Insulin resistance (IR) plays a vital role in the pathogenesis of Type 2 Diabetes Mellitus (T2DM). The mechanism of IR may be associated with inflammation, whereas the neutrophil-lymphocyte ratio (NLR) is a new indicator of subclinical inflammation. Scholars have rarely investigated the relationship between IR and NLR. This study aims to evaluate the relationship between IR and NLR, and determine whether or not NLR is a reliable marker for IR.The sample consists of a total of 413 patients with T2DM, 310 of whom have a HOMA-IR value of > 2.0. The control group consists of 130 age and BMI matched healthy subjects.The NLR values of the diabetic patients were significantly higher than those of the healthy control (P < 0.001), and the NLR values of the patients with a HOMA-IR value of > 2.0 are notably greater than those of the patients with a HOMA-IR value of ≤ 2.0 (P < 0.001). Pearson correlation analysis showed a significant positive correlation of NLR with HOMA-IR (r = 0.285) (P < 0.001). Logistic regression analysis showed that the risk predictors of IR include NLR, TG and HbA1c. NLR  = 7.231, 95% CI = 4.277–12.223) levels correlated positively with IR. The IR odds ratio increased by a factor of 7.231  for every one unit increase in NLR.Increased NLR was significantly associated with IR, and high NLR values may be a reliable predictive marker of IR.The online version of this article (doi:10.1186/s12902-015-0002-9) contains supplementary material, which is available to authorized users. Type 2 Diabetes Mellitus (T2DM) is characterized by insulin resistance and is associated with obesity and cardiovascular diseases . SeveralThe count of white blood cell (WBC) is a basic but cheap, readily available, and sensitive indicator of the inflammatory status . WBCs arHowever, there have been few studies evaluating the prognostic value of NLR in IR, especially patients who were newly diagnosed diabetes. In this study that lies in the selection of newly diagnosed diabetic subjects. We aim to evaluate the relationship between IR and inflammation by using NLR, and determine whether NLR can be used as a predictive and reliable marker.Conducted from July 2013 to January 2014 in the Department of Endocrinology of Zhujiang Hospital, Southern Medical University and Mingjing Diabetes Hospital, Guangdong, China, our study included 413 patients newly diagnosed with T2DM but without hypertension, any acute inflammation, infection, acute or chronic renal failure, chronic liver, heart diseases, or any microvascular complications of diabetes. The control group was comprised of 130 aged-matched healthy subjects. All participants were surveyed on the followings: age, sex, hyperlipidemia, smoking, family history, chronic disease, dietary compliance, used drugs, and other risk factors. The study protocols were conducted in accordance with the tenets of the Declaration of Helsinki and approved by the Medical Ethics Committee of Zhujiang Hospital of Southern Medical University and Mingjing Diabetes Hospital. Written informed consent was obtained from all patients.NLR was calculated as the simple ratio between the absolute neutrophil and lymphocyte count, which were both obtained from the same automated blood sample. NLR was computed for each subject. IR was also computed for each patient. The homeostasis model of IR (HOMA-IR) was used as a measure of IR . HOMA-IRDiabetes was diagnosed based on the World Health Organization consulting criteria   was used for continuous variables with normal distribution, whereas the Mann–Whitney U test was used for continuous variables without normal distribution. The χ2 test was used for categorical variables. Pearson’s correlation analyses were used to assess the relationships. Logistic regression analysis was used to assess the associations between IR and the other parameters evaluated. A value of P < 0.05 was accepted as level of significance (two-tailed). The SPSS statistical software  was used for statistical calculations.For continuous variables with normal distributions, data were expressed as mean ± standard deviation. Categorical variables were expressed as percentages. The Kolmogorov–Smirnov test was used to evaluate the distribution of variables. Student’s The groups were similar in terms of age, gender, body mass index, and smoking habits (P > 0.05). All baseline clinical characteristics of the groups are listed in Table The demographic and laboratory data of the groups are outlined in Table The diabetic patients were divided into two groups according to their HOMA-IR score after the demographic and laboratory data evaluation. Group 1: HOMA-IR ≤ 2.0; group 2: HOMA-IR > 2.0 ,20. GrouA logistic regression analysis was also carried out using the enter method to evaluate the risk factors for IR. The measurement of NLR, TG and HbA1c were dependent parameters, whereas age, gender, BMI, systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol (TC), HDL-C, LDL-C, and microalbuminuria were independent parameters. As shown in Table The present study had shown that the NLR values of the diabetic patients were significantly higher than those of the healthy control (P < 0.001), and the NLR values of the patients with a HOMA-IR value of > 2.0 are notably greater than those of the patients with a HOMA-IR value of ≤ 2.0 (P < 0.001).Many epidemiological studies have determined that DM is associated with chronic inflammation , which mIn addition, NLR was found to be a significant risk factor for IR with DM through logistic regression analysis. The pathological activation of innate immunity leads to inflammation of the islet cells, resulting in a decrease in pancreatic beta-cell mass and impaired insulin secretion . PatientHowever, some common physical conditions, such as dehydration and Prostate Specific Antigen of the blood specimen can affect the accuracy of the data. Furthermore, physical exercise and release of catecholamine (CA) can cause a drop in neutrophilic granulocyte and lymphocyte. NLR represents a combination of two markers where neutrophils represent the active nonspecific inflammatory mediator initiating the first line of defense, whereas lymphocytes represent the regulatory or protective component of inflammation . NLR is A logistic regression analysis of the following risk factors was conducted: NLR, TG and HbA1c. In our study, in conjunction with the rising of the level of HbAlc, the degree of IR increased significantly. HbA1c showed an association with early-phase insulin secretion assessed by insulinogenic index . HeianzaWe recommend that the NLR values of diabetic patients be calculated as NLR is a cheap, predictive, and prognostic marker for IR. High NLR values were independently related to IR.


ObjectiveWhile albuminuria is a marker for progressive chronic kidney disease (CKD) in patients with type 2 diabetes (T2DM), both albuminuric and normoalbuminuric patients appear prone to vascular injury. This pilot study examines the association between circulating endothelial cell (CEC) levels and vascular injury in patients with T2DM and CKD.Methods2). CEC levels were tested by Janssen Diagnostics, LLC using an immuno-magnetic bead-based assay. CEC levels were compared to levels in a previously tested normal population. Correlations between CEC levels and other vascular injury markers  were performed.In this cross-sectional study, eligible adult patients had T2DM, and stage 3 CKD  were significantly higher than the normal population , including in the normoalbuminuric subgroup . CEC levels were significantly correlated with uric acid levels .ConclusionsCEC levels in patients with T2DM and CKD, both albuminuric and normoalbuminuric, are significantly higher than a normal population, suggesting the presence of vascular injury in both groups. Future studies are needed to evaluate the role of CECs as a biomarker to predict outcomes in normoalbuminuric patients with CKD. Of these patients with T2DM and CKD only a small proportion will progress to end stage renal disease (ESRD) requiring dialysis or transplant2. Identifying patients with T2DM and CKD at high risk for progressive renal disease could lead to a decrease in the incidence of ESRD through the implementation of interventions known to slow progression3. Unfortunately, identifying which of these patients are at high risk remains a challenge, due to inaccurate biomarkers of progressive renal disease.Type 2 diabetes (T2DM) is the most common cause of pre-dialysis chronic kidney disease (CKD) in the United States affecting approximately 10 million Americans4. Despite this, they have been found to be a poor predictor of progression to ESRD in T2DM, and are in the normal range in up to 50% of patients with T2DM and CKD11. Patients with diabetes and normoalbuminuria are at risk for progressive renal function decline12, and those with diabetes, CKD and normoalbuminuria are at higher risk of cardiovascular events and all-cause mortality than diabetes patients without CKD13. Furthermore, patients with T2DM, CKD and normoalbumuria have a similar prevalence of micro and macroangiopathies as patients with T2DM and albuminuria7. Biomarkers that quantify underlying vascular injury and predict future renal and cardiovascular risk independent of urine microalbumin are needed in this population14.Urine microalbumin levels are the most commonly used biomarker for progressive diabetic renal damage15. Levels of these cells correlate with the degree of vascular injury, with higher levels seen in patients with atherosclerotic cardiovascular disease, small vessel vasculitis, renal transplant rejection, metastatic carcinoma and advanced chronic kidney disease18. In patients with T2DM and CKD, CEC levels may quantify the degree of underlying vascular damage independent of urine microalbumin, potentially acting as a seromarker for future renal or cardiovascular events. The purpose of this study was to determine whether CEC levels correlate with other markers of vascular injury in patients with T2DM and CKD including those with