Abstract 209: NAD(P)H Oxidase-Derived Superoxide Contributes to Impaired Cutaneous Microvascular Function in Chronic Kidney Disease

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Jennifer J DuPont ◽  
Meghan G Ramick ◽  
William B Farquhar ◽  
Raymond R Townsend ◽  
David G Edwards
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Xanthine Oxidase ◽  
Local Heating ◽  
Control Site ◽  
Healthy Control Group ◽  
Control Group ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Healthy Control

Endothelial dysfunction occurs in chronic kidney disease (CKD) and cardiovascular disease is the most common cause of death in these patients. Oxidative stress has been shown to be a mechanism of vascular dysfunction in CKD. We utilized the cutaneous circulation to test the hypothesis that superoxide derived from NAD(P)H oxidase and xanthine oxidase impair nitric oxide (NO)-dependent cutaneous vasodilation patients with CKD. Twenty subjects, 10 stage 3 and 4 CKD patients (61±4 years; 5 male/5 female; eGFR: 39 ± 4 ml·min -1 ·1.73m -2 ) and 10 healthy controls (HC) (55±2 years; 4 male/6 female; eGFR: >60 ml·min -1 ·1.73m -2 ) were instrumented with 4 intradermal microdialysis fibers in the forearm for the local delivery of 1) Ringers solution (Control), 2) 10 μM Tempol to scavenge superoxide, 3) 100 μM apocynin to inhibit NAD(P)H oxidase, and 4) 10 μM allopurinol to inhibit xanthine oxidase. Red blood cell (RBC) flux was measured via laser Doppler flowmetry during standardized local heating (42°C). After the local heating response was established, 10 mM L-NAME was infused into all four sites to quantify the NO-dependent portion of the response. Cutaneous vascular conductance (CVC) was calculated as RBC flux/mean arterial pressure and all data are presented as a percentage of maximum CVC achieved during 28mM sodium nitroprusside infusion at 43°C. The plateau in cutaneous vasodilation was attenuated in CKD at the control site (CKD: 77±3 vs. HC: 88±3 %, p<0.05). Tempol and apocynin augmented the plateau in cutaneous vasodilation in CKD patients (Tempol: 88±2, apocynin: 91±2 %, p<0.05 vs. CKD control site) but had no effect in the healthy control group. The NO-dependent portion of the response was reduced in CKD at the control site (CKD: 41±4 vs. HC: 58±2 %, p<0.05). Tempol and apocynin augmented NO-dependent portion of the response in CKD patients (Tempol: 58±3, apocynin: 58±4 %, p<0.05 vs. CKD control site) but had no effect in the healthy control group. Inhibition of xanthine oxidase did not alter the plateau in cutaneous vasodilation in either group (p>0.05). These data suggest that NAD(P)H oxidase is a source of superoxide and contributes to microvascular dysfunction in CKD.

scholarly journals NADPH oxidase-derived reactive oxygen species contribute to impaired cutaneous microvascular function in chronic kidney disease

2014 ◽  
Vol 306 (12) ◽  
pp. F1499-F1506 ◽  
Author(s):  
Jennifer J. DuPont ◽  
Meghan G. Ramick ◽  
William B. Farquhar ◽  
Raymond R. Townsend ◽  
David G. Edwards
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Nadph Oxidase ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Oxidase Inhibition

Oxidative stress promotes vascular dysfunction in chronic kidney disease (CKD). We utilized the cutaneous circulation to test the hypothesis that reactive oxygen species derived from NADPH oxidase and xanthine oxidase impair nitric oxide (NO)-dependent cutaneous vasodilation in CKD. Twenty subjects, 10 stage 3 and 4 patients with CKD (61 ± 4 yr; 5 men/5 women; eGFR: 39 ± 4 ml·min−1·1.73 m−2) and 10 healthy controls (55 ± 2 yr; 4 men/6 women; eGFR: >60 ml·min−1·1.73 m−2) were instrumented with 4 intradermal microdialysis fibers for the delivery of 1) Ringer solution (Control), 2) 10 μM tempol (scavenge superoxide), 3) 100 μM apocynin (NAD(P)H oxidase inhibition), and 4) 10 μM allopurinol (xanthine oxidase inhibition). Skin blood flow was measured via laser-Doppler flowmetry during standardized local heating (42°C). Ng-nitro-l-arginine methyl ester (l-NAME; 10 mM) was infused to quantify the NO-dependent portion of the response. Cutaneous vascular conductance (CVC) was calculated as a percentage of the maximum CVC achieved during sodium nitroprusside infusion at 43°C. Cutaneous vasodilation was attenuated in patients with CKD (77 ± 3 vs. 88 ± 3%, P = 0.01), but augmented with tempol and apocynin (tempol: 88 ± 2 ( P = 0.03), apocynin: 91 ± 2% ( P = 0.001). The NO-dependent portion of the response was reduced in patients with CKD (41 ± 4 vs. 58 ± 2%, P = 0.04), but improved with tempol and apocynin (tempol: 58 ± 3 ( P = 0.03), apocynin: 58 ± 4% ( P = 0.03). Inhibition of xanthine oxidase did not alter cutaneous vasodilation in either group ( P > 0.05). These data suggest that NAD(P)H oxidase is a source of reactive oxygen species and contributes to microvascular dysfunction in patients with CKD.

