CKD Population Research Articles

Chlorthalidone and Advanced Chronic Kidney Disease.

Chlorthalidone and Advanced Chronic Kidney Disease.

Genetic Variants Associated With Mineral Metabolism Traits in Chronic Kidney Disease.

Chronic kidney disease (CKD) causes multiple interrelated disturbances in mineral metabolism. Genetic studies in the general population have identified common genetic variants associated with circulating phosphate, calcium, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23). In this study we aimed to discover genetic variants associated with circulating mineral markers in CKD. We conducted candidate single-nucleotide variation (SNV) analysis in 3027 participants in the multiethnic Chronic Renal Insufficiency Cohort (CRIC) to determine the associations between SNVs and circulating levels of mineral markers. SNVs adjacent to or within genes encoding the regulator of G protein-coupled signaling 14 (RGS14) and the calcium-sensing receptor (CASR) were associated with levels of mineral metabolites. The strongest associations (P < .001) were at rs4074995 (RGS14) for phosphate (0.09 mg/dL lower per minor allele) and FGF23 (8.6% lower), and at rs1801725 (CASR) for calcium (0.12 mg/dL higher). In addition, the prevalence of hyperparathyroidism differed by rs4074995 (RGS14) genotype (chi-square P < .0001). Differential inheritance by race was noted for the minor allele of RGS14. Expression quantitative loci (eQTL) analysis showed that rs4074995 was associated with lower RGS14 gene expression in glomeruli (P = 1.03 × 10-11) and tubules (P = 4.0 × 10-4). We evaluated genetic variants associated with mineral metabolism markers in a CKD population. Participants with CKD and the minor allele of rs4074995 (RGS14) had lower phosphorus, lower plasma FGF23, and lower prevalence of hyperparathyroidism. The minor allele of RGS14 was also associated with lower gene expression in the kidney. Further studies are needed to elucidate the effect of rs4074995 on the pathogenesis of disordered mineral metabolism in CKD.

MO566: Relationship Between Cholesterol Intake and Development of Chronic Kidney Disease: A Community-Based Prospective Cohort Study

Abstract BACKGROUND AND AIMS Globally, the incidence and prevalence of CKD have been increased. Also, CKD DALYs and death due to CKD have been increased (DALYs: The disability-adjusted life-year).[1] CKD puts a lot of mental and economic burden on an individual’s life and lowers the quality of life.[2] As CKD progress, kidney-specific risk factor for cardiovascular events and disease are increased.[3] Dyslipidemia is generally known to be associated with the development and progression of chronic kidney disease.[4] However, it is unclear whether limiting cholesterol intake helps prevent CKD. Recent studies have reported that there is no association between cholesterol intake and cardiovascular disease.[5] The aim of our study is to analyze the relationship between cholesterol intake and the development of CKD in a general population. METHOD We included 9226 subjects without CKD from the Korean Genome and Epidemiology Study. The amount of daily cholesterol intake was assessed by food frequency questionnaire. The primary outcome was the development of CKD, which was defined as an estimated glomerular filtration rate (eGFR) of &amp;lt; 60 mL/min/1.73 m2 and/or proteinuria (≥1+). RESULTS The mean age was 55.7 ± 8.8 years and 39.6% of subjects were men. The cholesterol intake was only significantly correlated with serum HDL cholesterol but not with total and non-HDL cholesterol. Moreover, this significant relationship was disappeared after adjusting for daily fat intake. During median follow-up duration of 11.4 years, 778 (8.5%) CKD events occurred. In multivariable Cox analysis, serum total cholesterol was significantly associated with incident CKD (hazard ratio [HR] 1.005, 95% confidence interval [CI]: 1.003–1.007; P &amp;lt; 0.001). However, cholesterol intake was not associated with incident CKD both in subjects with dyslipidemia (HR: 1.001; 95% CI: 1.000–1.002; P = 0.205) and without dyslipidemia (HR: 0.999; 95% CI: 0.997–1.000; P = 0.134). CONCLUSION Cholesterol intake was not correlated with serum cholesterol levels with considering fat intake. In addition, cholesterol intake was not associated with increased risk of CKD in the general population. Therefore, it may not be necessary to limit cholesterol intake to prevent CKD in this population.