normoalbuminuria.Circulating endothelial cells (CECs) are a reliable serologic marker of vascular injury. These cells have been found to detach and circulate in human sera after sustained activation by inflammatory and thrombotic stimuliThis was designed as a cross-sectional study of CEC levels and other vascular injury markers in patients with T2DM and CKD. Recruitment occurred at the outpatient nephrology offices of a large northeastern hospital. This office has an annual caseload of approximately 1500 patients with T2DM and CKD, of whom 25% are minorities (black or hispanic). The study was approved by the local institutional review board , and all patients gave their written informed consent prior to study procedures.2 were considered for study inclusion. This inclusion criterion selected for a population at high risk for vascular injury that had not yet progressed to advanced CKD. Patients with prior evidence of renal artery stenosis, biopsy proven non-diabetic etiology of kidney disease, recurrent urinary tract infections, microhematuria, active malignancy, recent hospitalization and nephrotic range proteinuria were excluded. The exclusion criterion selected for patients with the highest likelihood of having diabetes related renal vascular injury, minimizing the possibility of elevations in CEC levels caused by alternative etiologies. Patients were selected to ensure approximately equal numbers of males and females, and normoalbuminuric and albuminuric subgroups.Patients aged 18–89 years with T2DM for ≥ 8 years, and stage 3 CKD with an estimated GFR between 30 and 60 mL/min/1.73mTwelve hundred electronic charts with the ICD 9 coding diagnoses of T2DM and stage 3 CKD were selected for review of inclusion/exclusion criteria. Of these charts, 800 patients met all inclusion/exclusion criteria and 103 consecutive patients were asked to participate in the study when they presented for a follow-up appointment at our outpatients offices. Of those patients who were approached, 40 (38%) signed consent forms and participated in a single study session apart from their regularly scheduled follow-up visit.All study procedures were performed during a single, morning 1-hour study session. For all patients, a complete history and physical including seated blood pressure was performed and baseline characteristics were recorded. For blood pressure readings, the lower of two seated measurements taken after 5 minutes of sitting was recorded. Comorbidities were defined by patient report or documentation in the patient’s problem list. Cardiovascular disease was defined as a prior history of coronary artery disease (CAD), congestive heart failure (CHF), peripheral vascular disease (PVD) or stroke.Blood and urine samples were collected from all patients at the time of recruitment. This included serum creatinine, uric acid, von Willebrand Factor antigen levels, high sensitivity C-reactive protein, morning urine microalbumin to creatinine ratios (UACR) and CEC levels. For low density lipoprotein (LDL) cholesterol, hemoglobin A1c (HbA1c), serum phosphorus and blood hematocrit, the most recent value from outpatient blood work taken within 6 months of the study visit was recorded. Patients with UACR < 30mg/g were classified as normoalbuminuric, while patients with a UACR ≥ 30mg/g were classified as albuminuric.20. Briefly, peripheral whole blood was obtained with a 21-G butterfly needle and the first 3mL was discarded to minimize falsely elevated CEC levels related to venipuncture19. Whole blood was then collected into a tube containing anticoagulant and preservative, maintained at 15–30°C and shipped overnight to the central laboratory where it was processed within 72 hours. Prior studies have shown no significant difference in CEC levels at 0, 24, 48 and 72 hours in normal patients19. The CEC levels in a normal healthy population from this study are quoted from previous studies performed using the CELLSEARCH® Circulating Endothelial Cell Kit 19.Levels of total CECs were measured by the Clinical Lab Services Group at Janssen Diagnostics, LLC (previously Veridex Corporation) using the CELLSEARCH® Circulating Endothelial Cell Kit . This system has provided valid and reproducible CEC levels in normal populations and in patients with chronic illness and malignancy, and the details have previously been described in detailCECs were isolated and enumerated by Janssen Diagnostics, LLC using the CELLSEARCH® Circulating Endothelial Cell Kit  in combination with the CELLTRACKS® AUTOPREP® System , and the CELLTRACKS ANALYZER II® . These systems use immunomagnetic bead technology and a semi-automated fluorescent microscope. Briefly, 4mL of blood were mixed with 10mL of dilution buffer containing 0.1% sodium azide and the mixture was centrifuged at 800g for 10min, placed in the sample preparation system, i.e. the CELLTRACKS® AUTOPREP® System , and processed within 1 hour of preparation. The sample preparation system then aspirated the plasma, leaving the buffy coat layer and red cells to be further processed. An anti-CD146 ferrofluid from a 3.0mL suspension of 0.012% magnetic nanoparticles conjugated to a mouse monoclonal antibody was added . The cells were then incubated inside the sample preparation system at room temperature for 12 to 13 minutes, at which time they underwent magnetic separation. The unbound cells and remaining plasma were then aspirated by the sample preparation system, and staining reagents with a permeablization buffer, to fluorescently label immunomagnetically bound cells, were added. These staining reagents included: 1) 4,6-diamidino-2-phenylindole (DAPI), a nuclear stain, 2) the mouse monoclonal CD105-PE which is specific for the protein endoglin and is expressed by endothelial cells; activated monocytes, stromal cells and pre-B cells, and 3) the mouse monoclonal pan-leukocyte antibody CD45 conjugated to allophycocyanin, in conjuction with a permeabilization buffer . Cells were then re-incubated and magnetic separation was repeated. Finally, the cells were re-suspended in approximately 300 µL of buffer and transferred to a chamber with two magnets that magnetically oriented cells into a monolayer for analysis. Analysis was performed within 24 hours using the CELLTRACKS ANALYZER II , a four-color semi-automated fluorescent microscope and a gray scale charged coupled device camera, capturing 175 frames per channel. The captured frames were analyzed by image analysis software. CECs candidates selected by the software were then manually identified by the operator as DAPI+, CD105+ and CD45- cells. A single CEC count was performed for each blood specimen.st quartile – 3rd quartile). Categorical variables are reported as proportions. Kolmogorov-Smirnov test was used to evaluate the normality of all continuous variables. A dichotomous grouping variable was created using urine microalbumin variable . Two independent samples t-test was used to compare normally distributed variables between albuminuric and normo-albuminuric groups and Wilcoxon rank-sum test was used for non-normally distributed variables. Fisher’s exact test was used to compare all categorical variables. Correlations analyses between levels of CECs and other vascular injury markers were performed using Pearson’s correlation for normally distributed continuous variables and Spearman’s for non-normally distributed continuous variables. There were three missing data points in this study . This missing data was ignored from analysis. All analyses were performed using SAS 9.4. Results were considered significant if p<0.05.The aim of this pilot trial was to study the feasibility of recruitment, and assessment procedures. The sample size of 40 was based on the feasibility of single center recruitment and the study budget. All normally distributed continuous variables are reported as mean±standard deviation, and all non-normally distributed variables as median   and stage 2 chronic kidney disease (CKD) and examine the association between circulating endothelial cell (CEC) levels and  surrogates biomarkers of vascular damage . Mean CEC levels were significantly higher (x1.8) than the normal population independently for albuminuria level and correlated with uric acid levels. Higher CEC levels have been already reported in severe renal disease  and cardiovascular disease . CEC are considered as markers of severe vascular damage with poor outcome.    The originality of this study is to identify that CEC levels are elevated also in normoalbuminuric patients with T2DM and CKD suggesting severe vascular injury despite the absence of significant albuminuria. Unfortunately, the predictive value of CEC levels either on cardiovascular disease or chronic kidney disease progression is missing. In addition, it would have been interesting to have data on endothelial progenitor cell (EPC) levels, which are markers of endothelial regeneration with vascular protective role.  As the authors mentioned, further prospective studies are needed to define the role and the predictive value of CEC in T2DM and CKD patients as biomarker of cardiovascular and kidney disease progression.I have read this submission. I believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard. Novel pilot study demonstrating significant increase in circulating vascular endothelial cells (CEC) in stage 3 chronic kidney disease with and without microalbuminuria suggesting significant vascular disease in patients with normal albuminuria and albuminuria compared to historical healthy controls. Significant correlation was also shown between CEC and serum uric acid.This is a preliminary study and prospective outcome studies will need to be performed to demonstrate any clinical predictive power of CECs. This limitation the investigators acknowledge.It would be interesting to measure CEC levels in T2DM without CKD  and follow them prospectively to see whether they are predictive of development of CKD.I have read this submission. I believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard.