scholarly journals Ascorbic acid or l-arginine improves cutaneous microvascular function in chronic kidney disease

2011 ◽  
Vol 111 (6) ◽  
pp. 1561-1567 ◽  
Author(s):  
Jennifer J. DuPont ◽  
William B. Farquhar ◽  
Raymond R. Townsend ◽  
David G. Edwards
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Ascorbic Acid ◽  
Kidney Disease ◽  
Local Heating ◽  
Microvascular Function ◽  
Doppler Flowmetry ◽  
Healthy Control ◽  
Cutaneous Vascular Conductance ◽  
Initial Peak

We sought to determine whether oxidative stress or a relative deficit of l-arginine plays a role in reducing cutaneous vasodilation in response to local heating in chronic kidney disease (CKD). Eight patients with stage 3–4 CKD and eight age- and sex-matched healthy control (HC) subjects were instrumented with four microdialysis (MD) fibers for the local delivery of 1) Ringers solution (R), 2) 20 mM ascorbic acid (AA), 3) 10 mM l-arginine (l-Arg), and 4) 10 mM NG-nitro-l-arginine methyl ester (l-NAME). Red blood cell (RBC) flux was measured via laser Doppler flowmetry. A standardized nonpainful local heating protocol (42°C) was used. Cutaneous vascular conductance (CVC) was calculated as RBC flux/MAP and all data were expressed as a percentage of the maximum CVC at each site (28 mM sodium nitroprusside, Tloc = 43°C). The plateau %CVCmax was attenuated in CKD (CKD: 76 ± 4 vs. HC: 91 ± 2%CVCmax; P < 0.05) and the NO contribution to the plateau was lower in CKD (CKD: 39 ± 7, HC: 54 ± 5; P < 0.05). The plateau %CVCmax in the CKD group was significantly greater at the AA and l-Arg sites compared with R (AA: 89 ± 2; l-Arg: 90 ± 1; R: 76 ± 4; P < 0.05) and did not differ from HC. Initial peak %CVCmax was also significantly attenuated at the R and l-Arg sites in CKD ( P < 0.05) but did not differ at the AA site. These results suggest that cutaneous microvascular function is impaired in stage 3–4 CKD and that oxidative stress and a deficit of l-arginine play a role in this impairment.

scholarly journals Evaluating the Serum Transforming Growth Factor-Beta 1 Level in Chronic Kidney Disease Caused by Glomerulonephritis

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Tuan Van Nguyen ◽  
Ky Duc Ngo ◽  
Minh Hoang Thi ◽  
Lan Thi Phuong Dam ◽  
Thuan Quang Huynh
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Healthy Control Group ◽  
Control Group ◽  
Healthy Control ◽  
Growth Factor Beta ◽  
Tgf Β1

Background: The transforming growth factor-beta 1 (TGF-β1) has been demonstrated as one of the main factors in the progression of fibrosis and sclerosis glomerular damages. Glomerulonephritis is one common cause of chronic kidney disease (CKD) with the promotion of inflammatory renal damage containing fibrosis and sclerosis glomerular. Objectives: This study aimed to evaluate the TGF-β1 level in CKD patients and compare it with the healthy control group. Methods: This cross-sectional case-control study was carried out on 212 subjects admitted to the Nghe An Friendship General Hospital in Vietnam from March 2018 to February 2020. The case group included 152 patients diagnosed with CKD caused by glomerulonephritis, and the control group included 60 healthy individuals. The TGF-β1 was determined in serum by ELISA method. Results: The serum TGF-β1 concentration of the healthy control group and CKD group was 13.45 ± 7.17 and 32.35 ± 11.74, respectively. The CKD group had a significantly higher TGF-β1 level than the control group (P < 0.05). The CKD group with the eGRP ≥ 60 mL/min/1.73 m2 group had a higher TGF-β1 level than the eGRP < 60 mL/min/1.73 m2 group, and the TGF-β1 level increased from stage 1 to stage 5 (P < 0.001). The TGF-β1 had a medium correlation to urea, creatinine, and hs-CRP. Conclusions: The concentration of TGF-β1 in the CKD group was higher than the control group so that it increased early from the first stage of the disease.

