Non-dialysis Patients Research Articles

Health Literacy in Non-dialyzed Chronic Kidney Disease Patients: A Cross-Sectional Study

Objective: To explore the current status and influencing factors of health literacy in non-dialyzed chronic kidney disease (CKD) patients, and to provide a basis for developing more comprehensive and effective interventions. Methods: 206 CKD patients hospitalized or followed up in outpatient clinics in the Department of Nephrology of a tertiary hospital in Baoding City were conveniently selected from June to August 2024. General information questionnaire, Health Literacy Scale for Chronic Disease Patients, Perceived Social Support Scale, and Positive Psychological Questionnaire were used to conduct the survey. Results: The health literacy score of non-dialyzed CKD patients was (91.04±15.17); The results of multiple linear regression analysis showed that the number of comorbidities, education level, per capita monthly household income, family support, and optimism were the influencing factors of health literacy in CKD patients. Conclusion: The health literacy of non-dialyzed CKD patients is low, and healthcare professionals should develop scientific and reasonable intervention programs based on their influencing factors in order to enhance the health literacy and delay disease progression.

Exposure to microplastics via hemodialysis: differences between women and men

Abstract Background Hemodialysis (HD) may contribute to microplastics (MPs) burden in dialysis patients. The aim of the study was to estimate any differences in exposure to MPs between cases (on dialysis patients) and controls (not on dialysis patients), investigating any sex differences. Methods We organized a case-control study. Both cases and controls were recruited at the Policlinic “G. Rodolico-San Marco” Hospital Nephrology Unit. Preparation and determination of MPs smaller than 10 µm in blood samples were carried out using a patented method (Italian Patent n. 102018000003337-07 March 2018, European Patent n.3788344 20 July 2022) and SEM-EDX electron microscopy analysis, respectively. Results A convenience sample was recruited including 15 dialysis (60.0% women) and 10 not on dialysis patients (60.0% women) with a median (IQR) age of 77.0 (59.0-83.0) in dialysis patients and 65.5 (49.3-79.0) in those not on dialysis. No significant differences were found between cases and controls on the consumption of bottled water (100% vs 80%, p = 0.07), bagged foods (93.3% vs 70%, p = 0.12) unlike the use of drugs (100% vs 70%, p = 0.02). Women in general declared a greater use of drugs than men (F 93.3%, M 80.0%, p = 0.32). Dialysis patients had higher MPs levels than non-dialysis patients [9132(4896-15847) vs 3554(1661-7340), p-value=0.06]. In particular, female dialysis patients had values comparable to males [9132 (4665-17205) p/d vs men: 10438 (3672-16699) p/d] while non-dialysis female patients had higher levels than males [3274 (1681- 7814) p/g vs 1661 (1661-3354) p/g]. No difference was detected about the diameter of the MPs (IQR) [dialysis patients 4.28 (3.72-4.66) µm vs non-dialysis patients [4.67 (4.15-5.08) µm]. Conclusions Future studies must focus on studying the relationship between exposure to MPs and their levels in dialysis patients as well as investigating the differences between men and women and the possible consequences of dialysis as a further source of exposure. Key messages • On dialysis patients, both men and women, had higher MPs exposition compared to not on dialyzed ones. • Not on dialysis women had higher MPs levels than not on dialysis men.

Comparison of long-term prognosis between coronary artery disease and peripheral artery disease in haemodialysis and non-dialysis patients