Acute respiratory distress syndrome (ARDS) with concomitant impairment of oxygenation and decarboxylation represents a complex problem in patients with increased intracranial pressure (ICP). Permissive hypercapnia is not an option to obtain and maintain lung-protective ventilation in the presence of elevated ICP. Pumpless extracorporeal lung assist (pECLA) devices  can improve decarboxylation without aggravation associated with invasive ventilation. In this pilot series, we analyzed the safety and efficacy of pECLA in patients with ARDS and elevated ICP after severe traumatic brain injury (TBI).The medical records of ten patients  with severe ARDS and severe TBI concurrently managed with external ventricular drainage in the neurointensive care unit (NICU) were retrospectively analyzed. The effect of pECLA on enabling lung-protective ventilation was evaluated using the difference between plateau pressure and positive end-expiratory pressure, defined as driving pressure (ΔP), during the 3 days preceding the implant of pECLA devices until 3 days afterward. The ICP threshold was set at 20 mmHg. To evaluate effects on ICP, the volume of daily cerebrospinal fluid (CSF) drainage needed to maintain the set ICP threshold was compared pre- and postimplant.2O to 11.9±0.5 cm/H2O (p = 0.011). In spite of this improved lung-protective ventilation, carbon dioxide pressure decreased from 46.6 ± 3.9 mmHg to 39.7 ± 3.5 mmHg (p = 0.005). The volume of daily CSF drainage needed to maintain ICP at 20 mmHg decreased significantly from 141.5 ± 103.5 ml to 62.2 ± 68.1 ml (p = 0.037).The ΔP values after pECLA implantation decreased from a mean 17.1 ± 0.7 cm/HFor selected patients with concomitant severe TBI and ARDS, the application of pECLA is safe and effective. pECLA devices improve decarboxylation, thus enabling lung-protective ventilation. At the same time, potentially detrimental hypercapnia that may increase ICP is avoided. Larger prospective trials are warranted to further elucidate application of pECLA devices in NICU patients. Acute respiratory distress syndrome (ARDS), according to the recent Berlin definition, is defined as impaired oxygenation caused by acute, diffuse, inflammatory lung injury  from 3 days preceding pECLA device implant until 3 days afterward were compared. All ventilation-related variables, such as VT in milliliters, Pplat in cm/H2O, Pmean in cm/H2O, PEEP in cm/H2O, blood pH level, and ΔP in cm/H2O (defined as Pplat minus PEEP) were recorded half-hourly , and PEEP was increased significantly . Both interventions caused a decrease of ΔP from a mean of 17.1 ± 0.7 cm/H2O to 11.9 ± 0.5 cm/H2O (p = 0.011), whereas Pmean remained unchanged   system. She recovered without sequelae and was discharged from the intensive care unit after 20 days.2 levels and reduced ΔP and occurs regardless of Pmean.In this report of a patient cohort with ARDS and TBI treated with implant of a pECLA device, we describe several important findings. First, pECLA is a safe and effective tool to enable LPV in patients with ARDS in the presence of severe brain injury. Second, in the critical situation of elevated ICP and concomitant demand for adjusted ventilation, the use of pECLA enables better ICP control under optimized ventilator settings. Third, the better control of ICP, as reflected in the reduced necessity to drain CSF, results from optimized pCOT ventilation  is the preferred approach [permissive hypercapnia [Though most patients with TBI die as a result of the underlying pathology or secondary complications rather than because of respiratory failure per se, ARDS contributes significantly to poor outcome and increased risk of death in these patients , 17. Theapproach , 20. LPVercapnia . In addiercapnia , 23.2, the autoregulatory pressure range is decreased and, depending on the pCO2 level, cerebral autoregulation is significantly impaired [2 > 70 mmHg, the pressure–flow relationship can approximate a linear relationship, as demonstrated in animal experiments [2 is effectively reduced to normal levels and can be controlled by adjusting the oxygen sweep flow to avoid unwanted hypocapnia. Normalization of pCO2 is accompanied by increased pH and avoidance of respiratory acidosis. This yields a significant reduction in drained CSF as a surrogate for improved ICP control. Interestingly, mean airway pressure does not contribute to this effect. After pECLA device implant, inspiratory pressure is decreased, but PEEP is increased, to improve oxygenation. As a consequence, mean airway pressure does not change significantly. Therefore, improved ICP control can be attributed predominantly to the normalization of pCO2. In ARDS, the combination of low VT and higher PEEP is superior to low VT with lower PEEP [In neurosurgical patients with TBI, permissive hypercapnia cannot be tolerated easily. Hypercapnia increases cerebral blood flow by cerebral vasodilation. More specifically, with increasing pCOimpaired , 8, 9. Ieriments . Thus, heriments , 25. pCOwer PEEP . Though wer PEEP . High peAn important limitation of our analysis is its retrospective nature; thus, residual confounding parameters might have been missed. In addition, the number of patients is too small to allow generalizability of the results or to provide any meaningful outcome data. However, the main aim of this study was to provide data on the safety and efficacy of this intervention.In this context, it is important to recognize that, for pECLA treatment, systemic anticoagulation to avoid clotting of the filter membrane is recommended. In patients with brain injury, this may increase the risk of decompensating intracerebral hematomas. However, in our series, no complications  attributable to anticoagulation were seen. Besides, owing to heparin-coating of the extracorporeal circuit, low-dose systemic anticoagulation is sufficient to avoid clotting of the extracorporeal circuit, thereby minimizing the risk of bleeding complications. In patients with extraordinarily high risk of bleeding, even a complete abdication of anticoagulation in venovenous ECMO was shown to be safe and feasible . Also, e2), which might have contributed to reduced right ventricular capacity.Owing to the relevant shunt volume of approximately 1500 ml of blood per minute over the extracorporeal circuit, a relevant increase in right heart preload occurs. This may have contributed to the right heart failure in one of our patients. This patient had no known preexisting cardiac disease; however, the patient was obese (body mass index 33 kg/mFor selected patients with concomitant severe brain and lung injury, the application of pECLA is effective to avoid hypercapnia and respiratory acidosis, thus enabling application of LPV guidelines as well as effective ICP control. Large prospective trials are necessary to further elucidate the application of pECLA devices and the influence of different ventilation pressures on ICP and outcome in NICU patients.pECLA is a safe and effective tool to enable LPV in patients with ARDS and TBI.2 and normalizes pH in patients vulnerable to hypercapnia.pECLA effectively reduces pCOpECLA enables better ICP control under optimized ventilator settings than without extracorporeal decarboxylation.


After three years of excessive confidence, overoptimistic expectations and performance of 15 to 20,000 renal denervation procedures in Europe, the failure of a single well-designed US trial—Symplicity HTN-3—to meet its primary efficacy endpoint has cast doubt on renal denervation as a whole. The use of a sound methodology, including randomisation and blinded endpoint assessment was enough to see the typical 25–30 mmHg systolic blood pressure decrease observed after renal denervation melt down to less than 3 mmHg, the rest being likely explained by Hawthorne and placebo effects, attenuation of white coat effect, regression to the mean and other physician and patient-related biases. The modest blood pressure benefit directly assignable to renal denervation should be balanced with unresolved safety issues, such as potentially increased risk of renal artery stenosis after the procedure , unclear long-term impact on renal function and lack of morbidity–mortality data. Accordingly, there is no doubt that renal denervation is not ready for clinical use. Still, renal denervation is supported by a strong rationale and is occasionally followed by major blood pressure responses in at-risk patients who may otherwise have remained uncontrolled. Upcoming research programmes should focus on identification of those few patients with truly resistant hypertension who may derive a substantial benefit from the technique, within the context of well-designed randomised trials and independent registries. While electrical stimulation of baroreceptors and other interventional treatments of hypertension are already “knocking at the door”, the premature and uncontrolled dissemination of renal denervation should remain an example of what should not be done, and trigger radical changes in evaluation processes of new devices by national and European health authorities. Accordingly, at 6 months the between-group difference in office blood pressure averaged 33/11 mmHg (P < 0.0001) [In 2009, Krum and colleagues  publisheStill, in this sunny landscape, many shadows remained. Only a minority of patients with resistant hypertension were found to be eligible for RDN , 6, 7•. As early as 2012, we and others , 15 haveDespite these caveats, publication of the Symplicity studies , 2••, 3 Based on mostly small, purely observational studies, RDN was associated with ancillary benefits such as decreased left ventricular mass , arteriahttp://www.tctmd.com/show.aspx?id=123265) stunned the medical community and device industry as a deep shock, and was quickly followed by definitive or temporary stopping of large ongoing research programmes (http://www.reuters.com/article/2014/01/24/us-covidien-divestment-idUSBREA0N18B20140124). A rapid opinion shift from excessive optimism to deep mistrust ensued [Symplicity HTN-3 ••, a lart ensued .P < 0.001 for both comparisons of the change from baseline). This corresponds to a modest 2.39 mmHg advantage in favour of the technique, lower than the preset superiority margin of 5 mmHg [p = 0.006) compared to a non-significant (p = 0.51) -3 mmHg in 25 patients from control group [p < 0.001 for both) [In contrast with Symplicity HTN-2 ••, the mf 5 mmHg ••. Discoor both) •• , at higher cardiovascular risk (slightly higher proportion of type 2 diabetes and dyslipidemia) and took more diuretics (99 vs. 89 %) and aldosterone antagonists (23 vs. 17 %). Furthermore, as expected in a US population, the Symplicity HTN-3 cohort included one-fourth of patients of African descent [The huge discrepancy between Symplicity HTN-3 on one side and most other studies including Symplicity HTN-2 on the other side raises concern. Can a single large US trial challenge all previous studies? Who is right? Symplicity HTN-2, Symplicity HTN-3, or both? Compared to Symplicity HTN-2 •• were m descent ••, while descent •• was th descent ••.blinded, while other studies were randomised but unblinded (Symplicity HTN-2) or purely observational [The aforementioned differences in study populations and in the RDN procedure itself may partly account for the less important blood pressure decrease in RDN-treated patients from Symplicity HTN-3 •• comparvational ••, 42••.vational . In othevational . As detavational , the Symvational , 19••. Cvational , 15. In vational .Some of the most enthusiastic exponents of RDN are already ready to “seek redemption” for RDN , withoutThe key message of Symplicity HTN-3 •• is simOn the other side, reason takes back her rights. All previous discrepancies are now easily understandable. If the blood pressure decrease observed in previous studies is mostly related to patient and physician-related biases, it is not unexpected that blood pressure outcome may critically depend on the expertise of centres, the way in which blood pressure is measured, and/ or the individual characteristics and psychology of patients. It is obvious that ambulatory blood pressure, which minimises observer-related bias and placebo effect , will behttp://www.tctmd.com/show.aspx?id=123265). At first sight, this may convey the impression that the Simplicity HTN-3 investigators have achieved at least one of their aims after all, and thus mitigate our disappointment. However, it should be pointed out that the primary safety endpoint—a composite of major adverse events, including death, endstage renal disease, an embolic event resulting in end-organ damage, renal-artery or other vascular complications, hypertensive crisis within 30 days or new renal-artery stenosis of more than 70 % within 6 months [The first announcement of the failure of Symplicity HTN-3 •• to ach6 months ••—was an6 months , in the 6 months .http://www.tctmd.com/show.aspx?id=120456), respectively. If confirmed on a larger scale, this frequency is not negligible, especially in view of the modest efficacy of the technique [Up to now, at least 13 cases of significant, de novo renal artery stenosis have been documented 3 to 6 months after RDN performed using four different renal ablation systems ••, 55–65echnique ••, 42••.echnique , some of2, a twofold to eightfold larger decrease than in other contemporary trials including patients at high cardiovascular risk (median follow-up: 29 to 56 months) [Long-term evolution of renal function is also a matter of concern. While glomerular filtration rate (GFR) at 6 months was similar in both RDN and control groups in Symplicity HTN-2 , in the  months) –70. WhetIn patients with resistant hypertension as a whole, the efficacy of RDN has been largely overestimated ••. OveraThe proportion of patients in whom RDN appears as the single option is thus very low (probably < 1 %) , 73. Furrationale [2 [While, as stated in a recent editorial, the “RDN bubble” has exploded  and overationale . Most inationale . Hence, ationale , but mayationale ••, whileonale [2 ••. Theseonale [2 .Identification of determinants of response to RDN should be done within the context of properly designed randomised controlled trials and independent registries. Selection criteria should be much stricter than previously. Candidates to RDN should undergo an in-depth screening in order to rule out secondary and white coat hypertension. Elderly patients, patients with isolated systolic hypertension and altered renal function  are unliRDN may find its place in the therapeutic arsenal of resistant hypertension and some other diseases characterised by sympathetic overactivity. It will never be a “miracle cure” of hypertension, or even the standard treatment for all patients with resistant hypertension , 44. In rationale [Different factors have jointly contributed to the uncontrolled and premature deployment of RDN in Europe: (1) the attractive underlying ationale ; (2) theationale ; (5) theationale • and theationale ; (6) theationale , 86; andationale .Thriving on what is viewed as the failure of RDN to meet its expectations, new treatment approaches of resistant hypertension such as electrical stimulation of baroreceptors  or creat


P < 0.001). In multivariate analysis, sST2 was an independent explanatory variable associated with carotid plaques . After adjustment for the osteoporotic risk factors, sST2 was significantly associated with higher cortical porosity  and cortical pore volume ; and had a trend to be associated with lower cortical vBMD . IL-33 was not associated with carotid plaque or vBMD/microstructure. In conclusion, plasma sST2 levels were independently correlated with both carotid plaque and compromised cortical vBMD/microstructure in PsA patients. IL-33/ST2 axis may be a link between accelerated atherosclerosis and osteoporosis in PsA.Psoriatic arthritis (PsA) patients have increased risk of both atherosclerosis and osteoporosis. Previous studies revealed that IL-33/ST2 axis may be related to both conditions; however, these associations were never evaluated in a single patients’ group. Here we explored the association among plasma levels of IL-33 and its decoy receptor soluble ST2 (sST2), carotid plaque determined by ultrasound, and volumetric bone mineral density (vBMD)/microstructure of distal radius measured by high-resolution peripheral quantitative computed tomography (HR-pQCT) in 80 PsA patients . Plasma sST2 levels were significantly higher in 33 (41%) patients with carotid plaques (11.2 ± 4.5 vs 7.7 ± 3.7 ng/ml,  Association between atherosclerosis and osteoporosis has been reported122Interleukin-33 (IL-33) is a recently discovered member of the Interleukin-1 (IL-1) cytokine family6Psoriatic arthritis (PsA) is a chronic inflammatory arthritis associated with psoriasis9111214In this study, we aimed to elucidate the association among plasma IL-33 and sST2 levels and (i) the presence of carotid plaque using high-resolution ultrasound, and (ii) vBMD/bone microstructure of distal radius using HR-pQCT in PsA patients.A total of 80  PsA patients were included. The mean age was 53.0 ± 10.1 years and disease duration was 14.3 ± 7.2 years. P = 0.002), had longer PsA disease duration , and an increased prevalence of high cardiovascular diseases (CVD) risk  (P = 0.085) and more patients were put on statins  in patients with plaques. CV events were more common in patients with plaques .Carotid plaque(s) were identified in 33 (41.3%) patients. The patients with carotid plaques were older  . There wP < 0.001). There was no difference in the prevalence of detectable IL-33 between patients with or without plaques (P = 0.752). After adjusting for the confounding factors, sST2 was an independent explanatory variable associated with the presence of carotid plaques  (P = 0.036). sST2 levels discriminated PsA patients with or without plaques with area under receiver operating characteristic curve (AUROC) of 0.757   . Older a< 0.001) . When ag< 0.001) .P > 0.1).On the other hand, mean or maximal IMT was not associated with plasma IL-33 or sST2 , cortical tissue mineral density (TMD) , and positively associated with cortical porosity (Ct. Po)  and pore volume  (P = 0.012) and pore volume , and had a trend to be associated with lower cortical vBMD   . The ass= 0.073) . Plasma = 0.073) .On the other hand, detectable IL-33 was not associated with the vBMD or microstructure at distal radius.P = 0.024), trabecular vBMD , vBMD for the central medullary region (mTb) , trabecular bone volume fraction (BV/TV)  and trabecular thickness . These differences remained significant after adjusting for age/gender or full adjustment except for total vBMD On the other hand, all patients had detectable plasma sST2. The association between plasma sST2 levels and carotid plaque was independent of traditional CV risk factors and the presence of CVD. The overall accuracy of sST2 in predicting carotid plaque was high 76%), and could be further increased to 82% when age was added to the predictive model. These results indicated that sST2 may be a good biomarker for atherosclerosis in PsA patients. sST2 had been proposed as a novel biomarker for CV events%, and co1920This is the first study to report the association between sST2, vBMD and bone microstructures. In multivariate analysis, only the positive association between sST2 and cortical porosity and cortical pore volume remained significant. The association between sST2 with compromised bone quality in terms of low cortical vBMD and TMD and was attenuated by adjusting for traditional osteoporotic risk factors, suggesting that the latter might partially mediate the effect of inflammation on osteoporosis. More importantly, compromised cortical bone quality was also the featured pattern of bone microstructural deficits in our PsA patients compared with controlsThe plasma sST2 was also positively associated with trabecular number. However, this result should be interpreted carefully. Identifying the transitional zone between cortical and trabecular region remained difficult using HR-pQCTIL-33 and ST2 are expressed in the normal and atherosclerotic vasculature of murine and human26et al. reported that IL-33 was expressed in osteoblasts, and prevented osteoclast formation from bone marrow precursor cells3133IL-33 inhibited receptor activator of NF-kB ligand (RANKL)-induced osteoclast formation through the regulation of anti-osteoclastic genes such as interferon regulatory factor-8 (IRF-8), which could be blocked by an anti-ST2 monoclonal antibodyP = 0.665] or CRP  in this cohort) and other important pathways, such as Wnt signaling pathwayWe also confirmed an association of atherosclerosis and compromised bone quality in PsA patients for the first time. However, the patients with carotid plaque had mainly compromised trabecular instead of cortical bone quality. It indicates that the extract underlying mechanism could be complicated and may not be explained by a single IL-33/ST2 axis. Other potential links between these two conditions, including chronic inflammation . Our study also has a few limitations. The lack of control subjects does not allow us to test the associations in general population. Since this is an observational cross-sectional study, causal inferences cannot be drawn. Increased sST2 may either be the culprit or a compensatory response, or even an “innocent bystander” to the pathogenesis of atherosclerosis and osteoporosis. However, the clinical correlation highlighted the potential utility of sST2 as a biomarker, and further studies should be performed for a better understanding of the underlying mechanism. It is also important to note the presence of carotid plaque may incompletely capture the complex process of atherosclerosis in multiple vascular bedsIn conclusion, plasma sST2 levels were independently associated with both carotid plaque and compromised cortical vBMD/microstructure in PsA patients, indicating that IL-33/ST2 axis may contribute to both atherosclerosis and osteoporosis. These associations were independent of other established biomarkers including CRP and other established CV/osteoporotic risk factors. Future studies are warranted to elucidate the potential use of sST2 for screening and management of patients with subclinical atherosclerosis and possibly osteoporosis. The detailed mechanism should be further investigated.Eighty consecutive PsA patients fulfilled the Classification of Psoriatic Arthritis criteria were recruited from the rheumatology clinic of The Prince of Wales Hospital for this cross-sectional study. The vBMD and microstructure of 53 out of the 80 patients comparing with age and gender matched controls had been published beforeEthics approval was obtained from Ethics Committee of The Chinese University of Hong Kong-New Territories East Cluster Hospitals (reference number: CRE-2012.082), and written informed consent was obtained from all participants according to the Declaration of Helsinki. The study was conducted in accordance with ICH-GCP.Clinical interview was performed by experienced rheumatologists using standardized data collection instruments as described beforeg for 15 minutes to obtain plasma. Plasma samples were stored at −70 °C immediately until analysis. Plasma IL-33 and sST2 levels were measured using Human IL-33 Quantikine enzyme-linked immunosorbent assay (ELISA) Kit and Human ST2/IL-1 R4 Quantikine ELISA Kit  in singlicate. According to the manufacturer’s instruction, the minimum detectable dose of IL-33 and sST2 was 0.519 pg/mL and 5.1 pg/mL, respectively. The intra-assay coefficient of variation (CV) was about 3% for IL-33 and 5% for sST2. The inter-assay CV was about 5% for IL-33 and 6% for sST2, respectively.Ten milliliters fasting ethylenediaminetetraacetic acid (EDTA) blood was collected. The EDTA blood samples were centrifuged at 2,000 Carotid mean and maximum IMT were measured at 6 carotid arterial segments using a high-resolution B mode ultrasound machine  by an experienced cardiologist (QS) as described before9vBMD and microstructure were measured at the distal radius of the non-dominant forearm using HR-pQCT  as described before15Images were first analyzed using a standard protocol provided by the manufacturerFor indices of cortical volumetric density and microstructure, a fully automated cortical compartment segmentation technique was used2 test for categorical variables. Univariate and multivariable logistic regression analysis were performed to determine the independent predictor for the presence of carotid plaque. All variables with P < 0.1 in the univariate analysis were included in the multivariate analysis as potential confounding factors. Binary logistic regression was also used to calculate the predicted probability of combined utility of sST2 and age. ROC curve was used to calculate the accuracy in discriminating patients with or without carotid plaques. Univariate and multivariate linear regression analysis were used to assess the correlation between sST2 and HR-pQCT parameters. These associations were adjusted for age and gender, as well as clinical characteristics which were associated with lower cortical vBMD of the distal radius in PsA patients as we reported before P < 0.05 is used.Results were expressed as mean ± SD or median (interquartile range) as appropriate. Plasma IL-33 level was only expressed as detectable or un-detectable. Comparisons between 2 groups were assessed using the student’s t test or Mann-Whitney U test for continuous variables and χHow to cite this article: Shen, J. et al. Carotid plaque and bone density and microarchitecture in psoriatic arthritis: the correlation with soluble ST2. Sci. Rep.6, 32116; doi: 10.1038/srep32116 (2016).