scholarly journals Role of mitochondria-derived reactive oxygen species in microvascular dysfunction in chronic kidney disease

2018 ◽  
Vol 314 (3) ◽  
pp. F423-F429 ◽  
Author(s):  
Danielle L. Kirkman ◽  
Bryce J. Muth ◽  
Meghan G. Ramick ◽  
Raymond R. Townsend ◽  
David G. Edwards
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Local Heating ◽  
Reactive Oxygen ◽  
Microvascular Dysfunction ◽  
Healthy Controls ◽  
Oxygen Species ◽  
Cutaneous Vasodilation

Cardiovascular disease is the leading cause of mortality in chronic kidney disease (CKD). Mitochondrial dysfunction secondary to CKD is a potential source of oxidative stress that may impair vascular function. This study sought to determine if mitochondria-derived reactive oxygen species contribute to microvascular dysfunction in stage 3–5 CKD. Cutaneous vasodilation in response to local heating was assessed in 20 CKD patients [60 ± 13 yr; estimated glomerular filtration rate (eGFR) 46 ± 13 ml·kg−1·1.73 m−2] and 11 matched healthy participants (58 ± 2 yr; eGFR >90 ml·kg−1·1.73 m−2). Participants were instrumented with two microdialysis fibers for the delivery of 1) Ringer solution, and 2) the mitochondria- specific superoxide scavenger MitoTempo. Skin blood flow was measured via laser Doppler flowmetry during standardized local heating (42°C). Cutaneous vascular conductance (CVC) was calculated as a percentage of the maximum conductance achieved with sodium nitroprusside infusion at 43°C. Urinary isofuran/F2-isoprostane ratios were assessed by gas-chromatography mass spectroscopy. Isofuran-to-F2-isoprostane ratios were increased in CKD patients (3.08 ± 0.32 vs. 1.69 ± 0.12 arbitrary units; P < 0.01) indicative of mitochondria-derived oxidative stress. Cutaneous vasodilation was impaired in CKD compared with healthy controls (87 ± 1 vs. 92 ± 1%CVCmax; P < 0.01). Infusion of MitoTempo significantly increased the plateau phase CVC in CKD patients (CKD Ringer vs. CKD MitoTempo: 87 ± 1 vs. 93 ± 1%CVCmax; P < 0.01) to similar levels observed in healthy controls ( P = 0.9). These data provide in vivo evidence that mitochondria-derived reactive oxygen species contribute to microvascular dysfunction in CKD and suggest that mitochondrial dysfunction may be a potential therapeutic target to improve CKD-related vascular dysfunction.

Local ascorbate administration augments NO- and non-NO-dependent reflex cutaneous vasodilation in hypertensive humans

2007 ◽  
Vol 293 (2) ◽  
pp. H1090-H1096 ◽  
Author(s):  
Lacy A. Holowatz ◽  
W. Larry Kenney
Keyword(s):  
Local Heating ◽  
Oxidant Stress ◽  
Control Site ◽  
No Synthase ◽  
Oral Temperature ◽  
Antioxidant Supplementation ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Reflex Cutaneous Vasodilation ◽  
Cutaneous Vascular Conductance

