Risk Of Chronic Kidney Disease In Patients Research Articles

Association of blood pressure and long-term change with chronic kidney disease risk among Chinese adults with different glucose metabolism according to the 2017 ACC/AHA guidelines.

Whether the definition of hypertension according to 2017 AHA/ACC guidelines and blood pressure (BP) changes was related to the increased risk of chronic kidney disease (CKD) remained debated. This prospective cohort study aimed to investigate the association of BP and long‐term BP change with CKD risk with different glucose metabolism according to the new hypertension guidelines. This study examined 12 951 participants and 11 183 participants derived from the older people cohort study, respectively. Participants were divided into three groups based on blood glucose and the risks were assessmented by the logistic regression model. During a 10 years of follow‐up period, 2727 individuals developed CKD (21.1%). Compared with those with BP < 130/80 mmHg, individuals with increased BP levels had significantly increased risk of incident CKD. Participants with BP of 130–139/80–89 or ≥140/90 mmHg had 1.51‐ and 1.89‐fold incident risk of CKD in patients with diabetes mellitus (DM). Compared with individuals with stable BP (−5 to 5 mmHg), the risk of CKD was reduced when BP decreased by 5 mmHg or more and increased when BP increased ≥5 mmHg among normoglycemia and prediabetes participants. Similar results were observed for rapid estimated glomerular filtration rate (eGFR) decline. In conclusion, the BP of 130–139/80–89 mmHg combined with prediabetes or DM had an increased risk of incident CKD and rapid eGFR decline in older people. Long‐term changes of BP by more than 5 mmHg among normoglycemia or prediabetes were associated with the risk of incident CKD and rapid eGFR decline.

Narrative Review of Carotid disease and the kidney.

Patients with chronic kidney disease (CKD) have an increased cardiovascular (CV) risk that is only in part explained by established risk factors. Carotid arteriosclerosis and atherosclerosis are increased in CKD, play a role in the causation of CV disease in these patients and can affect the progression of renal disease. The arterial stiffening process is evident even in CKD patients with a very mild reduction of glomerular filtration rate (GFR) whereas arterial thickening is evident in more advanced stages. Possible mechanisms include functional and structural alterations of the arterial wall. Arterial stiffness can mediate the effect of CKD on target organs (i.e., brain, kidney and heart). In this review we discuss the arterial phenotype of patients with CKD. This is characterized by increased common carotid artery stiffness and outward remodeling (enlargement and thickening of the arterial wall) and a normal/reduced stiffness paired with an inward remodeling (narrowing of the arterial wall) of muscular arteries. We also discuss the consequences of carotid dysfunction, including the involvement of large elastic arteries stiffness on ventricular-vascular coupling, the mechanisms linking carotid stiffening and increased cardio- and cerebrovascular risk in CKD patients, and the therapeutic options to improve carotid function.

404-P: Advanced Liver Fibrosis Is Associated with an Increased Risk of Chronic Kidney Disease in Patients with Type 2 Diabetes and NAFLD

Objectives: Nonalcoholic fatty liver disease (NAFLD) is associated with chronic kidney disease (CKD). However, the causal relationship between NAFLD and the development of CKD is uncertain, particularly in patients with type 2 diabetes. We aimed to investigate the association between the presence and severity of NAFLD and incident CKD in patients with type 2 diabetes. Research Design and Methods: In this longitudinal cohort study of patients with type 2 diabetes, 3,188 patients with preserved renal function were followed for the occurrence of incident CKD. NAFLD was defined as the presence of hepatic steatosis on ultrasonography without any other causes of chronic liver diseases. Advanced liver fibrosis of NAFLD was defined as NAFLD fibrosis score &amp;gt;0.675. CKD was defined as estimated glomerular filtration rate (eGFR) &amp;lt; 60 mL/min/1.73 m2. Results: At baseline, 1,729 (54.2%) patients had NAFLD, of whom 94 (5.4%) had advanced liver fibrosis. During the follow-up of 8.3 ± 3.6 years, 472 (14.8%) patients developed incident CKD, 220 (15.1%) in the non-NAFLD group, 226 (12.8%) in the hepatic steatosis alone group and 26 (27.7%) in the advanced liver fibrosis group. There was no increased risk of incident CKD in the NAFLD group compared with the non-NAFLD group (p = 0.79). However, among patients with NAFLD, advanced liver fibrosis was associated with an increased risk of CKD (adjusted hazard ratio [HR] 1.78 (95% confidence interval [CI] 1.14-2.76), p=0.011). Conclusions: Advanced liver fibrosis in NAFLD is independently associated with an increased risk of incident CKD in patients with type 2 diabetes. Disclosure D. Seo: None. Y. Cho: None. S. Ahn: None. S. Seo: None. S. Hong: None. Y. Lee: None. S. Kim: None. Funding National Research Foiundation (2017R1D-1A1B03034581)