MO611: Glycated Albumin Levels Predict The Type of Kidney Damage in Diabetic Patients

Abstract BACKGROUND AND AIMS Diabetes mellitus remains the most frequent cause of end-stage renal disease (ESRD) in developing countries. The main determinant of the onset of nephropathy in diabetes is hyperglycemia which brings to glycation of albumin and haemoglobin with higher concentration of AGEs (advanced glycation end products), finally leading to fibrosis, inflammation and albuminuria. Glycated albumin (GA) was introduced as an alternative to hemoglobin A1c (HbA1c) for glycemic control in the CKD population, with some advantages for diabetic patients with diabetic kidney disease (DKD), since it is not influenced by anemia and associated treatments and it is not affected by serum albumin levels. Although some evidences in literature demonstrated that GA is superior to HbA1c in assessing blood glucose control in DKD (Gan T et al. J Diabetes Complications. 2018); however, KDIGO Guidelines still recommend HbA1c, although underlying some limitations in the context of DKD, meaning that new markers are needed in order to monitor this class of diabetic patients. Kidney disease in diabetic patients can include different kind of renal damage ranging from real diabetic nephropathy (DN, with Kimmelstiel–Wilson lesions, glomerular basal membrane thickening, proliferation of mesangial matrix) to nondiabetic renal disease (NDRD), in the presence or absence of real DN, thus influencing prognosis and treatment. The purpose of the study was to evaluate the clinical utility of the GA dosage, alone or with other molecular and clinical markers as noninvasive biomarkers for the prediction of the progression and type of kidney damage in the diabetic patient. METHOD We enrolled 108 diabetic patients in follow-up at our center, 90 with a biopsy-proven diagnosis of kidney disease and 18 with no kidney dysfunction. Among the 90 patients, 51 had real diabetic nephropathy (DN) or mixed forms (DN + NDRD) and 39 had non-diabetic renal disease (NDRD). GA dosage was obtained by QuantILab® Glycated Albumin assay (Instrumentation Laboratory SpA, Milan, Italy). qPCR was used to evaluate urinary levels of miR27b-3p, a biomarker that predicts the kind of renal damage in diabetic patients and is related to kidney fibrosis (Conserva F et al. Sci Rep. 2019). Statistical analysis was performed using ‘SPSS Statistical Software.’ RESULTS We observed that GA values had a significantly different distribution among DN, NDRD and diabetic patients without renal dysfunction (P = 0.003); conversely, there was no statistical difference in HbA1c distribution although a trend was visible. In the entire cohort, only GA levels, but not HbA1c levels, were significantly correlated with fasting glucose (P = 0.001) and the duration of diabetes (P = .001). In the single classes, only in DN patients there was a significant correlation between GA and diabetes duration (P = .02) and GA and HbA1c (P = 0.01) but not in the NDRD class (P = 0.43). We then applied a multivariate logistic regression model to discriminate real DN and NDRD. We demonstrated that GA is the only significant predictor of real DN in a model corrected for sex, age and serum creatinine {P = 0.009; OR = 0.757–0.962; [95% confidence interval (CI)]}, whereas the same logistic regression model with HbA1c demonstrated no significance (P = 0.082). In the same cohort, we also evaluated miR-27b-3p expression levels, whose levels are correlated with renal fibrosis in DN, and we observed that there was a significant and direct correlation also with GA levels (P = 0.001), thus suggesting the possibility to integrate these biomarkers to predict the kind of renal damage in diabetic patients. CONCLUSION Our study described for the first time the role played by GA as a diagnostic marker in the identification of the different kind of renal damage in diabetic patients. All these evidences support the need to introduce GA as an index of glycemic control to be associated with other molecular markers, such as miRNAs, in order to noninvasively diagnose the kind of renal damage in diabetic patients.