Full expression of reflex cutaneous vasodilation (VD) is dependent on nitric oxide (NO) and is attenuated with essential hypertension. Decreased NO-dependent VD may be due to 1) increased oxidant stress and/or 2) decreased l-arginine availability through upregulated arginase activity, potentially leading to increased superoxide production through uncoupled NO synthase (NOS). The purpose of this study was to determine the effect of antioxidant supplementation (alone and combined with arginase inhibition) on attenuated NO-dependent reflex cutaneous VD in hypertensive subjects. Nine unmedicated hypertensive [HT; mean arterial pressure (MAP) = 112 ± 1 mmHg] and nine age-matched normotensive (NT; MAP = 81 ± 10 mmHg) men and women were instrumented with four intradermal microdialysis (MD) fibers: control (Ringer), NOS inhibited (NOS-I; 10 mM NG-nitro-l-arginine), l-ascorbate supplemented (Asc; 10 mM l-ascorbate), and Asc + arginase inhibited [Asc+A-I; 10 mM l-ascorbate + 5 mM ( S)-(2-boronoethyl)-l-cysteine-HCl + 5 mM Nω-hydroxy- nor-l-arginine]. Oral temperature was increased by 0.8°C via a water-perfused suit. NG-nitro-l-arginine was then ultimately perfused through all MD sites to quantify the change in VD due to NO. Red blood cell flux was measured by laser-Doppler flowmetry over each skin MD site, and cutaneous vascular conductance (CVC) was calculated (CVC = flux/MAP) and normalized to maximal CVC (%CVCmax; 28 mM sodium nitroprusside + local heating to 43°C). During the plateau in skin blood flow (ΔTor = 0.8°C), cutaneous VD was attenuated in HT skin (NT: 42 ± 4, HT: 35 ± 3 %CVCmax; P < 0.05). Asc and Asc+A-I augmented cutaneous VD in HT (Asc: 57 ± 5, Asc+A-I: 53 ± 6 %CVCmax; P < 0.05 vs. control) but not in NT. %CVCmax after NOS-I in the Asc- and Asc+A-I-treated sites was increased in HT (Asc: 41 ± 4, Asc+A-I: 40 ± 4, control: 29 ± 4; P < 0.05). Compared with the control site, the change in %CVCmax within each site after NOS-I was greater in HT (Asc: −19 ± 4, Asc+A-I: −17 ± 4, control: −9 ± 2; P < 0.05) than in NT. Antioxidant supplementation alone or combined with arginase inhibition augments attenuated reflex cutaneous VD in hypertensive skin through NO- and non-NO-dependent mechanisms.

scholarly journals Oral clopidogrel improves cutaneous microvascular function through EDHF-dependent mechanisms in middle-aged humans

2013 ◽  
Vol 305 (4) ◽  
pp. R452-R458 ◽  
Author(s):  
Jessica D. Dahmus ◽  
Rebecca S. Bruning ◽  
W. Larry Kenney ◽  
Lacy M. Alexander
Keyword(s):  
Local Heating ◽  
Reactive Hyperemia ◽  
Area Under The Curve ◽  
Control Site ◽  
Microvascular Function ◽  
Sensory Nerves ◽  
Controlled Study ◽  
Double Blind ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation

Platelet P2Y12-ADP and COX-1 receptor inhibition with oral clopidogrel (CLO) and low-dose aspirin (ASA), respectively, attenuates reflex-mediated cutaneous vasodilation, but little is known about how these medications affect local vasodilatory signaling. Reactive hyperemia (RH) results in vasodilation that is mediated by sensory nerves and endothelium-derived hyperpolarization factors (EDHF) through large-conductance calcium-activated potassium channels, whereas slow local heating (LH) elicits vasodilation largely through the production of nitric oxide (NO). We hypothesized that CLO and ASA would attenuate locally mediated cutaneous vasodilation assessed by RH and LH (0.5°C/min). In a randomized, cross-over, double-blind placebo-controlled study, nine healthy men and women (56 ± 1 yr) took CLO (75 mg), ASA (81 mg), and placebo for 7 days. Skin blood flow was measured (laser-Doppler flowmetry, LDF) and cutaneous vascular conductance (CVC) was calculated (LDF/mean arterial pressure) and normalized to maximal CVC (%CVCmax: 43°C and 28 mM sodium nitroprusside). RH response parameters, including area under the curve (AUC), total hyperemic response (THR), and the decay constant tau (λ) were calculated. NO-dependent vasodilation during LH was assessed by calculating the difference in %CVCmax between a control site and an NO synthase-inhibited site (10 mM l-NAME: intradermal microdialysis). CLO augmented the AUC and THR (AUCclo = 3,783 ± 342; THRclo = 2,306 ± 266% CVCmax/s) of the RH response compared with ASA (AUCASA = 3,101 ± 325; THRASA = 1,695 ± 197% CVCmax/s) and placebo (AUCPlacebo = 3,000 ± 283; THRPlacebo = 1,675 ± 170% CVCmax/s; all P < 0.0001 vs. CLO). There was no difference in the LH response or calculated NO-dependent vasodilation among treatments (all P > 0.05). Oral CLO treatment augments vasodilation during RH but not LH, suggesting that CLO may improve cutaneous microvascular function.