MO159CHA2DS2-VASC SCORE AS A PREDICTOR OF CARDIOVASCULAR MORTALITY IN CHRONIC KIDNEY DISEASE PATIENTS

Abstract Background and Aims Cardiovascular mortality is high in chronic kidney disease (CKD) patients. Recognizing patients with higher cardiovascular risk might help in their treatment. CHA2DS2-VASc score was originally used to predict cerebral infarction in patients with atrial fibrillation (AF). However, it is also useful in predicting outcome in different cardiovascular conditions, independent of the presence of AF. Therefore, the aim of our research was to assess the role of CHA2DS2-VASc score in cardiovascular mortality in CKD patients. Method Eighty-seven non-dialysis CKD patients from our outpatient clinic were included. At the time of inclusion, medical history data and standard blood results were collected and CHA2DS2-VASc score was calculated. Patients were followed for assigned time or until their death. Mean follow-up time was 1696.45±564.60 days. Results Descriptive statistics of our patients are presented in table 1. During follow-up 11 patients suffered from cardiovascular death. Univariate Cox regression analysis showed that CHA2DS2-VASc score is a significant predictor of cardiovascular mortality (HR: 2.19, CI: 1.42-3.37, p=0.001). In multivariate Cox regression analysis in which CHA2DS2-VASc score, serum creatinine, urinary albumin/creatinine, haemoglobin, high sensitivity CRP and intact PTH were included, CHA2DS2-VASc score was an independent predictor of cardiovascular mortality (HR: 2.04, CI: 1.20-3.45, p=0.008) (table 2). Conclusion CHA2DS2-VASc score is a simple and quick way to identify cardiovascular risk in CKD patients.

The impact of advanced glycation end products on bone properties in chronic kidney disease.

Chronic kidney disease (CKD) affects over 15% of Americans and results in an increased risk of skeletal fractures and fracture-related mortality. However, there remain great challenges in estimating fracture risk in CKD patients, as conventional metrics such as bone density assess bone quantity without accounting for the material quality of the bone tissue. The purpose of this review is to highlight the detrimental effects of advanced glycation end products (AGEs) on the structural and mechanical properties of bone, and to demonstrate the importance of including bone quality when assessing fracture risk in CKD patients. Increased oxidative stress and inflammation drive the production of AGEs in CKD patients that form nonenzymatic crosslinks between type I collagen fibrils in the bone matrix. Nonenzymatic crosslinks stiffen and embrittle the bone, reducing its ability to absorb energy and resist fracture. Clinical measurement of AGEs is typically indirect and fails to distinguish the identity and properties of the various AGEs. Accounting for the impact of AGEs on the skeleton in CKD patients may improve our estimation of overall bone quality, fracture risk, and treatments to improve both bone quantity and quality by reducing AGEs in patients with CKD merit investigation in order to improve our understanding of the etiology of increased fracture risk.

Optimal Protein Intake in Pre-Dialysis Chronic Kidney Disease Patients with Sarcopenia: An Overview.

Multi-factors, such as anorexia, activation of renin-angiotensin system, inflammation, and metabolic acidosis, contribute to malnutrition in chronic kidney disease (CKD) patients. Most of these factors, contributing to the progression of malnutrition, worsen as CKD progresses. Protein restriction, used as a treatment for CKD, can reduce the risk of CKD progression, but may worsen the sarcopenia, a syndrome characterized by a progressive and systemic loss of muscle mass and strength. The concomitant rate of sarcopenia is higher in CKD patients than in the general population. Sarcopenia is also associated with mortality risk in CKD patients. Thus, it is important to determine whether protein restriction should be continued or loosened in CKD patients with sarcopenia. We may prioritize protein restriction in CKD patients with a high risk of end-stage kidney disease (ESKD), classified to stage G4 to G5, but may loosen protein restriction in ESKD-low risk CKD stage G3 patients with proteinuria <0.5 g/day, and rate of eGFR decline <3.0 mL/min/1.73 m2/year. However, the effect of increasing protein intake alone without exercise therapy may be limited in CKD patients with sarcopenia. The combination of exercise therapy and increased protein intake is effective in improving muscle mass and strength in CKD patients with sarcopenia. In the case of loosening protein restriction, it is safe to avoid protein intake of more than 1.5 g/kgBW/day. In CKD patients with high risk in ESKD, 0.8 g/kgBW/day may be a critical point of protein intake.

A prognostic risk score for major amputation in dialysis patients with chronic limb-threatening ischemia after endovascular revascularization.