MO507: Prediction of CKD Progression and Cardiovascular Events Using Pulse Wave Velocity and Albuminuria

Abstract BACKGROUND AND AIMS Chronic kidney disease (CKD) is associated with an increased risk of cardiovascular disease (CVD) and death. Albuminuria has been identified as a risk factor, however, additional biomarkers predicting CKD progression and CVD are needed. Arterial stiffness is an easily measurable candidate that has been associated with CVD and mortality. We compared the ability of carotid-femoral pulse wave velocity (PWV) and urine albumin-creatinine (UAC) ratios to predict CKD progression, cardiovascular events (myocardial infarction or stroke) and mortality in a cohort of CKD patients. METHOD In stage, CKD stage 3–4 patients PWV and UAC were measured at baseline. The endpoint of CKD progression was defined as a 50% decline in estimated glomerular filtration rate (eGFR), the initiation of dialysis or renal transplantation. The composite endpoint was defined as the CKD progression endpoint, myocardial infarction, stroke or death. Endpoints were analyzed in a Cox regression analysis adjusted for age, gender, blood pressure, baseline eGFR, BMI and including both PWV and UAC. Data were collected from individual patient biochemistry files, the Danish National Nephrology Registry and the Danish Health Data Registry. RESULTS We included 182 patients [median age 69 (interquartile range 60–75) years, 68% males] with a mean eGFR 37 ± 12 mL/min/1.73 m2 and a UAC of 52 (5–453) mg/g. The mean PWV was 10.6 m/s. The median follow-up until the first event was 4 (3–6) years, with 44 and 89 patients reaching the CKD progression and the composite endpoints, respectively. UAC (mg/g) significantly predicted both the CKD endpoint [HR: 1.0005 (1.0002–1.0008)] and the composite endpoint [HR 1.0004 (1.0001–1.0007)] in adjusted cox regression. In contrast, PWV (m/s) was not associated with the CKD endpoint [HR: 0.99 (0.84–1.18)] nor the composite endpoint (HR: 1.03 (0.92–1.15)]. CONCLUSION In an ageing CKD population, UAC predicted both CKD progression and a composite endpoint of CKD progression, cardiovascular events, or death, while PWV at baseline did not.

Aspirin to target arterial events in chronic kidney disease (ATTACK): study protocol for a multicentre, prospective, randomised, open-label, blinded endpoint, parallel group trial of low-dose aspirin vs. standard care for the primary prevention of cardiovascular disease in people with chronic kidney disease

