% on insulin) received sLPD (Ketosteril®, 1 tablet/10kg) for 12mo. Monitoring and treatment followed the Best Practice Guidelines. The primary endpoint was proteinuria during intervention as compared to pre-enrolment. Serum levels of calcium, phosphates and iPTH were considered to assess MBD. Nutrition, inflammation (SGA, BMI, serum albumin, CRP) and compliance were safety parameters. Results In patients with advanced DKD and severe proteinuria, sLPD was associated with a 69 (63; 82) % reduction in proteinuria (data presented). Significant amelioration in MBD was noted: serum levels of calcium and phosphates were significantly ameliorated at the end of the study as compared to enrolment - 4.3 (4.2-4.9) vs 3.2 (3.1-3.5) mg/dL and 5.4 (4.9-6.1) vs 8.2 (7.8-8.9) mg/dL, respectively. Serum iPTH significantly decreased: 185 (168-212) vs 375 (354-585) pg/mL. The need for calcium supplementation decreased: 6.5 (6.0-6.7) vs 7.0 (6.8-7.3) g/day. Vitamin D was required by only 35% vs 65% of patients. Nutritional status was preserved and dietary compliance was very good throughout the study. Conclusion In patients with advanced DKD ketoanalogue supplemented low protein diet seems to be effective and safe as part of MBD management.

scholarly journals Is there a relationship between the prevalence of autoimmune thyroid disease and diabetic kidney disease?

2021 ◽  
Vol 16 (1) ◽  
pp. 611-619
Author(s):  
Magdalena Maria Stefanowicz-Rutkowska ◽  
Wojciech Matuszewski ◽  
Katarzyna Gontarz-Nowak ◽  
Elżbieta Maria Bandurska-Stankiewicz
Keyword(s):  
Diabetes Mellitus ◽  
Kidney Disease ◽  
Thyroid Disease ◽  
Autoimmune Thyroid Disease ◽  
Diabetic Kidney Disease ◽  
Microvascular Complications ◽  
Control Group ◽  
Anthropometric Parameters ◽  
Diabetic Kidney ◽  
Autoimmune Thyroid

Abstract Autoimmune thyroid disease (AITD) is more common among diabetes mellitus (DM) patients and may impact its microvascular complications. The present study aimed to assess the relationship between AITD and the prevalence of diabetic kidney disease (DKD) in patients with diabetes mellitus type 1 (DM1). Anthropometric parameters, parameters of metabolic control of DM, thyreometabolic status, and the UACR were assessed. DKD was diagnosed if patients’ UACR level was ≥30 mg/g or eGFR level was <60 mL/min. This study involved 144 patients with DM1 aged 36.2 ± 11.7 years: 49 men and 95 women. Significant differences in creatinine, eGFR, and UACR levels were found in patients with DKD. fT3 concentration was significantly lower among DKD patients. A significantly higher probability of DKD was found in DM1 patients with lower fT3 levels. Patients with DM1 and AITD had significantly lower creatinine levels than the control group. However, the study did not show any significant relationship between AITD and the occurrence of DKD in patients with DM1. Significantly lower fT3 concentrations in DKD patients may be caused by metabolic disorders in the course of DKD and require further cohort studies in a larger population of patients with DM1 and AITD.

Elevated Serum Levels of Carbohydrate Antigen 72–4 in Diabetic Kidney Disease

2021 ◽  
Author(s):  
Lei Shi ◽  
Jiali Meng ◽  
Bin Zhang ◽  
Jiandong Chen ◽  
Jianzhong Chen ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Elevated Serum ◽  
Serum Levels ◽  
Carbohydrate Antigen ◽  
Urinary Albumin ◽  
Renal Diseases ◽  
Diabetic Patients ◽  
Healthy Controls ◽  
Diabetic Kidney

AbstractThe aim of this study was to determine whether carbohydrate antigen 72–4 (CA72–4) is elevated in diabetic kidney disease (DKD), and examine the association between urinary albumin-to-creatinine ratio (UACR) and CA72–4 in patients with type 2 diabetes mellitus (T2DM). Non-dialysis patients with T2DM (n=296) and 90 healthy controls were recruited in this study. CA72–4 level was measured by electrochemiluminescence immunoassay. DKD was defined as UACR≥ 30 mg/g in the absence of a urinary infection or other renal diseases. We found that patients with DKD had significantly higher serum CA72–4 levels compared to those with normoalbuminuria and healthy controls. Positive rates of CA72–4 increased gradually and markedly from normoalbuminuria to microalbuminuria and to macroalbuminuria in diabetic patients (7.5, 11.2, and 17.4%, respectively; P for trend< 0.05). CA72–4 also showed a positive correlation with UACR (r=0.288, P< 0.01). Logistic regression analysis revealed the association of increased UACR with an increased odds ratio of elevation of CA72–4 levels (P for trend< 0.05) after multivariable adjustment. In conclusion, serum levels of CA72–4 increase abnormally with the increase in urinary albumin excretion, which affects the specificity of diagnosis of malignancies. An appropriate interpretation of CA72–4 is essential to prevent unnecessary and even hazardous diagnostic procedures in patients with T2DM.