Almost 38% of all patients with end-stage chronic kidney disease (CKD) have peripheral arterial disease of the lower limbs that can lead to chronic limb threatening ischemia (CLTI). The aim of this study was to assess the impact of several factors to conduct a stratification of the amputation risk in CKD patients with CLTI receiving endovascular revascularization. Observational, retrospective, single-center study of patients treated from 2010 to 2016. The primary endpoint was the major amputation. The study included adult CKD dialysis patients affected by CLTI (rest pain and/or trophic lesions) with indication to endovascular revascularization and excluded for open repair. A total of 82 patients were considered (58 men [70.7%], 24 women [29.3%] mean age 70.4±15.0 years). The number of major amputations was 28 (34.1%). The arterial lesion severity (TASC II-classification) and the trophic lesions extension (WIfI classification) were significantly associated with major amputation (OR and 95%CI, 1.20 [1.07-1.34], P=0.001; 2.65 [1.49-4.72], P=0.001; respectively). Based on the above-mentioned characteristics, a prognostic score was proposed to predict the major amputation risk. A score ≥23 was associated with a 67.6% probability of amputation in the following 12 months. The CLTI revascularization is associated with poor outcomes in CKD patients. The present clinical score provided a pragmatic tool to calculate the major amputation risk. An elevated score could facilitate the decision-making process in order to perform an endovascular treatment vs. conservative approach.

Chronic kidney disease and the outcomes of fibrinolysis for ST-segment elevation myocardial infarction: A real-world study.

In low-resource regions, fibrinolytic therapy is often the only option for ST-elevation myocardial infarction (STEMI) patients as primary percutaneous coronary intervention (PCI) is often not available and patients are hardly transferred to a medical center with PCI capacity within the first 120 minutes. Chronic kidney disease (CKD) is one of the most frequently encountered complications of STEMI. However, the evidence for the efficacy of fibrinolytic therapy in STEMI patients with CKD is still limited. The aim of this study is to test whether CKD modifies the association between fibrinolytic therapy and short-term major adverse cardiovascular events (MACEs) among patients with STEMI. This is a real-world study analyzing the data from 9508 STEMI patients (mean age: 64.0±12.4 years; male: 70.1%) in the third phase of Clinical Pathways in Acute Coronary Syndromes program (CPACS-3), which is a large study of the management of acute coronary syndromes (ACS) in 101 county hospitals without PCI capacity in China. CKD was defined as an estimated glomerular filtration rate of less than 60 mL/min per 1·73 m2 at the admission. The primary outcome is short-term MACEs, including all-cause death, recurrent myocardial infarction, or nonfatal stroke. Patients were recruited consecutively between October 2011 and November 2014. Out of them, 1282 patients (13.5%) were classified as having CKD. Compared with non-CKD patients, CKD patients were less likely to receive fibrinolytic therapy than non-CKD patients (26.4% vs. 38.9%, P<0.001), more likely to experience a failed fibrinolytic therapy (32.8% vs. 16.9%), and had a higher risk of short-term MACEs (19.7% vs. 5.6%). After full adjustment, use of fibrinolytic therapy was associated with a significantly lower risk of short-term MACEs in non-CKD patients (relative risk [RR] = 0.87, 95% confidence interval [CI]: 0.76-0.99), but not in CKD patients (P for interaction = 0.026). Further analysis stratified by the success of fibrinolysis showed that compared with patients who did not receive fibrinolytic therapy, patients with successful fibrinolysis had a lower risk of short-term MACEs that was similar between patients with (RR = 0.71, 95% CI: 0.55-0.82) and without CKD (RR = 0.67, 95% CI: 0.55-0.92), while patients with unsuccessful fibrinolysis had a similarly higher risk in CKD patients (RR = 1.25, 95% CI: 1.09-1.43) and non-CKD patients (RR = 1.30, 95% CI: 1.13-1.50). CKD reduced the likelihood of successful fibrinolysis and increased the risk of short-term MACEs in patients with STEMI. Attention should be paid to how to improve the success rate of fibrinolytic therapy for STEMI patients with CKD. The CPACS-3 study was registered on www.clinicaltrials.gov (NCT01398228).