P0195THE RELATIONSHIP BETWEEN CALCIFICATION INHIBITOR LEVELS IN CHRONIC KIDNEY DISEASE AND THE DEVELOPMENT OF ATHEROSCLEROSIS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Can Sevinc ◽  
Gulay Yilmaz ◽  
Sedat Ustundag
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Carotid Artery ◽  
Linear Relationship ◽  
Vascular Calcification ◽  
Intima Media Thickness ◽  
Control Group ◽  
Fetuin A ◽  
Healthy Control ◽  
The Mean

Abstract Background and Aims Atherosclerosis and its associated cardiovascular diseases starting from the early stages of chronic kidney disease (CKD) are the most important cause of increased morbi-mortality in the CKD process. In studies performed in patients with end-stage renal disease (ESRD), it is observed that the calcification occured in the vascular structures was an important component of the atero-arteriolosclerosis process. The number of studies investigating the relationship between vascular calcification and the development of atherosclerosis and increased morbi-mortality in the process of CKD are quite small and limited to patients undergoing hemodialysis (HD) treatment for ESRD. We aimed to investigate the factors affecting the development of atherosclerosis and the role of calcification inhibitors fetuin-A, matrix-Gla protein (MGP), osteoprotegerin (OPG) in atherosclerosis progress. Method Our study was planned to investigate the relationship of serum OPG, MGP and fetuin-A levels with the development of atherosclerosis in the stage 2-3-4-5 chronic kidney patients who did not require dialysis treatment. Thirty-two (17 female, 15 male) healthy individuals and 92 (49 females, 43 males) CKD cases were included. The healthy control group did not have a history of regular use of medication for any reason, known acute or chronic disease. Chronic kidney disease group, with no acute disease, no history of known malignancy and cerebrovascular disease. The patients' GFR was also calculated with CKD-EPI Formula. The mean carotid artery intima media thickness was calculated by dividing the sum of right and left carotid artery intima media thickness. Statistical analysis was performed with IBM SPSS Statistics 20.0.0. Results The laboratory data of the healthy control group, stage 2 CKD group, stage 3 CKD group, stage 4 CKD group and stage 5 CKD groups were statistically compared with the healthy control group, between themselves and the whole CKD group, the results were given in Table-1. Chronic kidney disease group divided into two groups; carotid artery intima media thickness less than 0.750 millimeters (without subclinical atherosclerosis) and those above 0.750 millimeters (with subclinical atherosclerosis). The mean C-IMT, CRP, FETUIN-A, OPG and MGP of the two groups were compared statistically and the results are shown in Table-2. In chronic kidney patients, age (r = 0.493, p &lt;0.001), BMI (r = 0.337, p = 0.001), CRP (r = 0.301, p = 0.004), TG (r = 0.245, p = 0.019 ), urea (r = 0.228, p = 0.029), SBP (r = 0.212, p = 0.043), fasting blood sugar (r = 0.212, p = 0.043) have positive linear relationship, fetuin-A (r = -0.409, P = 0.001), OPG (r = -0.235, p = 0.024), GFR (r = -0.209, p = 0.046) have a negative linear relationship with CIMT. The multiple relationships between CIMT and other variables are given in Table-3. The mean CIMT (r =-0.417, p = 0.001), right CIMT (r = -0.412, p = 0.001), left CIMT (r = -0.410, p = 0.001), urea (r = -353, p = 0.007), CRP (r = -0.322, p = 0.014), UPE (r = -0.301, p = 0.022), creatinine (r = -0.277, p = 0.035), age (r = -0.262, p = 0.047) show a negative linear relationship with Fetuin-A. Multiple relationships between fetuin-A and other variables are given in Table-4. Conclusion Our study shows that; In particular, fetuin-A levels, which is a vascular calcification inhibitor, begin to decline from the early stages of CKD and is significantly lower in patients with atherosclerosis. This suggests that fetuin-A may be used as an early marker in CKD with increased cardiovascular mortality. On the other hand, contradictions related to the levels of OPG and MGP in CKD and its role in the development of atherosclerosis continue. The results in our study also support this situation. Reducing mortality and morbidity in CKD primarily depends on reducing the risk of cardiovascular events. Pre-recognition of these risks is important, so large-scale studies on vascular calcification inhibitors are needed.