Several studies have shown that the progression of communicating hydrocephalus is associated with diminished cerebral perfusion and microangiopathy. If communicating hydrocephalus similarly alters the cerebrospinal fluid circulation and cerebral blood flow, both may be related to intracranial mechanoelastic properties as, for instance, the volume pressure compliance. Twenty-three shunted patients with communicating hydrocephalus underwent intraventricular constant-flow infusion with Hartmann’s solution. The monitoring included transcranial Doppler (TCD) flow velocities (FV) in the middle (MCA) and posterior cerebral arteries (PCA), intracranial pressure (ICP), and systemic arterial blood pressure (ABP). The analysis covered cerebral perfusion pressure (CPP), the index of pressure-volume compensatory reserve (RAP), and phase shift angles between Mayer waves (3 to 9 cpm) in ABP and MCA-FV or PCA-FV. Due to intraventricular infusion, the pressure-volume reserve was exhausted (RAP) 0.84+/-0.1 and ICP was increased from baseline 11.5+/-5.6 to plateau levels of 20.7+/-6.4 mmHg. The ratio dRAP/dICP distinguished patients with large 0.1+/-0.01, medium 0.05+/-0.02, and small 0.02+/-0.01 intracranial volume compliances. Both M wave phase shift angles  and CPP  displayed a gradual decline with decreasing dRAP/dICP gradients. This study showed that in communicating hydrocephalus, CPP and dynamic cerebral autoregulation in particular, depend on the volume-pressure compliance. The results suggested that the alteration of mechanoelastic characteristics contributes to a reduced cerebral perfusion and a loss of autonomy of cerebral blood flow regulation. Results warrant a prospective TCD follow-up to verify whether the alteration of dynamic cerebral autoregulation may indicate a progression of communicating hydrocephalus. The cauume load . Before ume load ,5. On thThe ventricular constant-flow infusion with Hartmann’s solution is a diagnostic means for the evaluation of the dynamics of cerebrospinal fluid circulation. In patients with ventricular dilation of various origin, it has been shown that flow velocity responses to slow spontaneous blood pressure changes can still be detected during ventricular volume load ,7. It isTwenty three patients  with shunted hydrocephalus of communicating idiopathic, posttraumatic, and other origin were examined with the CSF infusion test which is routinely performed to obtain measure of the CSF dynamics . The trahttps://www.nice.org.uk/guidance/ipg263). The infusion study data with TCD monitoring was analyzed anonymously as a part of the standard clinical audit. The clinical audit was commissioned by the head of Hydrocephalus Clinic, Addernbrookes Hospital and approved by audit facilitator. In this study patient data were collected during routine care and were analyzed retrospectively.The infusion studies were performed as a part of clinical routine diagnostics of patients referred to the Hydrocephalus Clinic, Addenbrooke’s Hospital, Cambridge UK for shunt control. The infusion studies are clinical routine in our hospital for 20 years and are performed in more than 300 patients per year. This standard diagnostic procedure in patients with CSF disorders is approved by National Institute of Clinical Excellence, UK  was initiated at a constant rate of 1.5 ml/min and was continued until a steady-state intracranial pressure plateau (equilibrium between infused and resorbed CSF fluid) was achieved. The infusion was stopped when the intracranial pressure (ICP) reached the plateau level or exceeded 40 mmHg.The monitoring began at ICP baseline, included the plateau pressure, and was continued after the cessation of infusion, until ICP decreased to steady baseline levels. The monitoring included ICP, arterial blood pressure (ABP), and the cerebral blood flow velocity (FV): The ICP was continuously monitored via a pressure transducer at a Hartmann’s solution-filled tube connected to the intraventricular catheter or shunt antechamber.www.medschl.cam.ac.uk/icmplus) captured the time-averaged values of ICP, ABP, FV, and cerebral perfusion pressure (CPP = ICP-ABP). The data were sampled at a rate of 50Hz and were digitalized. The artefacts were manually removed after recording.The arterial blood pressure was monitored non-invasively using a servo-controlled finger plethysmograph . The hand was kept steady at the level of the heart during the entire recording. The cerebral blood flow velocity (FV) in the left MCA and right PCA were measured with TCD . The 2 MHz probes were held in position using a headband . A personal computer running the in-house software  which are induced by peripheral sympathetic regulation and are transferred to cerebral circulation . The spoAll values are given as mean +/- standard deviation. Statistical significance was set at p<0.05. For the comparison between baseline and plateau as well as between subgroups of different intracranial volume compliance we applied the ANOVA using SPSS (12.0.1). The relationship between volume compliance and phase shift angles or CPP, was assessed using linear regression analysis.Twenty-three data files depicting time courses of ICP, ABP and FV (MCA and PCA) during 5+/-3 min ICP baseline and during 5+/-3 min ICP plateau were included in the analysis. Via ventricular infusion, the ICP was led to a plateau of 20.7+/-6.4 mmHg. RAP marked the exhaustion of volume compensatory reserve 0.84+/-0.1. For the physiological and derived parameters at baseline and plateau pressure levels please see Unlike RAP and ICP, mean values of ABP, MCA-FV, PCA-FV, CPP as well as MCA- and PCA-phase shift angles did not significantly change between baseline and plateau. Although baseline ICP and RAP varied among patients dRAP and dICP were significantly correlated and suggested similar intracranial compliance among patients of three subgroups . ResponsPhase-shift angles between M waves in ABP and MCA-FV as well as between ABP and PCA-FV were ranging between -58.9 and +171.0grad . Lower dThe comparison of phase shifts between baseline and plateau in most cases revealed no significant differences. Under conditions of low pressure compliance of 0.01+/-0.01/mmHg only, the ventricular volume load led to a decline of M wave phase shift in the PCA.This study showed that cerebral perfusion pressure and dynamic cerebral autoregulation in patients with communicating hydrocephalus are depending on the ventricular pressure compliance. CPP and M wave phase shift angles at baseline as well as during controlled ventricular volume load were correlated with dRAP/dICP. The transient ventricular volume load did however, neither alter the dynamic cerebral autoregulation nor CPP significantly. There are many hypotheses about the link between communicating hydrocephalus and alterations of cerebral blood flow and perfusion –27. ImagBy means of the TCD-based analysis of dynamic cerebral autoregulation in patients with communicating hydrocephalus we did not find any regional differences between the M wave phase shifts in the anterior and posterior parts of circulation. The advantage of TCD lies in the time resolution of seconds and less. The method thus detects gradual differences of the autoregulatory response to spontaneous blood pressure oscillations of a frequency of 3 to 9 cycles per minute. M wave phase shifts may depend on the degree of carotid or MCA stenosis as well as the sufficiency of collateral blood supply –33. Our Mase et al (2006) hypothesized that indeed, the most important factor in the underlying pathophysiology of communicating hydrocephalus is the alteration of intracranial compliance . We haveThe gradients dRAP/dICP distinguished subgroups of low, medium, and high pressure compliance in patients with communicating hydrocephalus and provided information about the mechanoelastic characteristics of the cerebrospinal system . RecentlThis study showed that cerebral perfusion pressure and dynamic cerebral autoregulation in particular, depend on the cerebrospinal pressure compliance. These results suggested that the alteration of mechanoelastic characteristics contributes to a reduced cerebral perfusion and a loss of autonomy of cerebral blood flow regulation. Results warrant a prospective study with TCD and MRI in order to investigate whether impaired dynamic cerebral autoregulation and low cerebrospinal compliance in communicating hydrocephalus are related to small vessel disease.