BackgroundChronic kidney disease (CKD) is a very common long-term condition and powerful risk factor for cardiovascular disease (CVD).Low-dose aspirin is of proven benefit in the secondary prevention of myocardial infarction (MI) and stroke in people with pre-existing CVD. However, in people without CVD, the rates of MI and stroke are much lower, and the benefits of aspirin in the primary prevention of CVD are largely balanced by an increased risk of bleeding.People with CKD are at greatly increased risk of CVD and so the absolute benefits of aspirin are likely to be greater than in lower-risk groups, even if the relative benefits are the same. Post hoc evidence suggests the relative benefits may be greater in the CKD population but the risk of bleeding may also be higher. A definitive study of aspirin for primary prevention in this high-risk group, recommended by the National Institute for Health and Care Excellence (NICE) in 2014, has never been conducted. The question has global significance given the rising burden of CKD worldwide and the low cost of aspirin.MethodsATTACK is a pragmatic multicentre, prospective, randomised, open-label, blinded endpoint adjudication superiority trial of aspirin 75 mg daily vs. standard care for the primary prevention of CVD in 25,210 people aged 18 years and over with CKD recruited from UK Primary Care.Participants aged 18 years and over with CKD (GFR category G1-G4) will be identified in Primary Care and followed up using routinely collected data and annual questionnaires for an average of 5 years. The primary outcome is the time to first major vascular event (composite of non-fatal MI, non-fatal stroke and cardiovascular death [excluding confirmed intracranial haemorrhage and other fatal cardiovascular haemorrhage]). Deaths from other causes (including fatal bleeding) will be treated as competing events. The study will continue until 1827 major vascular events have occurred. The principal safety outcome is major intracranial and extracranial bleeding; this is hypothesised to be increased in those randomised to take aspirin. The key consideration is then whether and to what extent the benefits of aspirin from the expected reduction in CVD events exceed the risks of major bleeding.DiscussionThis will be the first definitive trial of aspirin for primary CVD prevention in CKD patients. The research will be of great interest to clinicians, guideline groups and policy-makers, in the UK and globally, particularly given the high and rising prevalence of CKD that is driven by population ageing and epidemics of obesity and diabetes. The low cost of aspirin means that a positive result would be of relevance to low- and middle-income countries and the impact in the developed world less diluted by any inequalities in health care access.Trial registrationISRCTN: ISRCTN40920200. EudraCT: 2018-000644-26. ClinicalTrials.gov: NCT03796156

Evaluation of Drug-Related Problems in Chronic Kidney Disease Patients.

BackgroundChronic kidney disease (CKD) is a challenging global health problem with increasing prevalence worldwide. Concurrence of CKD and comorbidities results in the use of multiple medications and exposing patients to polypharmacy. Polypharmacy in CKD is common across all the stages of the disease and leads to poor medication adherence, higher healthcare costs, and drug-related problems, such as drug-drug interactions (DDIs) and adverse drug reactions (ADRs). DDIs and ADRs in CKD patients may lower the quality of life, increase the length of hospital stay, and augment the risks of morbidity and mortality.MethodologyThis was a hospital-based, prospective, cross-sectional study conducted in a secondary care hospital. The study population comprised 130 adult CKD patients admitted to the nephrology department including those on maintenance hemodialysis. Study-related data were obtained from the electronic patient case records. Medications prescribed to the patients were analyzed for potential DDIs (pDDIs) using Portable Emergency and Primary Care Information Database (PEPID 12.1) drug interaction checker. All observed and reported suspected ADRs related to the prescribed drugs were evaluated for causality, severity, preventability, and predictability.ResultsOut of the 130 patients, majority were males (n = 71, 54.6%), in the age group of 61-70 years (n = 45, 34.6%), and belonged to CKD stage 5 (n = 105, 80.8%). The mean number of drugs prescribed was 11.1 ± 3.8 per patient. The prevalence of pDDIs was found to be 89.2%. Upon analysis by the PEPID database, 708 pDDIs with 215 different pairs of interacting drugs were identified. Polypharmacy (odds ratio (OR): 62.34, 95% confidence interval (CI): 7.97-487.64, p < 0.001) was identified as an independent predictor of the occurrence of pDDIs. Negative binomial regression analysis revealed that dyslipidemia (incidence rate ratio (IRR): 2.7, 95% CI 2.09-3.48, p < 0.001) and diabetes (IRR: 1.2, 95% CI 1.01-1.54, p = 0.040) increased the probability of occurrence of pDDI by 2.7 and 1.2 folds, respectively. Furthermore, the likelihood of pDDI increased with every one-day increase in the length of hospital stay (IRR: 1.02, 95% CI 1.00-1.03, p = 0.015) by 1.02 times and polypharmacy (IRR: 6.30, 95% CI 3.04-13.02, p < 0.001) by 6.3 times. The incidence of ADRs was found to be 10.7%. Majority of suspected ADRs were possible (n = 7, 50.0%), of mild and moderate severity (n = 7, 50.0%), and non-preventable (n = 8, 57.1%) type.ConclusionsThis study investigated two important drug-related problems, pDDIs, and ADRs, in the CKD population. High proportion of CKD patients in the study had pDDIs. Comorbid conditions such as dyslipidemia and diabetes mellitus, length of hospital stay, and polypharmacy were significantly associated with increased likelihood of pDDIs. Furthermore, there was a burden of ADRs in the study population, of which most ADRs were possible and of mild to moderate severity. Prevention, identification, and resolution of these problems in CKD patients is important and can be achieved through medication optimization, which requires a proactive interdisciplinary collaboration between clinicians, clinical pharmacists, and other healthcare professionals.