Abstract Background Patients on hemodialysis (HD) have been consistently recognized as a population with a high risk for cardiovascular diseases. However, it has not been clear which vascular disease had more impact on clinical prognosis. The aim of this study was to compare coronary artery disease (CAD) and peripheral artery disease (PAD) among HD and non-HD patients undergoing coronary artery bypass graft (CABG) and lower extremity bypass (LEB) surgery. Methods A total of consecutive 1,867 patients who initially and successfully underwent cardiovascular bypass surgery (242 CABG and 620 LEB in HD patients, 604 CABG and 401 LEB in non-HD patients) were enrolled in this study. They were followed up for up to 10-year. The primary endpoint was all-cause mortality. Results Cumulative mortality rates for 10-year were 15.6%, 21.8%, 38.7% and 58.9% after CABG in non-HD patients, LEB in non-HD patients, CABG in HD patients and LEB in HD patients, respectively (Figure). HD patients consistently had higher risk of mortality after cardiovascular bypass surgery compared to non-HD patients [adjusted hazard ratio (aHR) 3.04, 95% confidence interval (CI) 2.21-4.36, p<0.0001]. Similar results were observed after CABG and LEB in both, respectively (aHR 2.50, 95%CI 1.75-3.61, p<0.0001 for CABG and aHR 3.07, 95%CI 3.07, 95%CI 2.21-4.36, p<0.0001). Also, patients with LED tended to have higher risk of mortality compared to those with CABG (aHR 1.25, 95%CI 1.0.99-1.57, p=0.057) in entire cohort. However, the risk of mortality was significantly higher after LED than CABG in HD patients (aHR 1.34, 95%CI 1.02-1.81, p=0.042) but not in non-HD patients (aHR 1.00, 95%CI 0.67-1.49), p=0.98). In addition, HD patients with LEB had markedly higher risk of mortality compared to non-HD patients with CABG (aHR 3.50, 95%CI 2.62-4.74, p<0.0001). Conclusion Long-term prognosis was consistently poorer after cardiovascular surgery regardless of CABG or LEB in HD patients than in non-HD patients. The risk of mortality was also significantly higher after LEB than CABG in HD patients but not non-HD patients, and HD patients with LEB was considered to have the highest mortality risk in the study. Thus, PAD might be at more advanced atherosclerotic status than CAD in this high-risk population.

Does gut microbiota dysbiosis impact the metabolic alterations of hydrogen sulfide and lanthionine in patients with chronic kidney disease?

BackgroundChronic Kidney Disease (CKD) is characterized by a methionine-related metabolic disorder involving reduced plasma levels of hydrogen sulfide (H2S) and increased lanthionine. The gut microbiota influences methionine metabolism, potentially impacting sulfur metabolite dysfunctions in CKD. We evaluated whether gut microbiota dysbiosis contributes to H2S and lanthionine metabolic alterations in CKD.MethodsThe gut microbiota of 88 CKD patients (non-dialysis, hemodialysis, and transplant patients) and 26 healthy controls were profiled using 16 S-amplicon sequencing. H2S and lanthionine concentrations were measured in serum and fecal samples using the methylene blue method and LC-MS/MS, respectively.ResultsThe CKD population exhibited a tenfold increase in serum lanthionine associated with kidney dysfunction. Despite lanthionine retention, hemodialysis and transplant patients had significantly lower serum H2S than healthy controls. Fecal H2S levels were not altered or related to bloodstream H2S concentrations. Conversely, fecal lanthionine was significantly increased in CKD compared to healthy controls and associated with kidney dysfunction. Microbiota composition varied among CKD groups and healthy controls, with the greatest dissimilarity observed between hemodialysis and transplant patients. Changes relative to the healthy group included uneven Ruminococcus gnavus distribution (higher in transplant patients and lower in non-dialysis CKD patients), reduced abundance of the short-chain fatty acid-producing bacteria Alistipes indistinctus and Coprococcus eutactus among transplant patients, and depleted Streptococcus salivarius in non-dialysis CKD patients. A higher abundance of Methanobrevibacter smithii, Christensenella minuta, and Negativibacillus massiliensis differentiated hemodialysis patients from controls. No correlation was found between differentially abundant species and the metabolic profile that could account for the H2S and lanthionine alterations observed.ConclusionsThe metabolic deregulation of H2S and lanthionine observed in the study was not associated with alterations in the gut microbiota composition in CKD patients. Further research on microbial sulfur pathways may provide a better understanding of the role of gut microbiota in maintaining H2S and lanthionine homeostasis.