Study the association between the total caloric intake, protein, lipid, and some classes of fatty acids of the diet, and their effects on blood pressure in a sample of Egyptian obese women with and without visceral obesity.Five hundred forty-nine obese women were included in the study with mean age of 38.1 ± 11.56 years and mean Body mass index [BMI] of 36.17 ± 7.23. They enrolled in a program for losing weight. Visceral fat was determined using ultrasound. Blood pressure was measured 3 times and the mean was recorded. Twenty four hours dietary recall was reported.Thirty point four percentages of samples has visceral obesity ≥ 7cm; they were the older, showed higher values of BMI, visceral obesity and blood pressure. Significant difference was found between groups regarding mean value of BMI, visceral obesity, both systolic blood pressure SBP and diastolic blood pressure DBP and most of the daily macronutrients intake. In groups (2&3) positive significant correlation was recorded between (SBP) & (DBP) and total daily intake of total calories, carbohydrate, total fat, saturated fatty acids and cholesterol, and negative significant correlation with total daily intake of total protein, animal and vegetable protein, linolenic and linoleic fatty acids, while oleic fatty acid showed negative correlation with SBP&DBP in all groups.This study emphasizes the hypothesis that the macronutrients composition of diet influences blood pressure in different ways, in obese patients with visceral obesity. Elevated blood pressure (BP) continues to be a major public health concern because of its high global prevalence and its concomitant increase as risk of cardiovascular disease , 2. StudEnergy balance and macronutrient balance are the cornerstones upon which any theories of obesity must be built. Obesity can only occur when energy intake remains higher than energy expenditure for an extended period of time. However the macronutrient composition of the diet can also affect energy balance. Fat is a key nutrient because it is poorly regulated at both the level of consumption and oxidation . DietarySaturated fatty fats (SFAs) have a bad file and several experimental studies in the rat showed a progressive increase in blood pressure in response to a highly saturated diet . MoreoveLittle is known about the relation of different dietary protein types with blood pressure. Altorf-Van , reporteThe aim of this study focuses on the quantitative concern of total caloric, protein, lipid, and some classes of fatty acids of the lipid fraction of the diet, and their effects on blood pressure in a sample of Egyptian obese women with and without visceral obesity.2. All women were subjected to thorough clinical examinationFive hundred forty nine obese women, shared as volunteers in this study. They were enrolled in a program for losing weight in National Research Centre (NRC) Egypt that lasted for 24 month, after taking approval from Ethical Committee of NRC and written informed consent from each of them. Their mean age was 38.1 ± 11.56 years and had a mean BMI of 36.17 ± 7.23 kg/m2). All participants had BMI >29 kg/m2.Relevant anthropometric measurements were reported including height and weight using standardized equipment, and following the recommendations of the International Biological Program . Body maBlood pressure for each of them was measured 3 times in the same setting and the mean value was recorded. Systolic and diastolic blood pressures were measured throughout for each subject in the sitting position using standardized mercury sphygmomanometer with an appropriate blood pressure cuff that covers at least two thirds of the right upper arm length and does not encroach on the antecubital space.Visceral fat was determined by using ultra sound device. Ultrasound (US) examination to each participant was done to evaluate visceral fat at the umbilicus (USVF) in cm. Intrabdominal fat thickness measurement was obtained using the “Medison Sonoace X8” ultrasonography equipment. For the visceral fat, a 3.5 MHz transducer was transversely positioned 1 cm above the umbilical scar on the abdominal midline, without exerting any pressure over the abdomen. Visceral fat thickness attempted corresponding to the measurement in centimeters between the internal surface of the abdominal rectus muscle and the posterior aortic wall in the abdominal midline, during expiration. Cutoff point of umbilical visceral fat thickness ≥7 cm was assessed for diagnosis of visceral obesity . In the Collecting detailed data about food intake was done through 24 hour recall that repeated for 3 days. Analysis of food items was done using World Food Dietary Assessment System, (WFDAS), 1995, USA, University of California.All values were expressed as mean value ± SD. Two tailed student t-test was used to compare between the two groups. Correlation between the different parameters was tested by Pearson test. P values <0.05 were considered statistically significant. SPSS windows software version 17.0  was used.Sample distribution, according to the degree of visceral obesity (VO) presented in Means ± SD per daily intake of the different macronutrients of the different groups presented in Tables Data of this study revealed that overweight and obese women in the different three groups consumed high amount of calories, protein and fat in their daily diet compared to the RDAs, where it reached 124.01% and 184.74% of the RDAs for the mean daily caloric and protein intake respectively in group (3).Positive significant correlations were found between both SBP and DBP and the mean daily intake of total calories, carbohydrate, total fat, SFAs, and cholesterol in groups (2&3) that had higher degree of BMI and visceral obesity, which is in line with that reported by Najafian , who staOn the other hand, negative significant correlations were found between SBP & DBP and the daily intake of the total protein, vegetable and the animal protein in groups (2&3). Friedman et al , observeObservational studies indicate that dietary saturated fat is positively associated with blood pressure , 22, andThe role of individual fatty acids in blood pressure regulation is unclear. Data of this study revealed high negative significant correlation between the monounsaturated fatty acids (MUFA), the oleic fatty acid and both SBP and DBP in the overweight women (group 1) and in the same time obese women who had BMI ≥30 and visceral obesity that support its important healthy effect in control of BP level. Mediterranean dietary pattern has been proposed as a healthy choice for the prevention of cardiovascular disease, part of its beneficial impact can be mediated through a favorable effect on blood pressure (BP). A major characteristic of the Mediterranean diet is a high supply of energy coming from MUFA, . IncreasIn conclusion, consumption of healthy diet characterized by balanced macronutrients, protein, fat and carbohydrate, rich in monounsaturated, polyunsaturated fatty acids may contribute to prevention and control of adverse blood pressure levels.


P < 0.001), 2.28 (1.13–4.58) (P < 0.05), 3.55 (1.70–7.42) (P < 0.001), and 9.42 (4.22–21.02) (P < 0.001), respectively. In subgroups analysis, the multivariable relative odds ratio of chronic kidney disease was highest in patients with both resistant hypertension and severe sleep apnea [13.42 (4.74–38.03)] (P < 0.001). Severe sleep apnea, stage III hypertension, and resistant hypertension are independent risk factors for chronic kidney disease. Patients with both severe sleep apnea and resistant hypertension have the highest risks.Hypertension, blood pressure variation, and resistant hypertension have close relations to sleep apnea, which lead to target organ damage, including the kidney. The complex relationships between sleep apnea and blood pressure cause their interactions with chronic kidney disease ambiguous. The aim of the study was to elucidate the separate and joint effects of sleep apnea, hypertension, and resistant hypertension on chronic kidney disease. A cross-sectional study was done to see the associations of sleep apnea, hypertension, and resistant hypertension with chronic kidney disease in 998 subjects underwent overnight polysomnography without device-therapy or surgery for their sleep-disordered breathing. Multivariate logistic regression was used to analyze the severity of SA, hypertension stage, resistant hypertension, and their joint effects on CKD. The multivariable relative odds (95% CI) of chronic kidney disease for the aged (age ≥65 years), severe sleep apnea, stage III hypertension, and resistant hypertension were 3.96 (2.57–6.09) ( Recognizing and controlling the risk factors for CKD may improve outcomes.Chronic kidney disease (CKD) is a serious global health problem, Previous studies have reported a high prevalence of SA among patients with CKD, and SA has been reported to potentially be a risk factor for CKD.,5 However, most of previous studies were conducted mainly in subjects with the estimated glomerular filtration rate (eGFR) between 60 and 90 mL/min/1.73 m2,,6–9 and the effect of SA on CKD (eGFR < 60/mL/min/1.73 m2) is unknown. In addition, SA has been reported to be associated with hypertension and resistant hypertension,,11 which are well-known risk factors for deteriorating renal function.,13 SA has also been aroused to be associated with blood pressure variation, which is closely associated with organ damage. Therefore, the interactions of SA, hypertension, and RH on CKD need to be clarified. The aim of the study was to clarify the interactions of SA, hypertension, and RH on CKD.Sleep apnea (SA) is defined as the presence of >5 complete or partial breathing disruptions, each lasting for at least 10 seconds per hour during sleep. SA is a common disease and reportedly affects ∼20% of the general population.22.1Sandman Elite System, Tyco Inc., Ottawa, Canada) at China Medical University Hospital, and did not undergo surgery or device-based therapy for sleep-disordered breathing, were enrolled in this study.From January 2007 to December 2009, all patients, who underwent single night polysomnography (2.2 The patients with CKD were defined as those with an eGFR <60 mL/min/1.73 m2 for 3 months or longer. Patients who were ≥ 65 years were considered as “Aged.” Hypertension was defined as a blood pressure >140/90 mm Hg. Resistant hypertension (RH) was defined as a failure to adequately control blood pressure control (<140/90 mm Hg) after treatment with 3 kinds of antihypertensive drugs, of which one was a diuretic. The stage of hypertension was defined according to JNC7 and the Taiwan hypertension guidelines. Stage 1 hypertension was defined as systolic blood pressure/diastolic blood pressure 140–159/90–99 mm Hg, stage 2 as ≥160/ ≥100 mm Hg, and stage 3 as ≥180/ ≥110 mm Hg. Diabetes mellitus (DM) was defined as HbA1c>6.5% or fasting glucose ≥126 mg/dL or a random plasma glucose level ≥200 mg/dL. Hypercholesterolemia was defined as a serum cholesterol level ≥ 200 mg/dL. The body mass index (BMI) was calculated as the body weight, measured at the night of the polysomnography study, divided by the square of the height (kg/m2). A diagnosis of SA was according to the American Academy of Sleep Medicine 2007 manual. The severity of SA was estimated using the apnea–hypopnea index (AHI), with a score ≥30 been defined as severe SA, 5 to 30 as mild to moderate SA, and <5 was as no SA. A written informed consent was obtained from all the patients before commencement of polysomnography study. This study was approved by the Institutional Review Board of our hospital (reference number: DMR101-IRB2-129).We performed this cross-sectional study to investigate the individual and synergistic effects of SA, hypertension stage, and RH on CKD. Clinical data and diagnoses were obtained from the patients’ medical history, image study, medical records, and standardized questionnaires. The data collected in from night polysomnography and medical records were reviewed by physicians, and the eGFR was calculated using the CKD–EPI formula.2.3P < 0.05. SAS software version 9.3  was used for all data analyses.Descriptive statistics were presented as frequencies and percentages, or means ± standard deviations. For the comparisons of means and proportions, ANOVA  tests were performed for continuous variables and trend tests were used for categorical variables. We performed multivariate logistic regression analysis, and the odds ratios (ORs) with 95% confidence intervals (CIs) were estimated after adjusting for covariates. In multivariate regression analysis, the variables were chosen based on variables that were important in the literature and clinical practice. All tests were considered statistically significant when 32. When the patients were classified into 3 groups according to the severity of hypertension, the mean age, BMI, and AHI score increased from the HTN (−) group (the patients without hypertension), to the group with hypertension stage 1 to 3, to the RH group. The prevalence rates of CKD and DM were significantly different among these 3 groups with the lowest rates in the HTN (–) group and highest in the RH group. There were also significant differences in gender between these 3 groups. The proportion of male was higher than the proportion of female in all the 3 groups , 5 ≤ AHI <30 (n = 499), and group with AHI<5 (n = 214). The mean age and BMI were significantly different among these 3 groups. The patients with an AHI ≥30 were older and had a higher BMI than those in the other groups. There were also significant differences in gender with more males in the AHI ≥30 group (85.6%), followed by the 5 ≤ AHI <30 group (69.7%), and AHI<5 group (56.5%). In addition, there were significant differences in hypertension, DM, and CKD between the 3 groups with higher prevalence rates in the groups. The percentages of these comorbidities were associated with groups with a higher AHI. There was no significant difference in hypercholesterolemia among the groups. There was a significant difference in smoking among the 3 groups, with the group with an AHI ≥30 having the highest percentage (24.6%) , severe SA, stage 3 hypertension, and RH significantly increased the OR of CKD, whereas BMI and DM did not , as this is not reliable in the older patients with low muscle mass6The present study explored the effects of SA, hypertension, and RH on CKD. The patients with stage 3 hypertension and RH had a higher risk of CKD, especially when also had severe SA. It is necessary to do polysomnography in patients with disordered sleep, and severe SA may need to be treated because of its high CKD risk.