POS-903 ADVERSE EVENTS FOLLOWING IMMUNISATION (AEFI) OF COVID-19 VACCINES IN KIDNEY PATIENTS- A CASE SERIES

Patients with kidney diseases have been prioritised for covid 19 vaccination due to their higher risk for worse outcomes from covid 19 infections. Data on vaccine efficacy and safety have generally been inferred from studies of non-CKD population. The immune response from vaccinations may trigger various diseases with an immunopathogenesis. We report a series of 3 patients with kidney diseases who developed adverse events worth noting following vaccination Case 1: 67 years old, Male, with underlying primary membranous nephropathy, treated with oral cyclophosphamide and steroids and was in partial remission with proteinuria of 1.1g/24H. He came with relapsed nephrotic range proteinuria of 5.3g/24H 2 weeks after the 1stdose of Pfizer–BioNTech COVID-19 vaccine. Anti- PLA2R titre repeated was 41.8 RU/ml from 1574 RU/ml. Proteinuria self-reduced to 1.6g/24H about 1 month post vaccination with conservative management. Case 2: 60 years old, male, with underlying ESRF on regular haemodialysis and diabetes mellitus, became acutely delirious with Glasgow Coma Scale (GCS) ranging 10 to 13, 3 days after 1stdose Sinovac CoronaVac covid-19 vaccine. Multiple investigations ruled out organic causes. Patient did not respond to empirical treatment of meningo-encephalitis but responded with intravenous methylprednisolone and recovered full GCS on day 2 of methylprednisolone. Cerebrospinal fluid was normal. MRI brain showed non-specific finding with focus T2W/ FLAIR hyperintensity at splenium of corpus callosum. Patient likely had Acute Disseminated Encephalomyelitis post- vaccination with rapid response to steroids. Case 3: 28 years old, female, with underlying Systemic Lupus Erythematosus (SLE) with renal, muco-cutaneous, and joint involvement had been in remission on maintenance therapy of Myfortic and low dose steroids; developed progressive generalised pustular lesions immediately day 3 post second dose Sinovac CoronaVac covid-19 vaccine. Skin biopsy done suggestive of acute generalised exanthematous pustulosis (AGEP). She had no history of concomitant medications, viral infections, or drug allergies either before or after the COVID-19 vaccination. Skin lesions improving with steroids and potassium permanganate wet dressing with emollients. Even though benefits from vaccination far outweighs potential risks, health professional should be alert to the various adverse events that may occur following covid-19 vaccination. Patients with kidney diseases may experience different adverse events post vaccination unique to their underlying kidney diseases. Further studies are needed for better understanding of the effects of vaccination in the CKD population.

Bone mass measurement by DXA should be interpreted with caution in the CKD population with vascular calcification