Hepcidin, GDF-15 and their Impact on Iron Metabolism in CKD

Background Anemia is an important complication in chronic kidney disease (CKD). We studied the diagnostic accuracy of hepcidin and growth differentiation factor-15 (GDF-15) as early markers of iron deficiency anemia (IDA) in non-dialysis (ND-CKD) patients. Materials and Methods This was a cross-sectional, case-control study comprising 100 cases of CKD (newly diagnosed and non-dialyzed) and 40 healthy controls. Serum levels of hepcidin and GDF-15 were estimated using ELISA-based assays. Receiver operator characteristics were used to evaluate the diagnostic validity of hepcidin and GDF-15 for absolute and functional iron deficiency anemia. Results About 33% of the cases were females with a mean age of 47.64 (± 13.68) years. The predictive value of hepcidin for diagnosing functional IDA in CKD was found to be 69.1% (95% CI: 52.5% to 82.7%), and that of GDF-15 was found to be 68.8% (95% CI: 52.6% to 82.1%). Hepcidin significantly correlated with hemoglobin (r = 0.278, p = 0.005) and serum iron (r = 0.222; p = 0.025). GDF-15 positively correlated with ferritin (r = 0.346, p < 0.0001) and hsCRP (r = 0.223, p = 0.0088) and negatively correlated with eGFR (r = -0.462, p < 000001), Hb (r = -0.481, p < 0.00001) and TIBC (r = -0.353, p < 0.0001). Conclusion Hepcidin and GDF-15 could predict functional IDA in our patients but not absolute IDA.

Coronary artery bypass grafting in dialysis patients: a propensity score-matched analysis

BackgroundPatients undergoing dialysis treatment have long been recognized as having an elevated risk of developing coronary artery disease necessitating coronary artery bypass grafting (CABG). However, the prognostic implications of CABG in dialysis-dependent patients remain underexplored. This study aimed to comprehensively assess both short- and long-term outcomes in dialysis-dependent patients undergoing CABG.MethodsIn this retrospective analysis, we meticulously matched 55 dialysis-dependent patients with 55 non-dialysis patients, controlling for baseline characteristics including age, sex, etiology, and date of surgery. All patients underwent CABG treatment at our institution between January 2014 and June 2022. We conducted a comparative analysis of postoperative complications and survival rates between the two groups.ResultsOur findings revealed that the dialysis-dependent group exhibited a significantly higher incidence of postoperative complications compared to the non-dialysis group (92.7% vs. 61.8%; p < 0.001). Furthermore, the 5-year survival rates were notably diminished among dialysis patients relative to their non-dialysis counterparts (46.2 ± 7.9% vs. 58.2 ± 12.1%, p = 0.045). Consistently, dialysis patients exhibited decreased 5-year cardiac-event-free rates in contrast to non-dialysis patients (31.6 ± 7.6% vs. 58.8 ± 11.3%, p = 0.041). Predictably, several baseline parameters were identified as significant risk factors contributing to adverse outcomes among dialysis patients, including a history of smoking, diabetes mellitus, congestive heart failure upon admission, and the requirement for intraoperative concomitant surgery (p = 0.006, p = 0.043, p = 0.017, p = 0.003, respectively).ConclusionsThis study underscores the poorer prognosis associated with CABG treatment in dialysis-dependent patients. Notably, baseline factors such as a smoking history, diabetes mellitus, congestive heart failure upon admission, and the need for intraoperative concomitant surgery were all independently linked to increased mortality in this patient population.

Real-world fracture risk, osteoporosis treatment status, and mortality of Japanese non-dialysis patients with chronic kidney disease stages G3-5.