scholarly journals Features of microvasculature regulation in patients with chronic kidney disease on peritoneal dialysis

2016 ◽  
Vol 15 (1) ◽  
pp. 65-72
Author(s):  
G. I. Lobov ◽  
A. N. Isachkina ◽  
A. S. Gurkov
Keyword(s):  
Chronic Kidney Disease ◽  
Peritoneal Dialysis ◽  
Kidney Disease ◽  
Blood Plasma ◽  
Control Group ◽  
Doppler Flowmetry ◽  
Signaling Function ◽  
Endogenous Ouabain ◽  
Increased Activity ◽  
In Blood Plasma

Introduction and aim. Chronic kidney disease (CKD) is one of the most common non-infectious diseases, in which arterial hypertension (AH) is progressing. The mechanisms of AH in CKD are complex and understudied. This research was conducted with the objective to investigate the mechanisms of microvascular tonus increase in the group of patients with the 5th stage of CKD who were treated with peritoneal dialysis. Materials and methods. Patients from dialysis department were included in the study (76 people). Blood flow in microvessels was measured by laser Doppler flowmetry (LDF). Results of LDF used for the calculation of neurogenic (HT), myogenic (MT) and endothelium-dependent tonus (EDT) microvessels. Cardiotonic steroid concentration in plasma was measured by competitive immunofluorescence using antibodies to ouabain and marinobufagenin. The activity of Na/K-ATPase was measured by spectrophotometry. Results and discussion. HT microvessels in patients with CKD was increased by 21.4±3,88 %, MT - 33.4±5,62 %, EDT 17.1±3.14 % compared with the control group. Endogenous ouabain (EO) concentration in plasma of patients with CKD was on average 0.311±0.032 nM/L, in the control - 0.296±0.031 nM/L. Marinobufagenin (MBG) concentration in the plasma of patients with CKD was 2.10; 0.89; 3.07 nM/L (median, 25th and 75th percentile), and in control - 0.347; 0.103; 0.427 nM/L. The activity of Na/K-ATPase in patients with CKD was 1.54±0.18 μmol Pi/mL/hr, vs. 3.07±0.44 μmol Pi/mL/h in the control. The correlation between the value of MT of microvascular and MBG concentration in blood plasma of patients with CKD was found (rs = 0.736). Conclusions. Our results show that high NT of microvessels of patients with CKD and is connected with increased activity of the central structures of the sympathetic nervous system, while increase of EDT is connected with endothelial dysfunction and increase of MT is connected with increasing concentration of MBG (not EO) in blood plasma. We believe that the MBG causes contraction of smooth muscle cells of blood vessels by activating signaling function of Na/K-ATPase.

Evaluation of Serum Omentin-1 Levels in Chronic Kidney Disease Patients with and without Type 2 Diabetes Mellitus

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Magda Shukry Mohammed ◽  
Rania Sayed Abd Elbaky ◽  
Hanan Mahmoud Ali ◽  
Tahani Abdelsalam Naguib
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Chronic Kidney Disease ◽  
Type 2 Diabetes Mellitus ◽  
Kidney Disease ◽  
Control Group ◽  
Roc Curve Analysis ◽  
Healthy Control ◽  
Patient Groups

Abstract Background Omentin-1 a new anti-inflammatory adipokine has been identified as a major visceral (omental) secretory adipokine which plays important roles in glucose homeostasis, lipid metabolism, insulin resistance and diabetes. Objectives This study aimed to investigate the level of Omentin-1 in chronic kidney disease patients with and without type 2 diabetes mellitus. Methods The study included 70 patients who further subdivided into three subgroups (20 T2DM, 25T2DM+CKD, 25CKD) and 20 healthy subjects formed the control group. They subjected to full clinical examination, weight, height, waist and hip circumference and BMI was calculated.Lipid profile, omentin-1, kidney function test, UACR, and HbA1c were measured. Results Serum omentin-1 level was lower in all patient groups compared to healthy control. It’s level was lower in groups with T2DM than CKD only group. It had a negative correlation with HbA1c, cholesterol total, TGs, LDL-c and e-GFR, and a positive correlation with s.creatinine, UACR, BUN, HDL-c. The best cut off point of serum omentin-1 was  &lt; =330 ng/ml to differentiate group 3(T2DM+CKD) from control group using ROC curve analysis. Conclusion The results of the present study suggest that diabetes mellitus may be associated with lower omentin levels in CKD population .

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