Altered HDL proteome predicts incident CVD in chronic kidney disease patients

Patients with chronic kidney disease (CKD) are at high risk for CVD. However, traditional lipid risk factors, including low HDL levels, cannot completely explain the increased risk. Altered HDL proteome is linked with both CVD and CKD, but the role of HDL proteins in incident CVD events in patients with CKD is unknown. In this prospective case-control study, we used targeted proteomics to quantify 31 HDL proteins in 92 subjects (46 incident new CVD and 46 one-to-one matched controls) at various stages of CKD. We tested associations of HDL proteins with incident CVD using matched logistic regression analysis. In the model fully adjusted for clinical confounders, lipid levels, C-reactive protein, and proteinuria, no significant associations were found for HDL-C, but we observed inverse associations between levels of HDL proteins paraoxonase/arylesterase 1 (PON1), paraoxonase/arylesterase 3 (PON3), and LCAT and incident CVD. Odds ratios (per 1 SD) were 0.38 (0.18–0.97, P = 0.042), 0.42 (0.20–0.92, P = 0.031), and 0.30 (0.11–0.83, P = 0.020) for PON1, PON3, and LCAT, respectively. Apolipoprotein A-IV remained associated with incident CVD in CKD patients in models adjusted for clinical confounders and lipid levels but lost significance with the addition of C-reactive protein and proteinuria to the model. In conclusion, levels of four HDL proteins, PON1, PON3, LCAT, and apolipoprotein A-IV, were found to be inversely associated with incident CVD events in CKD patients. Our observations indicate that HDLs' protein cargo, but not HDL-C levels, can serve as a marker—and perhaps mediator—for elevated CVD risk in CKD patients.

Bone Mineral Density Is Inversely Associated With Mortality in Chronic Kidney Disease Patients: A Meta-Analysis.

Low bone mineral density (BMD) is suggested to be associated with increased mortality in the general health population, but the relationship in chronic kidney disease (CKD) patients is still unclear. We performed a meta-analysis to investigate the association of BMD in different sites with risk of all-cause mortality in CKD patients. We searched PubMed, EMBASE, and Web of Science to identify eligible cohort studies that evaluated the association between BMD at different sites and risk of all-cause mortality in CKD patients. Twelve cohort studies were identified, which included 2828 CKD patients and 1052 deaths. Compared with normal/high level of total body BMD, lower total body BMD was associated with 25% higher risk of all-cause mortality. The pooled relative risk (RR) was 1.25 (95% confidence interval [CI] 1.09, 1.42) with little heterogeneity across studies. Regarding BMD measured at different sites, the risk of all-cause mortality was highest for lower BMD at hip/femoral neck (pooled RR=1.69; 95% CI 1.20, 2.40). The pooled RRs were 1.26 (95% CI 1.04, 1.53) and 1.17 (95% CI 1.00, 1.37) for lower BMD at arm and spine, respectively. Similarly, the risk of death for per SD decrease in BMD was also higher at hip/femoral neck (pooled RR=1.43, 95% CI 1.15, 1.77) compared with arm (pooled RR=1.03, 95% CI 1.00, 1.06) and spine (pooled RR=1.17, 95% CI 0.98, 1.39). In conclusion, lower BMD values at hip, arm, spine, as well as the whole body are associated with increased risk of all-cause mortality in CKD patients. The excess risk is highest for patients with lower BMD at hip/femoral neck, suggesting BMD measured at hip region may be the best indicator of mortality risk in CKD patients. © 2022 American Society for Bone and Mineral Research (ASBMR).

Thyroid dysfunction and cardiovascular events in patients with chronic kidney disease: A protocol of systematic review and meta-analysis.

Background:Cardiovascular disease is the main cause of death in patients with chronic kidney disease (CKD). Studies have found that hypothyroidism can significantly increase cardiovascular risk. Meanwhile, hypothyroidism is a common complication of CKD, but the correlation between hypothyroidism and cardiovascular risk in CKD patients has not been verified and paid enough attention. We therefore plan to conduct a systematic review and meta-analysis to explore whether hypothyroidism was independently predictive for the cardiovascular risk in patients with CKD.Methods:We will search in PubMed, Embase Database, Web of Science, China National Knowledge Infrastructure (CNKI), China Biology Medicine Database (CBM), and Wanfang Database, and include the cross-sectional studies, case--control studies, and cohort studies that explore the association between hypothyroidism and cardiovascular risk in CKD patients. According to the eligibility criteria, two researchers will independently screen the retrieved literature, evaluate the methodological quality, and extract data. We will combine the extracted data based on STATA and TSA software.Results:This systematic review will assess the association between hypothyroidism and cardiovascular risk in CKD patients based on the incidence of cardiovascular events in CKD people with hypothyroidism.Conclusions:This study will provide more evidence for the correlation between hypothyroidism and cardiovascular risk in CKD patients, which will contribute to the management and clinical practice of CKD population.Ethics and dissemination:This protocol is based on available literatures so that the ethical approval and informed consent are not applicable. The results of this study will be published in a peer-reviewed journals or relevant conferences.Protocol registration number:INPLASY2020100022.