Few studies have investigated fracture risk and mortality in a Japanese chronic kidney disease (CKD) stages G3-5 population using a large-scale clinical database. This retrospective cohort study extracted data from 1 April 2008 to 30 April 2023. A single age-sex-matched control without CKD was matched with each non-dialysis CKD (estimated glomerular filtration rate < 60mL/min/1.73m2) patient. The incidences of all and hip fractures and all-cause mortality after the index date were calculated. Among 76,598 (38,299 per group) individuals matched, the incidence of all fractures did not differ between the CKD and control groups (5.7% vs 5.8%; hazard ratio [HR] 1.022 [95% confidence interval CI 0.952-1.098], P = 0.542). The CKD group had higher risk of hip fracture than the control group (incidence of hip fracture, 1.7% vs 1.3%; HR 1.415 [95% CI 1.234-1.622], P < 0.001). Multivariable regression analysis showed an increased risk for hip fracture in the CKD vs control groups, and a greater difference in this risk was observed with younger age. Osteoporosis treatment and bone mineral density (BMD) measurements were 10.0% and 5.3% in the CKD group and 4.4% and 4.4% in the control group, respectively. Mortality was also higher in the CKD group (HR 1.413 [95% CI 1.330-1.501], P < 0.001). Japanese patients with CKD had higher risk of hip fracture than those without. Treatment and BMD measurement for fracture are insufficient in Japanese patients with CKD, and more adequate management of fracture risk is needed.

Screening for Peripheral Vascular Disease: The Role of Ankle-Brachial Index (ABI) and Estimated Glomerular Filtration Rate (eGFR) Changes in Chronic Kidney Disease.

Background Chronic kidney disease (CKD) is a significant public health issue worldwide, closely linked with cardiovascular events such as atherosclerosis, peripheral arterial disease (PAD), stroke, coronary artery disease (CAD), and heart failure. The ankle-brachial index (ABI) is a simple tool that compares blood pressure in the ankle and arm, helping to detect PAD and assess the risk of cardiovascular events. An increased ABI signifies an increased risk of cardiovascular disease (CVD), whereas a diminished ABI correlates with angiographically verified atherosclerosis along with heightened death rates. Recent research indicates a U-shaped relationship between ABI and mortality, underscoring the necessity for early detection and action to mitigate potential consequences. Aim This study aimed to correlate ABI changes with estimated glomerular filtration rate (eGFR) changes in CKD patients to screen for the development of peripheral vascular disease. Materials and methods This prospective cross-sectional study was conducted in the outpatient department of a tertiary care hospital in India, focusing on patients diagnosed with CKD admitted to the general medicine department. The inclusion criteria were CKD patients with an eGFR less than 60 ml/min/1.73 m², accompanied by indicators of renal damage such as albuminuria, reduced kidney size on ultrasound, abnormal urinary sediment, or biopsy-proven kidney disease. Patients with peripheral vascular disease, with end-stage renal disease (on dialysis), with limb amputations, with hemodynamic instability, or who declined participation were excluded. eGFR was calculated using the Modification of Diet in Renal Disease (MDRD) equation, and the ABI was measured at baseline, three months, and six months. ABI values below 0.9 indicated peripheral vascular disease, and the study aimed to correlate changes in ABI with eGFR to assess vascular disease development in non-dialyzed CKD patients. Results By the end of the third month, a positive correlation was observed between ABI and eGFR (r=0.259), which persisted at the end of the sixth month (r=0.245). Conclusion The study concludes that a direct relationship exists between decreasing eGFR and ABI, which increases susceptibility to PAD and CVD. A low ABI is linked to an accelerated decline in eGFR, indicating that systemic atherosclerosis predicts kidney function deterioration.

Identification of serum biomarkers for chronic kidney disease using serum metabolomics

This study aimed to identify biomarkers for chronic kidney disease (CKD) by studying serum metabolomics. Serum samples were collected from 194 non-dialysis CKD patients and 317 healthy controls (HC). Using ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS), untargeted metabolomics analysis was conducted. A random forest model was developed and validated in separate sets of HC and CKD patients. The serum metabolomic profiles of patients with chronic kidney disease (CKD) exhibited significant differences compared to healthy controls (HC). A total of 314 metabolites were identified as significantly different, with 179 being upregulated and 135 being downregulated in CKD patients. KEGG enrichment analysis revealed several key pathways, including arginine biosynthesis, phenylalanine metabolism, linoleic acid metabolism, and purine metabolism. The diagnostic efficacy of the classifier was high, with an area under the curve of 1 in the training and validation sets and 0.9435 in the cross-validation set. This study provides comprehensive insights into serum metabolism in non-dialysis CKD patients, highlighting the potential involvement of abnormal biological metabolism in CKD pathogenesis. Exploring metabolites may offer new possibilities for the management of CKD.