Methamphetamine (MA) is a prevalently abused psychostimulant in the world. Previously published studies and case reports indicated potential associations between MA and body mass index (BMI) and cardiovascular factors . However, these associations have not been studied clearly. This study aimed to investigate BMI and cardiovascular factors in the MA-dependent patients.A total of 1019 MA-dependent patients were recruited between February 2, 2008 and March 11, 2013. A case report was used to gather information on sociocharacteristics and drug-dependent history. Meanwhile, a number of 1019 age- and sex-matched controls’ information were collected from the physical examination center. We measured BMI, blood pressure, and fasting blood glucose among the participants.2, P < 0.001), lower fasting blood glucose  and higher systolic blood pressure  compared with the control group after adjustment of possible confounders. Additional, we only found the duration of MA use was independently associated with BMI .MA-dependent patients had significantly lower BMI (20.4 ± 0.1 vs 23.9 ± 0.1 kg/mThis study demonstrated that MA dependence was associated with BMI and cardiovascular factors. In addition, we found a negative association between duration of MA use and BMI. The influence of MA on blood glucose has been reported by most animal experiment. In animal experiment, temporal increase in blood glucose has been observed,Given the prevalent use/abuse and the serious cardiovascular effect of MA, an enhanced understanding of cardiovascular responses is needed. It is surprised that little research has investigated cardiovascular responses among MA-dependent patients compared with the healthy population. In our present study, the first purpose was to compare the BMI and cardiovascular factors between a larger Chinese population with MA dependence and healthy controls. Furthermore, we aimed to examine the influence of potential-risk clinical features on BMI and cardiovascular factors among the MA-dependent patients.The total of 1019 studied individuals were selected from Sanyang Detoxification Institute between February 2, 2008 and March 11, 2013. All individuals met the following inclusion criteria: age 18 years or above; were only using MA; had a positive result on the urine test for MA at admission; satisfied DSM-IV criteria for MA dependence; have been withdrawal for 1 to 7 days; and signed informed consent. The individuals were excluded if they had dependence on other drugs and had any seriously illness that needed pharmacological treatment.A total of 1019 healthy age- and sex- matched individuals selected from the regular medical examination at The First Affiliated Hospital of Wenzhou Medical University served as control group, if they had no illegal dependence and serious diseases. All healthy individuals were selected at the same period with the studied ones.The study was approved by the Human Research and Ethics Committee of Wenzhou Medical University. Written informed consents were signed from all participants.A case report form that included sociodemographic characteristics, age at onset, duration of MA use, routes of drug administration, and daily dose was conducted by the inpatients at admission. The control groups’ sociodemographic data were collected from the physical examination center at The First Affiliated Hospital of Wenzhou Medical University.2). The right arm blood pressure of seated participants was obtained under resting condition. Fasting blood glucose was measured on the second day of admission. All data were recorded by trained operators who blind to the research design.The participants’ height and weight were measured at admission. The BMI was counted as weight divided by the square of height . P < 0.05 was considered to be statistically significant.We compared the sociodemographic variables, BMI, and cardiovascular factors between MA-dependent patients and healthy controls using analysis of variance (ANOVA), Mann–Whitney P > 0.5). Among the patients, they had a mean age at onset of MA use of 27.0 ± 7.5 years (range 11–51years). The average duration of MA use was 52.1 ± 58.6 months (range 1–228 months). The routes of MA administration were smoking (91.6%), intranasal administration (5.9%), oral (0.9%), intravenous injection (0.9%), and others (0.7%). The mean dose of MA use was 0.13 ± 0.13 g/day (range 0.05–3.0 g/day).The characteristics of MA-dependent patients and healthy controls are presented in Table 2, P < 0.001), fasting blood glucose , and diastolic blood pressure , whereas systolic blood pressure was significantly higher among MA-dependent patients .In unadjusted analysis Table , compareP < 0.001). However, with the effects of BMI, sex and age adding to the ANOVA as covariates, the significant difference in fasting blood glucose and systolic blood pressure were still existent, except for diastolic blood pressure .In adjusted analysis Table , there wP = 0.04) was independently related to BMI. However, information on MA-dependent history such as the duration of MA use, age at onset, and daily dose of MA use was not found to be related to systolic blood pressure and glucose .Among the patients, with BMI, systolic blood pressure and fasting blood glucose separately used as a dependent variable and sex, age, the duration of MA use, age at onset, routes of MA administration, and daily dose used as independent variables in the stepwise multiple regression analysis, we only found that the duration of MA use . Additionally, an animal experiment revealed that elevated blood pressure was attributed to injection of MA administration in rats, which may be correlated to catecholamine liberation.23 In contrast to our findings, Burchell et al10 reported that hypotension was found in MA-dependent patients during medical treatment. However, the patients were admitted to the hospital with serious metabolic acidosis. A recent study performed by Celotto et al24 found that acute metabolic acidosis caused the reduction in blood pressure. In our study, patients who have seriously disease were excluded. Therefore, the discrepancy may be explained by difference in inclusion criteria.Furthermore, we found that MA dependence was associated with increased blood pressure. Two previous researches are consistent with our findings. For example, a study conducted by Pike et al9 Contrary to above results, studies have indicated that MA only increased glucose levels at short time following MA administration in rats.8 The discrepancy between our study and previous studies demonstrating blood pressure severely increased after MA administration may be explained by the tolerance that develops with MA administration over several days.25In addition, our study showed that fasting blood glucose in MA-dependent patients was lower than controls, which resembles with previous study. For example, a study reported that the hypoglycemic influence of MA was noted in the mouse. Additionally, this study also demonstrated MA-induced insulin secretion through its direct influence on the pancreas.26 In contrast with this result, a genetic study demonstrated that appetite regulation genes may be significant markers of risk of developing obesity.27 Further studies should be conducted to clarify the relationship between dietary intake and BMI among the MA-dependent patients.There are some limitations in our study. First, we cannot make a conclusion about a casual relationship between MA dependence and BMI and cardiovascular factors because of the cross-sectional design. Second, the information about MA dependence stemmed from self-report of patients, which may lead to deviation with the actual situation. Third, measurement error and observer bias were present in our research as a result of retrospective study. Fourth, we did not examine dietary intake of participants, which may have a biased influence on the results. However, a previous study indicated that the lower BMI of drug abusers could not account by dietary intake.In summary, our study indicated that MA-dependent patients had increased systolic blood pressure, reduced BMI, and fasting blood glucose. Additionally, the duration of MA use was negatively related to BMI. Further studies investigating the causal relationship between MA dependence and BMI and cardiovascular factors should be carried out to develop better treatments to prevent MA complication.