Global longitudinal strain and chronic kidney disease prognostic impact on acute coronary syndrome

Abstract Background Impaired left ventricular ejection fraction (LVEF) and chronic kidney disease (CKD) have been associated with poorer outcomes in acute coronary syndrome (ACS). Increasing evidence on global left ventricular longitudinal strain (GLS) suggests superiority over left ventricular ejection fraction (LVEF) in risk stratification. Methods This study was based on a retrospective analysis of consecutive patients admitted to a Coronary Care Unit between 2009 and 2016. Baseline characteristics and echocardiographic parameters, including LVEF, were assessed. For each patient, a two-dimensional speckle tracking of the left ventricle was assessed and average GLS was calculated using 2, 3 and 4-chamber views. Blood creatinine was measured during hospital stay and used to estimate glomerular filtration rate (GFR) with Modification of Diet in Renal Disease (MDRD) equation. A cox regression analysis was performed to determine mortality prediction value of average GLS, LVEF and GFR in this population. Receiver operating characteristic (ROC) curve analysis was conducted and area under the curve (AUC) was estimated. Results A total of 85 patients (66.7±12.7 years old; 78.8% males) were enrolled. LVEF mean was 49.4±9.8% and average GLS was −16.0±4.0%. GFR median was 80.0±48.9 ml/min/1.73m2. In cox regression analysis, worse average GLS was associated with greater mortality (HR 0.721; 95% CI 0.599–0.867; P=0.001). GFR was inversely related to death (HR 0.967; 95% CI 0.944–0.991, P=0.008). In cox regression analysis using average GLS and GFR as covariates, both proved to be independent predictors of mortality (for average GLS, HR 0.748; 95% CI 0.610–0.918, P=0.005; for GFR, HR 0.974; 95% CI 0.949–0.999; P=0.044). The AUC of average GLS to predict mortality was 0.78 (P&amp;lt;0.001, sensitivity 50.7% and specificity 100%) and for average GLS and GFR combined was 0.85 (P&amp;lt;0.001, sensitivity 84.0% and specificity 77.8%). Although LVEF proved to be a mortality predictor, the AUC obtained by ROC curve analysis was inferior to average GLS, with statistical significance (P=0.043). Conclusions GLS and CKD proved to be independent predictors of mortality in ACS patients. GLS showed superiority when compared to LVEF in risk stratification and in the future it might replace LVEF. The model combining GLS and GFR emphasized the increased risk of CKD patients and how they should be seen as high-risk patients. ROC curve analysis Funding Acknowledgement Type of funding source: None

The Role of Prognostic and Predictive Biomarkers for Assessing Cardiovascular Risk in Chronic Kidney Disease Patients.

Chronic kidney disease (CKD) is currently defined as the presence of proteinuria and/or an eGFR < 60 mL/min/1.73m2 on the basis of the renal diagnosis. The global dimension of CKD is relevant, since its prevalence and incidence have doubled in the past three decades worldwide. A major complication that occurs in CKD patients is the development of cardiovascular (CV) disease, being the incidence rate of fatal/nonfatal CV events similar to the rate of ESKD in CKD. Moreover, CKD is a multifactorial disease where multiple mechanisms contribute to the individual prognosis. The correct development of novel biomarkers of CV risk may help clinicians to ameliorate the management of CKD patients. Biomarkers of CV risk in CKD patients are classifiable as prognostic, which help to improve CV risk prediction regardless of treatment, and predictive, which allow the selection of individuals who are likely to respond to a specific treatment. Several prognostic (cystatin C, cardiac troponins, markers of inflammation, and fibrosis) and predictive (genes, metalloproteinases, and complex classifiers) biomarkers have been developed. Despite previous biomarkers providing information on the pathophysiological mechanisms of CV risk in CKD beyond proteinuria and eGFR, only a minority have been adopted in clinical use. This mainly depends on heterogeneous results and lack of validation of biomarkers. The purpose of this review is to present an update on the already assessed biomarkers of CV risk in CKD and examine the strategies for a correct development of biomarkers in clinical practice. Development of both predictive and prognostic biomarkers is an important task for nephrologists. Predictive biomarkers are useful for designing novel clinical trials (enrichment design) and for better understanding of the variability in response to the current available treatments for CV risk. Prognostic biomarkers could help to improve risk stratification and anticipate diagnosis of CV disease, such as heart failure and coronary heart disease.

Statin use and the risk of chronic kidney disease in patients withpsoriasis: A nationwide cohort study in Taiwan.