BackgroundKDIGO guidelines suggest the use of dual-energy X-ray absorptiometry (DXA) to assess bone mineral density (BMD) in patients with CKD 3a-5D. Previous studies have demonstrated an association between trabecular bone mass loss and coronary artery calcification (CAC) progression. This study aimed to prospectively investigate the relationship between BMD changes, quantified by DXA, and CAC progression in the non-dialyzed CKD population. MethodsIn this post hoc study, BMD by DXA was measured at the lumbar spine and total hip at baseline and 12-months. Patients were categorized according to BMD changes into 3 different groups: LOSS, UNCHANGED and GAIN. CAC quantification was obtained by multislice computed tomography at baseline and 12-months. Results87 patients (55.6 ± 10.7 years, 62% males, 30% diabetic, eGFR = 39.2 ± 18.1 mL/min/1.73m2) were enrolled. CAC was found in 41 (47%) of the patients at baseline and CAC progression in 25 (64%) of them. Considering the lumbar spine and total hip BMD changes together, 24%, 48%, and 25% of the patients were in the LOSS, UNCHANGED and GAIN groups, respectively. Compared to the UNCHANGED or LOSS groups, the GAIN group had an increase in calcium score (p = 0.04) and a higher proportion of patients with CAC progression (p = 0.01). In the logistic regression analysis, CAC progression was 4.5 times more likely to be in the GAIN group. ConclusionsThe association between the increase in BMD values and the progression of vascular calcification was the result of two concomitant processes overlapping, leading to a misinterpretation of DXA results. Thus, the use of DXA for the evaluation of bone mass, especially at the lumbar spine, must be applied with restraint and its results very carefully interpreted in CKD patients.

120 Safety and efficacy of renal artery denervation for uncontrolled-resistant hypertension in a high risk population with CKD: the Verona real-world experience

Abstract Aims To evaluate the safety and the efficacy of catheter-based radiofrequency renal sympathetic denervation (RSD) in a daily practice population of patients with uncontrolled resistant hypertension on top of medical therapy. Methods and results Consecutive unselected patients with uncontrolled resistant hypertension undergoing RSD were enrolled. Office and ambulatory blood pressure (BP) monitoring were collected at baseline and 3, 6, and 12 months after RSD. Efficacy was assessed also in patients with an estimated glomerular filtration rate below 45 ml/min/1.73 m2. Patients were defined responders to RSD if systolic BP decreased by at least 5 mmHg at ambulatory BP or by 10 mmHg at office BP at the last follow-up available. Fifty-four patients with multiple comorbidities underwent RSD for uncontrolled-resistant hypertension from 2012 to 2021. Baseline office and ambulatory BP was 161.0/87.2 ± 24.1/15.6 mmHg and 155.4/87.5 ± 19.3/14.6 mmHg, respectively. At 12-month follow-up a significant reduction of office and ambulatory systolic BP, respectively by − 15.66 ± 29.73 mmHg (P &amp;lt; 0.01) and by − 11.3 ± 23.1 mmHg (P &amp;lt; 0.05), was noticed. BP reduction at 12-month follow-up among patients with eGFR &amp;lt;45 ml/min was similar to that obtained in patients with higher eGFR. Among patients treated before July 2020 with available follow-up (45/54) 36 patients (80%) were classified as responders. Combined hypertension, higher ambulatory systolic BP and lower E/E’ at baseline emerged as predictors of success of RSD at univariate analysis. Among responders and non-responders, the average medication number showed no significant difference at baseline and during follow-up. No major complications were observed and renal function was stable up to 12 months, even in patients with lowest eGFR at baseline. Conclusions RSD is safe and feasible in patients with uncontrolled resistant hypertension on top of medical therapy, even in a high-risk CKD population with multiple comorbidities, with a significant reduction of systolic BP and a trend of reduction of the diastolic BP up to 12 months. 775 Figure

A cohort study of the relationship between anaemia, mean corpuscular volume and mortality among a CKD population in South Africa.