In the multivariate analysis, adjusting for age, gender, diabetes, smoking and, left ventricular concentric hypertrophy, PF was significantly associated with the presence of CAC (OR: 1.88 95% CI: 1.03–3.43 per standard deviation). PF remained associated with CAC even with additional adjustments for estimated glomerular filtration rate or serum phosphorus . PF is independently associated with CAC in non-dialysis dependent CKD patients.Pericardial fat (PF) a component of visceral adipose tissue has been consistently related to coronary atherosclerosis in the general population. This study evaluated the association between PF and coronary artery calcification (CAC) in non-dialysis dependent chronic kidney disease (CKD) patients. This is a post-hoc cross sectional analysis of the baseline of a prospective cohort of 117 outward CKD patients without manifest coronary artery disease . CAC scores, PF volume and abdominal visceral fat (AVF) areas were measured by computed tomography. The association of PF as a continuous variable with the presence of CAC was analyzed by multivariate logistic regression. CAC  was present in 59.2% patients. Those presenting CAC were on average 10 years older, had a higher proportion of male gender , and had higher values of waist circumference , PF volumes (224.8±107.6 vs. 139.1±85.0 cm Chronic kidney disease (CKD) is highly prevalent affecting roughly 7% of the general adult population and up to one in three elder individuals Coronary artery calcification (CAC), a marker of subclinical vascular disease that is highly prevalent in CKD, reliably predicts the risk for overall mortality and cardiovascular events in dialytic Pericardial fat (PF) comprises all fatty tissues in the mediastinum surrounding the myocardium, especially over the epicardial coronary track There is limited evidence associating epicardial and pericardial fat with CAC in CKD individuals This is a post hoc analysis from a prospective cohort that comprised 117 stage 2–5 non-dialysis chronic kidney disease (ND CKD) patients followed at the outpatient clinic of the Nephrology Division, Federal University of São Paulo (UNIFESP) in Sao Paulo, Brazil The exclusion criteria were: age <18 years, presence of chronic inflammatory diseases, current malignancy, HIV infection, viral hepatitis, chronic steroid usage, and previous manifestations of coronary heart disease. The majority was using angiotensin converting enzyme inhibitors (82.2%); 22.9% angiotensin receptor blockers, 77.1% diuretics, 41.5% beta-blockers, 34% patients were on statins and 4.2% on recombinant human erythropoietin. Thirty patients (29.1%) were using sevelamer, six (5.0%) calcium based phosphate binders, and six (5.0%) calcitriol.2) was calculated. Blood samples were drawn in the fasting state. The biochemical parameters including serum creatinine, ionic calcium, phosphorus, alkaline phosphatase, lipid profile, hemoglobin, albumin and intact parathyroid hormone (iPTH) were measured by chemiluminescence immunoassay . High-sensitivity C-reactive protein (CRP) was measured by an immunometric assay . Proteinuria was directly measured by 24-hour urine samples and the glomerular filtration rate (eGFR) was estimated by the simplified “Modification of Diet in Renal Disease” (MDRD) equation. Abnormal proteinuria was defined as excretion >300 mg/24 hours. The diagnosis and classification of CKD was determined according to KDIGO guidelines criteria All patients underwent clinical evaluation, where their personal and familiar previous medical history and physical exam were addressed. Diabetes was defined as a fasting glucose >126 mg/dL or current usage of any anti-diabetic medication. Hypertension was ascertained by average blood pressure over 140×90 mmHg in two subsequent measurements after 15 minutes resting in sitting position or usage of any anti-hypertensive medication. Current smoking was defined as any cigarette consumption in the last month and ever smoking as any previous daily cigarette sustained consumption for at least 6 months. Body weight (kg), height (m), waist circumference (cm), as well as systolic and diastolic arterial pressure (mmHg) were measured as previously described 2 and >95 g/m2 respectively in men and women was considered elevated A two-dimensional color Doppler echocardiogram was performed in each patient according to the recommendations of the American Society of Echocardiography CAC was quantified by multi-slice computed tomography . The tomographic axial slices were acquired with a 2.5 mm thickness, prospective acquisition and synchronization to EKG, with a 0.4 seconds rotation, temporal reconstruction by 6 frames per second, and W-ray tube voltage of 120 kV and 350 mA. CAC was quantified as previously described by Agatston et al. 3) was calculated from measurements of each PF axial slice area (in cm2). In each tomography slice a semi-automatic selection by radiodensity window ranging from −30 to −200 Hounsfield units using the limiar technique (threshold) was made. For the segmentation, a tool from the Osirix software, which detects tissues within the mentioned thresholds surrounding the selection point was used. By this technique fat areas demarked in each axial slice, and fat outside PF borders were manually delimitated to display the final axial area  University of Sao Paulo Medical School Hospital (HCFMUSP) with supervision from the Cardiac Tomography and Resonance Service at the same hospital. The images obtained for CAC measurement were recovered and uploaded on an I- Mac Apple computer with and Intel Core i3 processor running MacOSx version 10.6. The Osirix Imaging Software , open source version 3.9 ial area . The PF ial area  and 3. I2) were measured by computed tomography  at the level of the 4th and 5th  were obtained by delineating and computing the adipose tissue surface using an attenuation range of −150 to −50 Hounsfield units.Abdominal visceral fat (AVF) and subcutaneous abdominal fat (SAF) areas  and 95% confidence intervals (CI). The direct comparison of CAC presence discrimination by PF and AVF was made by their individual receiver operating characteristic curves. P values <0.05 were considered statistically significant. The analyses were made using, the SPSS software for Macintosh .Data normality was tested by the Kolmogorov-Smirnov test. Normally distributed data were expressed as mean ± standard deviation, while non-normal data were expressed as median and interquartile ranges. Categorical variables were depicted as percent frequency (proportions). Chi-square test or Fisher's exact test were used to compare categorical variables when pertinent. Continuous variables were analyzed by Student's t test or by Mann-Whitney's test. The correlation between PF with the other markers of adiposity: waist circumference, BMI, AVF and SAF was tested by Pearson's test. Univariate and multivariate logistic regression analysis were performed to evaluate the association between presence of CAC and other variables. PF was expressed in standard deviation (SD) units rather than cm3 in women, p<0.001). Regarding other adiposity markers, PF volume correlated with AVF area , waist circumference , BMI  and SAF area . PF was not related with eGFR  and was not different in diabetic compared to non-diabetic patients .The PF was related with age  and was higher in men (220.4±110.5 vs.135.4±76.0 cm3 (p<0.01).Overall, 61 patients (59.2%) had CAC and among those the median (interquartile ranges- IQR) calcium score was 219 (IQR 25.5–756.0) AU. Forty-two patients (40.8%) had no coronary calcification (CAC score  = 0), in 23 patients (22.4%) CAC score was between 1–100 AU, and in 38 (36.9%) CAC score was >100 AU. The distribution of PF within CAC = 0, CAC>0–100 and CAC>100 groups were respectively, 139.1±85.0; 221.0±119.3 and 227.1±101.5 cmThis study addressed the association of PF volume with CAC presence measured by computed tomography in non-dialysis dependent CKD patients. PF was independently associated with CAC even after adjustment for parameters previously related with CAC in this population. The results suggest a role of PF, a component of the visceral fat compartment adjacent to the heart, on the pathophysiology of coronary vascular calcification development in CKD patients.PF is considered as part of the visceral adipose tissue compartment vasa vasorum or through systemic circulation Notwithstanding the known endocrine effects of abdominal visceral adipocytes on the coronary arteries 2. In that study CAC and serum levels of interleukin-6 were associated with epicardial fat volume (the dependent variable). The current study addresses this association by two different aspects: first, PF that comprises not only epicardial fat, that is located directly over the coronary arteries, but also within the rest of the pericardial sac was measured; second, we depart from PF to CAC (the dependent variable) as the physiopathological premise is PF being a promoter of CAC rather than the opposite.In CKD patients Turkmen et al. found a positive association of epicardial fat, a subset of PF located below the visceral pericardial sac, with CAC presence in peritoneal dialysis patients The results of this study reinforce the possible role of ectopic fat accumulation on the rather complex pathophysiology of CAC in CKD patients This is a post-hoc analysis of a cohort of CKD patients. However, all the data including clinical, laboratory and computed tomography parameters were collected concomitantly. So far there is no gold standard in the literature to adequately quantify the different components of thoracic ectopic adipose tissue that comprises pericardial, epicardial and intra-thoracic components. Therefore, the comparison of this study with previous results should be made with care. However, it is important to reinforce the high reliability of our measurement technique, confirmed by the high inter-observer index.On the multivariate analysis the confounding effect of hypertension for CAC is paramount. As more than 95% of the sample was hypertensive, using simply categorical labeling would not identify all the differential spectrum of exposition burden. Systolic arterial pressure as well would not discriminate this hemodynamic burden, since the sample had a good average control due to antihypertensive medication. So, concentric hypertrophy was used as marker of hypertension burden in our population. Indeed Ertük PF volume measured by computed tomography was associated with CAC presence in non-dialysis dependent CKD population. Further studies are required to evaluate this association.


Progranulin (PGRN) is expressed in many cell types, including adipocytes. It has been recognized as an adipokine related to obesity, insulin resistance and type 2 diabetes mellitus (T2D) and its levels depend on kidney function. However, the association of PGRN with diabetic kidney disease remains unknown.To evaluate serum and urinary levels of PGRN in patients with T2D and chronic kidney disease (CKD) stages 3-5 and compare to patients with T2D and glomerular filtration rate  >60 mL/min and with control individuals without T2D.Case-control study. Cases were defined by the presence of T2D and CKD stages 3-5, evaluated by estimated GFR<60 mL/min, and controls were formed by patients with T2D and GFR>60mL/min (diabetic control group); and by individuals without T2D (non-diabetic control group). PGRN was determined with enzyme-linked immunosorbent assay in blood and urine samples after overnight fasting. The study groups were compared by ANOVA with Tukey or Kruskal-Wallis with Dunn tests for continuous and χ2 test for categorical variables. The Spearman's correlation coefficient was used. This study was approved by the Ethics Committee of Hospital involved, and all subjects signed the informed consent.114 patients were included . There were no differences in age, gender, ethnicity and body mass index (BMI) between groups. PGRN serum levels were increased in patients with T2D and CKD stages 3-5, when compared to control groups . On the other hand, urinary PGRN was decreased in cases compared to T2D control group . There was a positive correlation between serum PGRN and BMI , waist circumference ; ultra-sensitive C reactive protein  and interleukin-6  and a negative correlation with GFR  in all patients. Urinary PGRN was positively associated to urinary albumin excretion .PGRN serum levels seems to be a marker of obesity and inflammatory state that is affected by decrease in GFR; while urinary PGRN could be a marker of diabetic kidney disease.