BackgroundPsoriasis is associated with hyperlipidemia. Few studies have examined the association among psoriasis, hyperlipidemia, and chronic kidney disease (CKD). It remains a topic of debate whether statin treatment for hyperlipidemia prevents the development of CKD in patients with psoriasis.ObjectiveWe investigated whether there is an association among psoriasis, hyperlipidemia and CKD. If so, we asked whether statin treatment for hyperlipidemia reduces the risk of CKD in patients with psoriasis.MethodsA Taiwan nationwide population-based cohort study between 1997 and 2010 included 2,912 patients with psoriasis and 8,736 matched patients without psoriasis (1:3 propensity score matched according to age, sex, and region); 104,609 patients without psoriasis but with hyperlipidemia and 104,609 matched patients without psoriasis or hyperlipidemia (1:1). The hazard ratios, relative risks, and 95% confidence intervals were calculated using Cox proportional hazards model.ResultsPsoriasis significantly increased the risk of CKD (adjusted hazard ratio 2.48, 95% confidence interval 1.81–3.40), and so did hyperlipidemia (adjusted hazard ratio 2.93, 95% confidence interval 2.79–3.08). Compared to treatment without statins, statin treatment for hyperlipidemia reduced the risk of CKD in patients with psoriasis (adjusted relative risk 0.58, 95% confidence interval 0.55–0.62).ConclusionAs well as hyperlipidemia, psoriasis significantly increased the risk of CKD. Statin treatment for hyperlipidemia reduced the risk of CKD in patients with psoriasis.

Product of Serum Calcium and Phosphorus (Ca x Pi) as a Predictor of Cardiovascular Disease Risk in Patients with Chronic Kidney Disease

INTRODUCTION: Most of the chronic kidney disease (CKD) patients develop cardiovascular disease (CVD) in their later stages. Various traditional CVD risk factors are highly prevalent in CKD but mortality of these patients cannot be fully justified by these CVD markers. So this study was designed to determine serum calcium and phosphorus product (Ca×Pi) to predict CVD risk in CKD patients.&#x0D; MATERIAL AND METHODS We followed the guidelines of NKF-KDOQI for CKD diagnosis and staging. Further the patients were classified into 3 different groups based on Ca×Pi product; &lt;40 mg2/dl2 (group 1), 40-55 mg2/dl2 (group 2) and &gt;55 mg2/dl2 (group 3). We then evaluated CVD risk by various traditional risk factors like age, BMI, BP, smoking history, dyslipidemia, previous history of CVD, LVH, arrhythmia, VHD, cardiomyopathy, and IHD.&#x0D; RESULTS: Higher level of Ca×Pi was associated with presence of LVH (32.30% in group 1, 31.42% in group 2 and 46.66% in group 3), Arrythemia (13.84% in group 1, 28.57% in group 2 and 46.67% in group 3), VHD (5.71% in group 2 and 10.00% in group 3), Cardiomyopathy (1.53% in group 1, 8.57% I group 2 and 6.66% in group 3), IHD (6.15% in group1, 11.42% in group 2 and 13.33% in group 3) and hypercholesterolemia, hypertriglyceridemia and increased LDLc.&#x0D; CONCLUSION: This study found that higher Ca×Pi increases with decline in glomerular filtration rate (GFR) and associated with CVD risks and CVD. So, this study raise a potential need to evaluate the level of calcium and phosphorus in all CKD patients and the level should be monitored more thoroughly to prevent CVD.

Prebiotic Therapy with Inulin Associated with Low Protein Diet in Chronic Kidney Disease Patients: Evaluation of Nutritional, Cardiovascular and Psychocognitive Parameters.

A relationship between dysbiotic gut microbiome and chronic kidney disease (CKD) has been recently documented; it contributes to CKD-related complications, including cardiovascular disease. Aim: We tested how a low-protein diet (LPD)—with or without oral inulin supplementation as a prebiotic—modulates some inflammatory, atherosclerosis and endothelial dysfunction indices and nutritional markers, as well as psychocognitive functions in CKD patients. We conducted a prospective, case–control study on CKD patients on conservative therapy, divided in two groups: the intervention group treated with LPD (0.6 g/kg/day) plus inulin (19 g/day) and a control group treated with LPD without inulin, for six consecutive months. Clinical and hematochemical parameters as well as instrumental, and psychocognitive assessments (by SF-36 survey and MMSE, HAM-D, BDI-II) were recorded in all the participants at baseline (T0), at three months (T1) and at six months (T2). A total of 41 patients were enrolled: 18 in the intervention group and 23 in the control group. At T2, in both groups, we observed a significant reduction of serum nitrogen and phosphorus (p ≤ 0.01) and serum uric acid (p ≤ 0.03), and an improvement in metabolic acidosis (bicarbonates, p ≤ 0.01; base excess, p ≤ 0.02). Moreover, at T2 the intervention group showed a reduction in serum insulin (p = 0.008) and fasting glucose levels (p = 0.022), HOMA-IR (p = 0.004), as well as lower total serum cholesterol (p = 0.012), triglycerides (p = 0.016), C-reactive protein (p = 0.044) and homocysteine (p = 0.044) and higher HDL (p < 0.001) with respect to baseline. We also observed a significant amelioration of some quality of life and functional status indices (SF-36 survey) among the intervention group compared to controls, without a significant improvement in the cognitive state (MMSE). On the other hand, an amelioration in mood (by HAM-D and BDI-II) was found in the intervention group and in controls (only by BID-II). In conclusion, LPD in association with oral inulin supplementation improved glycemic and lipid metabolism and ameliorated the systemic inflammatory state, likely reducing cardiovascular risk in CKD patients and this may represent a promising therapeutic option, also improving quality of life and mood.