The burden of chronic kidney disease is increasing globally and prompt identification, coupled with improved management of CKD patients have increased the population of pre-dialysis patients. We, therefore, aimed to evaluate the predictors of survival among pre-dialysis CKD patients in South Africa. We conducted a cohort study of 256 consecutive consenting Black non-dialysis requiring CKD patients attending the renal outpatient clinic of a tertiary Hospital in South Africa from 1st June 2016 to 1st December 2016. Socio-demographic and clinical information of the participants were obtained. Descriptive statistics, Kaplan-Meier curves and Cox proportional hazard regression analyses were conducted to evaluate factors affecting the survival of the participants. The mean age of the participants was 52.8±14.3 years and 48.0% were females, 52% were males. The death rate increased with worsening haemoglobin level from 0.96 among patients with mild anaemia to 4.29 per 100-person years among patients with severe anaemia. Anaemic patients with GFR < 30mls/min had significantly increased risk of death (HR 11.51, 95% CI 1.62-78.32, P < 0.001). Mortality in pre-dialysis CKD patients was associated with anaemia and hyperphosphatemia. Clinical interventions targeted at preventing these conditions may improve outcomes among this group of CKD patients.

Stressors and Resilience: An Integrative Model for Understanding Chronic Kidney Disease

Stressors and Resilience: An Integrative Model for Understanding Chronic Kidney Disease

An Updated View on the Antiviral Therapy of Hepatitis C in Chronic Kidney Disease.

Background: Hepatitis C virus infection remains common in patients with chronic kidney disease, including those on maintenance dialysis. The relationship between hepatitis C virus infection and chronic kidney disease is bi-directional; in fact, HCV is both a cause and consequence of chronic kidney disease. According to a systematic review with meta-analysis of observational studies (n = 23 studies) (n = 574,081 patients on long-term dialysis), anti-HCV positive serologic status was an independent and significant risk factor for death in patients with advanced chronic kidney disease on long-term dialysis. The overall estimate for adjusted mortality (all-cause death risk) with HCV was 1.26 (95% CI, 1.18; 1.34) (p < 0.0001). Interferon-based therapies are biased by low efficacy/safety in chronic kidney disease, but the advent of direct-acting antiviral drugs has made a paradigm shift in the treatment of HCV-infection. These medications give interruption of viral replication because they target specific non-structural viral proteins; four classes of DAAs exist-NS3/4A protease inhibitors, NS5A inhibitors, NS5B nucleoside and non-nucleoside polymerase inhibitors. All-oral, interferon-free, ribavirin-free combinations of DAAs are now available. Aim: The goal of this narrative review is to report the available treatment options for HCV in advanced chronic kidney disease. Methods: We have made an extensive review of the medical literature and various research engines have been adopted. Results: Some combinations of DAAs are currently recommended for HCV in advanced CKD (including patients on maintenance dialysis): elbasvir/grazoprevir; glecaprevir/pibrentasvir; and sofosbuvir-based regimens. Solid evidence, based on registration and “real life” studies supports their efficacy (SVR rates > 90%) and safety even in patients with advanced CKD. No dosage adjustment is necessary and treatment duration is 8–12 weeks. However, recent data highlight that many patients with advanced CKD remain untreated, and numerous barriers to antiviral treatment of HCV still exist. Whether successful antiviral therapy with DAAs will translate into improved survival in the advanced CKD population is another point of future research.

The effect of pre-ESRD care program on potentially inappropriate medication in advanced CKD patients

Abstract Background Due to the multiple comorbidities and the associated complications among advanced CKD population, assessing potentially inappropriate medications (PIM) in these patients is an important task for physicians and multidisciplinary care team members. This study aimed to investigate the impact of the national pre-ESRD pay-for-performance (P4P) program on prescribing quality in Taiwan. Methods We conducted a retrospective cohort study using data from National Health Insurance Research Database (NHIRD) maintained by the Health and Welfare Data Science Center, Ministry of Health and Welfare (HWDC, MOHW). The incidents of CKD in year 2010 were observed until the end of 2017. Adult patients who initiated maintenance dialysis therapy were enrolled. To identify the use of PIM that should be avoided in advanced CKD patients, the Beers 2019 criteria and latest Taiwan Manual of Renal Injury Prevention and Drug Safety were applied. We measured PIM use in one year before starting long-term dialysis. Results Among 7,828 participants underwent continuous dialysis treatment, 2,119 (27.1%) were P4P patients. Most (90.4%) participants were prescribed one or more PIMs before ESRD initiation. After adjusted age, sex, Charlson Comorbidity Index (CCI) and the number of nephrologist visits, the logistic regression showed lower probability of PIM use in the P4P enrollees (OR = 0.56, 95% CI = 0.47-0.66). The effect of P4P on PIM was more prominent in the subgroups of patients who were female and CCI≤3. Conclusions The implementation of the pre-ESRD P4P program might reduce PIM use among CKD patients. Our results underline the strategy of financial incentives in the payment design to improve prescribing patterns. Key messages Prescribing potentially inappropriate medications is common among patients who were approaching ESRD. The study highlights the importance of implementing the pre-ESRD P4P program to reduce PIM use in advanced CKD patients.