scholarly journals Adiponectin level in diabetic kidney disease the relationship with glycemic control and microvascular complications; a mystery unresolved

2018 ◽  
Vol 6 (1) ◽  
pp. 18
Author(s):  
Effat A. E. Tony ◽  
Mohamed H.Mostafa ◽  
Refaat F. Abdelaal ◽  
Abeer A. Tony ◽  
Tahra El- Shereif ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Therapeutic Potential ◽  
Microvascular Complications ◽  
Multivariate Logistic Regression Analysis ◽  
Vascular Complications ◽  
Predictive Biomarkers ◽  
Therapeutic Interventions ◽  
Diabetic Patients ◽  
Diabetic Kidney

Background: Defining new predictive biomarkers in diabetic kidney disease (DKD) would provide a window of opportunity for preventive and/or therapeutic interventions to prevent or delay the onset of irreversible long-term micro and or macro vascular complications. Adiponectin (ADPN) has been variously associated with diabetic microvascular complications; however, no comprehensive clinical data exist examining the association between adipocytokines and the presence of these complications.Aim of study: we aimed to measure the plasma levels of adiponectin in patients with type 2 diabetes mellitus, to assess whether these levels vary with the different stages of DKD according to their e GFR and to evaluate its relation to their microvascular complications and glycemic control.Methods: This is a prospective observational study including 100 T2DM classified into two groups according to their albuminuria levels and estimated GFR. Participants subjected to thorough history taking and clinical examination. Serum level of ADPN was assessed in all patients.Results: Serum ADPN levels were significantly lower in T2DM patients with nephropathy (P = 0.001), while their levels were non-significantly higher in patients with non-proliferative retinopathy or neuropathy. Their levels were lowered with more advanced stages of DKD with nephropathy and the decrement was dependent on their severity (P<0.001). Levels of ADPN with cutoff value of < 22600 (μg/mL) had ability to diagnose microvascular complications in our diabetic patients with sensitivity (81%) and specificity (27%). Multivariate logistic regression analysis showed that the odds ratio for the presence of nephropathy in the lowest tertile of ADPN was 1.09 (95% CI; 11.45- 13.08, P= 0.06), therefore, ADPN was not an independent risk factor for diabetic nephropathy. However, its higher level was independently associated with increased odds for the presence of neuropathy in particular. Conclusions: ADPN plays a role in the pathogenesis of microvasculopathy in diabetic patients and help to identify high-risk patients and modulate the therapeutic potential in the prevention of DKD.  

Hypoadiponectinemia is associated with aortic stiffness in nondialysis diabetic patients with stage 3–5 chronic kidney disease

Vascular ◽  
2021 ◽  
pp. 170853812110076
Author(s):  
Ssu-Chin Lin ◽  
Tsung-Jui Wu ◽  
Du-An Wu ◽  
Bang-Gee Hsu
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Aortic Stiffness ◽  
Diabetic Kidney Disease ◽  
Applanation Tonometry ◽  
Serum Adiponectin ◽  
Control Group ◽  
Multivariable Logistic Regression Analysis ◽  
Diabetic Patients ◽  
Diabetic Kidney

Objectives Albuminuria and serum adiponectin levels are factors that have been associated with the development of cardiovascular disease in patients with diabetes mellitus. Here we investigated the relationship between serum adiponectin levels and aortic stiffness in nondialysis diabetic kidney disease patients with stage 3–5 chronic kidney disease. Methods Fasting blood samples were obtained from 80 nondialysis diabetic kidney disease patients with stage 3–5 chronic kidney disease. Carotid-femoral pulse wave velocity (cfPWV) was measured using applanation tonometry; cfPWV values of >10 m/s were defined as aortic stiffness. Serum adiponectin levels were determined by enzyme immunoassay. Results Forty-two patients (52.5%) with nondialysis diabetic kidney disease were diagnosed with aortic stiffness. The patients in this group were older ( p =  0.011), had higher systolic blood pressure ( p =  0.002) and urine albumin-to-creatinine ratios ( p =  0.013), included fewer females ( p =  0.024), and had lower serum adiponectin ( p =  0.001) levels than those in the control group. Multivariable logistic regression analysis revealed that serum adiponectin was independently associated with aortic stiffness (odds ratio = 0.930, 95% confidence interval: 0.884–0.978, p =  0.005) and also positively correlated with cfPWV values by multivariable linear regression ( β = –0.309, p =  0.002) in nondialysis diabetic kidney disease patients. Conclusions The results suggested that serum adiponectin levels could be used to predict aortic stiffness in nondialysis diabetic kidney disease patients with stage 3–5 chronic kidney disease.