P0873GLA-RICH PROTEIN (GRP) AS AN EARLY AND NOVEL MARKER ASSOCIATED WITH VASCULAR CALCIFICATION AND CKD-MINERAL AND BONE DISORDER (MBD) IN DIABETIC PATIENTS WITH CKD: A PILOT COHORT STUDY

Abstract Background and Aims Cardiovascular disease (CVD) is the most life-threatening complication in chronic kidney disease (CKD) patients. In addition to traditional risk factors, most patients with CKD display abnormal mineral metabolism with underlying hormonal dysregulation, defined as chronic kidney disease-mineral and bone disorder (CKD-MBD). CKD-MBD involves changes in mineral ion homeostasis, bone quality and turnover, cardiovascular and soft tissue calcifications, which highly contribute for cardiovascular complications. Vascular calcification (VC) is associated with significant morbidity and mortality and a strong predictor of cardiovascular risk in CKD patients. Early preventive measures, including new diagnostic/prognostic tools, are required to reduce the development and progression of VC, left ventricular hypertrophy and arterial stiffness, which are crucial for the prevention of CVD outcomes in CKD patients. Gla-rich protein (GRP) is a vitamin K-dependent protein with a dual capacity to function as an inhibitor of pathological calcification and anti-inflammatory agent in the cardiovascular system, whose clinical utility is unknown. Our aim with this study was to evaluate the potential of GRP as a new marker for CKD-MBD and vascular calcification, in type 2 diabetic patients with chronic kidney disease (CKD) stages 2-4. Method In an observational prospective study including all eligible type 2 diabetic patients with CKD stages 2-4 (n=80) followed in outpatient nephrology consultation from 2010 to 2017, we explored correlations between levels of GRP in serum with mineral metabolism and inflammation markers, CKD developmental stage, vascular calcification and pulse pressure (PP). Vascular calcification score (VCS) was evaluated using the plain x-ray of the hands and pelvis (Adragão score), and increased cardiovascular risk was considered for VCS≥3. Measurements of GRP in serum were performed using a recently developed sandwich ELISA assay. Descriptive statistics, ANOVA and post hoc analysis with Scheffe test were used for analysis. Forward stepwise logistic regression (likelihood ratio) analysis was applied to identify predictive factors for VCS and PP, and ROC curves were used to assess the sensitivity and specificity of GRP in relation to these exposure factors. Results Spearman’s correlation analysis revealed the strong positive correlation between levels of serum GRP and eGFR (r=0.863, p&amp;lt;0.0001) and α klotho (r=0.647, p&amp;lt;0.0001), while a negative correlation with phosphate (P) (r=-0.715, &amp;lt;0.0001), FGF23 (r=-0.676, &amp;lt;0.0001), VCS (r=-0.822, p&amp;lt;0.0001), PP (r=-0.533, p&amp;lt;0.0001), calcium x phosphate (CaxP) (r=-0.302, p=0.006) and IL-6 (r=-0.349, p=0.002). Serum GRP levels were found to progressively decreased from stage 2 to stage 4 CKD. Multivariate analysis identified low levels of eGFR and GRP, and high levels of FGF-23 as independent risk factors for both the VCS and PP. The area under the ROC curves for GRP was 0.865±0.046, 95% CI (0.776-0.955), p&amp;lt;0.0001 for VCS and 0.782±0.054, 95% CI (0.677-0.887), p&amp;lt;0.0001 for PP. Conclusion Reduced levels of GRP were associated with higher levels of vascular calcification promoters such as P, FGF-23 and CaxP, and with lower levels of the VC inhibitor α-Klotho, indicating a correlation between GRP and the dysregulation of phosphate metabolism characteristic of CKD-MBD. In addition, this pilot cohort study indicates that GRP levels might be a significant clinical predictor of vascular calcifications in diabetic patients with CKD. Funding This research was funded by the Portuguese Society of Nephrology (SPN) through project funding 2016, by the Portuguese national funds from FCT - Foundation for Science and Technology through the transitional provision DL57/2016/CP1361/CT0006 and project UID/Multi/04326/2019. Acknowledgments To SPN by the attribution of the Jacinto Simões award (2018) financed by Fresenius medical care.