Elevated Levels of Renalase, the β-NAD(P)H Isomerase, Can Be Used as Risk Factors of Major Adverse Cardiovascular Events and All-Cause Death in Patients with Chronic Kidney Disease.

Background: Renalase is an enzyme and a cytokine involved in cell survival. Since its discovery, associations between it and both cardiovascular and kidney disease have been noted. Recognizing this, we conducted a study in which we followed patients with chronic kidney disease. Material and methods: The study involved 90 CKD patients with varying stages of the disease and 30 healthy controls. Renalase was measured with an ELISA kit, and patients were followed-up after a median of 18 months. During the follow-up, we asked about the occurrence of MACE, all-cause mortality and the need for dialysis initiation. Results: In CKD subgroups, RNSL correlated with all-cause death only in the HD group (Rs = 0.49, p < 0.01). In the whole CKD population, we found a positive correlation of RNSL concentration and both MACE occurrence (Rs = 0.38, p < 0.001) and all-cause death (Rs = 0.34, p < 0.005). There was a significant increase in MACE occurrence probability in patients with elevated renalase levels (>25 μg/mL). Conclusions: Elevated renalase levels can be used as a risk factor of MACE in patients with CKD, but its long-term utility needs further research. High renalase levels are a risk factor of death among CKD patients. In HD patients, all deaths were observed among patients with >30 μg/mL; this level could be used as a “red flag” marker in future studies.

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

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

Cardiovascular and Renal Outcomes of the New Intensive Blood Pressure Target in a CKD Population in Korea

Cardiovascular and Renal Outcomes of the New Intensive Blood Pressure Target in a CKD Population in Korea

A Population Health Survey-Based Prediction Equation for Incident CKD: The CKD Population Risk Tool CKDPort/PREDICT-CKD LIFESTYLE

A Population Health Survey-Based Prediction Equation for Incident CKD: The CKD Population Risk Tool CKDPort/PREDICT-CKD LIFESTYLE

Identification of Common Medication Therapy Problems in a High-Risk CKD Population

Identification of Common Medication Therapy Problems in a High-Risk CKD Population

Magnetic resonance imaging determination of tissue sodium in patients with chronic kidney disease.

Excess sodium is a major modifiable contributor to hypertension and cardiovascular risk. Knowledge of sodium storage and metabolism has derived mainly from indirect measurements of dietary sodium intake and urinary sodium excretion, however both attempt to measure body sodium and fluid in a two-compartment model of intracellular and extracellular spaces. Our understanding of total body sodium has recently included a storage pool in tissues. In the last two decades, sodium-23 magnetic resonance imaging (23 Na MRI) has allowed dynamic quantification of tissue sodium in vivo. Tissue sodium is independently associated with cardiovascular dysfunction and inflammation. This review explores (i) The revolution of our understanding of sodium physiology, (ii) The development and potential clinical adoption of 23 Na MRI to provide improved measurement of total body sodium in CKD and (iii) How we can better understand mechanistic and clinical implications of tissue sodium in hypertension, cardiovascular disease and immune dysregulation, especially in the CKD population.