539-P: The Trend of Diabetic Kidney Disease with Low eGFR and Absence of Albuminuria in Type 2 Diabetic Patients in Japan from 1996-2015

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 539-P
Author(s):  
YOSHINORI KAKUTANI ◽  
MASANORI EMOTO ◽  
KATSUHITO MORI ◽  
YUKO YAMAZAKI ◽  
AKINOBU OCHI ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Diabetic Kidney ◽  
Type 2 Diabetic

scholarly journals Metabolic Changes and Oxidative Stress in Diabetic Kidney Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1143
Author(s):  
Midori Sakashita ◽  
Tetsuhiro Tanaka ◽  
Reiko Inagi
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Stress Responses ◽  
Diabetic Kidney Disease ◽  
Renin Angiotensin System ◽  
Therapeutic Agents ◽  
Metabolic Changes ◽  
Diabetic Kidney ◽  
Glucose Levels ◽  
Patients With Diabetes

Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease, and it is crucial to understand the pathophysiology of DKD. The control of blood glucose levels by various glucose-lowering drugs, the common use of inhibitors of the renin–angiotensin system, and the aging of patients with diabetes can alter the disease course of DKD. Moreover, metabolic changes and associated atherosclerosis play a major role in the etiology of DKD. The pathophysiology of DKD is largely attributed to the disruption of various cellular stress responses due to metabolic changes, especially an increase in oxidative stress. Therefore, many antioxidants have been studied as therapeutic agents. Recently, it has been found that NRF2, a master regulator of oxidative stress, plays a major role in the pathogenesis of DKD and bardoxolone methyl, an activator of NRF2, has attracted attention as a drug that increases the estimated glomerular filtration rate in patients with DKD. This review outlines the altered stress responses of cellular organelles in DKD, their involvement in the pathogenesis of DKD, and discusses strategies for developing therapeutic agents, especially bardoxolone methyl.

N6 -(2-hydroxyethyl)-adenosine from Cordyceps cicadae protects against diabetic kidney disease via alleviation of oxidative stress and inflammation

2018 ◽  
Vol 43 (2) ◽  
pp. e12727 ◽  
Author(s):  
Xiaohong Wang ◽  
Aiqiong Qin ◽  
Fang Xiao ◽  
Opeyemi J. Olatunji ◽  
Shuyuan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Diabetic Kidney ◽  
Cordyceps Cicadae

scholarly journals Sulodexide Protects Renal Tubular Epithelial Cells from Oxidative Stress-Induced Injury via Upregulating Klotho Expression at an Early Stage of Diabetic Kidney Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yu Ning Liu ◽  
Jingwei Zhou ◽  
Tingting Li ◽  
Jing Wu ◽  
Shu Hua Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Epithelial Cells ◽  
Diabetic Kidney Disease ◽  
Early Stage ◽  
Collaborative Study ◽  
Oxidative Activity ◽  
Dependent Manner ◽  
Diabetic Kidney ◽  
Collaborative Study Group

The hypoalbuminuric effect of sulodexide (SDX) on diabetic kidney disease (DKD) was suggested by some clinical trials but was denied by the Collaborative Study Group. In this study, the diabetic rats were treated with SDX either from week 0 to 24 or from week 13 to 24. We found that 24-week treatment significantly decreased the urinary protein and HAVCR1 excretion, inhibited the interstitial expansion, and downregulated the renal cell apoptosis and interstitial fibrosis. Renoprotection was also associated with a reduction in renocortical/urinary oxidative activity and the normalization of renal klotho expression. However, all of these actions were not observed when SDX was administered only at the late stage of diabetic nephropathy (from week 13 to 24). In vitro, advanced glycation end products (AGEs) dose-dependently enhanced the oxidative activity but lowered the klotho expression in cultured proximal tubule epithelial cells (PTECs). Also, H2O2 could downregulate the expression of klotho in a dose-dependent manner. However, overexpression of klotho reduced the HAVCR1 production and the cellular apoptosis level induced by AGEs or H2O2. Our study suggests that SDX may prevent the progression of DKD at the early stage by upregulating renal klotho expression, which inhibits the tubulointerstitial injury induced by oxidative stress.

scholarly journals Diabetic Kidney Disease in Childhood and Adolescence: Conventional and Novel Renoprotective Strategies

2020 ◽  
pp. 68-77
Author(s):  
Samuel N Uwaezuoke ◽  
Adaeze C Ayuk
Keyword(s):  
Diabetes Mellitus ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Microvascular Complications ◽  
Clinical Syndrome ◽  
Clinical Staging ◽  
Childhood And Adolescence ◽  
Diabetic Kidney ◽  
Haemodynamic Changes ◽  
End Stage

Diabetic kidney disease (DKD) is defined as a clinical syndrome consisting of persistent macroalbuminuria, progressive decline in glomerular filtration rate (GFR), hypertension, increased cardiovascular disease events, and the associated mortality of these conditions. The disease evolves from the microvascular complications of poorly controlled Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM). The pathogenic pathways comprise renal haemodynamic changes, ischaemia and inflammation, and overactive renin–angiotensin–aldosterone system (RAAS), through which several events cascade down from hyperglycaemia to renal fibrosis. Conventional and novel renoprotective strategies target modifiable DKD risk factors and specific stages of the pathogenic pathways, respectively. Although these strategies may slow DKD progression to end-stage kidney disease (ESKD), novel drugs are still undergoing trials for validation in human participants. This narrative review appraises these renoprotective strategies and highlights the current clinical staging and pathogenesis of the disease.

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