1525-P: Serum Uric Acid Level Is an Independent Risk Factor for Glomerular Filtration Rate Decline in Patients with Untreated Type 2 Diabetes

Decline in kidney function is a major concern for patients with type 2 diabetes. The importance of serum uric acid level as the risk factor for chronic kidney disease (CKD) remains unconfirmed. We therefore evaluated the relationship between baseline serum uric acid level and the risk of incident CKD among men with untreated type 2 diabetes at baseline examination in a 10-11 years prospective cohort study. We included 717 middle-aged Japanese subjects with fasting plasma glucose level ≥126 mg/dL or HbA1c ≥6.5% at baseline who were not taking hypoglycemic medications nor insulin, who had an estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2, who did not have proteinuria nor malignant tumors, and who were not taking anti-hypertensive medications nor urate-lowering medications at baseline. CKD was defined as eGFR &amp;lt;60 ml/min/1.73 m2. Cox proportional hazards models were used in the multivariate analysis. During the 5961 person-years follow-up period, 87 subjects developed CKD. Higher serum uric acid level was associated with an increased risk of CKD after adjustment for age, body mass index, systolic blood pressure, diastolic blood pressure, HbA1c, smoking habits (nonsmokers, past smokers, and current smokers), regular leisure-time physical activity (yes/no), daily alcohol consumption (g ethanol/day), and eGFR at baseline. Multiple-adjusted hazard ratios of CKD for quintile 4 (6.2-6.9 mg/dL) and quintile 5 (≥7.0 mg/dL) of serum uric acid levels were 1.30 (95% CI, 0.73-2.30) and 1.80 (95% CI, 1.04-3.11), respectively, compared with quintile 1 to 3 (0.7-6.1 mg/dL). Moreover, when we modeled serum uric acid level as a continuous variable, serum uric acid level per 1.0 mg/dL increase was significantly associated with a 25% increased risk of incident CKD. In conclusion, higher serum uric acid level is independently and significantly associated with an increased risk of CKD in patients with untreated type 2 diabetes. Disclosure Y. Okada: None. K.K. Sato: None. M. Shibata: None. S. Uehara: None. H. Koh: None. K. Oue: None. H. Kambe: None. M. Morimoto: None. T. Hayashi: None.

P0673INVERSE ASSOCIATION OF TRANSFERRIN SATURATION WITH MORTALITY RISK IN CHRONIC KIDNEY DISEASE

Abstract Background and Aims Transferrin saturation (TSAT) is an indicator of iron deficiency or overload, but its relationship with mortality in patients with different stages of chronic kidney disease (CKD) is unclear. We investigated the association of TSAT with mortality in CKD patients. Method In 479 CKD patients (97 CKD3-4 patients, 298 CKD5 non-dialysis patients and 84 peritoneal dialysis patients; median age 58 years, 67% males, 33% cardiovascular disease, CVD, and 29% diabetes), biomarkers of iron status (plasma iron, TSAT, transferrin and ferritin), systemic inflammation (high sensitivity C-reactive protein, hsCRP, and interleukin-6, IL-6) and nutritional status were assessed. During median follow-up of 35.6 months, 139 (29%) patients died, and 176 (37%) patients underwent renal transplantation. Patients were stratified into low (n=157) and high (n=322) TSAT tertile groups. All-cause and CVD mortality risk were analyzed with competing risk regression with renal transplantation as competing risk. Results TSAT [median 23% (IQR 17-30%)] was negatively associated with presence of DM and CVD, body mass index, hsCRP, IL-6, Framingham´s CVD risk score (FRS), erythropoietin resistance index (ERI) and iron supplementation, and positively associated with hemoglobin, ferritin and s-albumin. In competing risk analysis, low tertile of TSAT was independently associated with increased all-cause mortality risk (sHR=1.50, 95%CI 1.05-2.14) after adjusting for CKD stages, 1-SD of FRS, 1-SD of hemoglobin, 1-SD of hsCRP, 1-SD of ESA dose and iron supplementation (Figure 1). Conclusion TSAT was inversely associated with mortality risk in CKD patients. When evaluating clinical outcomes of CKD patients, iron status using TSAT as a predictive marker, should be considered.

Hyperurikemie z perspektivy nefrologického pacienta

Hyperuricemia is a common laboratory finding in different types of patients. Except of those with acute or chronic gout, it is frequently found in patients with metabolic syndrome, patients with malignancies or renal impairment - acute kidney injury (AKI) and chronic kidney disease (CKD). Hyperuricemia might cause renal dysfunction or might be a part of laboratory abnormalities associated with loss of renal function as well. There is also large body of evidence of hyperuricemia as a potential cardiovascular (CV) risk factor, which might even more increase CV risk in CKD patients. Association of asymptomatic hyperuricemia and progression of CKD remaines controversial, as well as indication for hypouricemic treatment in this clinical setting.