Sulforaphane supplementation improves biochemical parameters in non-dialysis patients with chronic kidney disease

Sulforaphane supplementation improves biochemical parameters in non-dialysis patients with chronic kidney disease

The Impact of Uric Acid-Lowering Therapy on the Progression of Non-dialysis Chronic Kidney Disease: A Prospective Cohort Study.

Background Hyperuricemia treatment can positively influence the progression of chronic kidney disease (CKD). This study aimed to evaluate the impact of uric acid-lowering therapy on the progression of CKD after three months. Materials and methods A prospective cohort study was conducted on 126 patients with non-dialysis CKD in Can Tho Central General Hospital, Vietnam, from December 2018 to December 2019. Adopting a questionnaire survey method to collect information, including demographic characteristics, body mass index (BMI), personal history, previous medical history, diet, and use of drugs with the potential to affect the uric acid levels in the blood. Participants also underwent necessary tests, such as serum uric acid, serum creatinine, and blood lipids. Data were analyzed using SPSS software version 26.0(IBM Corp., Armonk, NY). Results The prevalence of hyperuricemia in patients with non-dialysis CKD was 77.8%, and the average serum uric acid was 494.21 ± 131.57 µmol/L. Patients with a high-purine diet were about 18.85 times as likely to have hyperuricemia as those with a low-purine diet (p < 0.001, OR = 18.85, 95%CI: 4.233-83.938). BMI, stages of CKD, and hypertension were associated with the hyperuricemia rate (p < 0.05). After three months of treatment, 46.2% of patients achieved the serum uric acid target, and the patient group combined allopurinol with changing diet had a higher rate than the patient group changing diet only (p = 0.02). There was a moderate inverse correlation between the difference in serum uric acid and the difference in estimated glomerular filtration rate (eGFR) after treatment (r = -0.5, p = 0.001). Conclusions The effective management of hyperuricemia by combining nonpharmacological (changing diet) and/or pharmacological (allopurinol) therapies may meaningfully improve the glomerular filtration rate in non-dialysis CKD patients with hyperuricemia.

Oral Liposomal Iron Versus Injectable Iron Sucrose for Anemia Treatment in Non-dialysis Chronic Kidney Disease Patients: A Non-inferiority Study.

Introduction Anemia is a prevalent and persistent complication in chronic kidney disease (CKD), particularly in advanced stages, contributing to the deterioration of renal function and diminishing patients' quality of life. Iron supplementation constitutes a cornerstone of anemia management in this population. Among various iron formulations, liposomal iron has emerged as a promising option due to its enhanced efficacy in replenishing iron reserves and improved tolerability. Objective This study aims to assess the comparative effects of intravenous and liposomal oral iron on hemoglobin levels in non-dialysis CKD patients. Additionally, it seeks to evaluate the rate of hemoglobin correction, iron reserve status during treatment, and therapeutic tolerance to these interventions. Materials and methods A randomized controlled trial enrolled CKD patients (stages 3-5, not on dialysis) with iron deficiency anemia (hemoglobin ≤ 12 g/dL, ferritin ≤ 100 ng/mL, transferrin saturation ≤ 25%). Participants were allocated to receive either daily oral liposomal iron (Group OS) at a dosage of 30 mg or intravenous iron-hydroxide sucrose complex weekly (Group IV) for three months. Follow-up extended through the treatment phase and two months post-withdrawal. Results Thirty-one CKD patients were randomized into two groups: 14 received intravenous iron (IV group) and 17 received oral iron (OS group). After excluding four patients, the final cohort comprised 27 individuals (IV group: n=13, OS group: n=14). Both iron treatments resulted in progressive hemoglobin increases, with the IV group showing a mean increase of 14.65% (p=0.049) compared to 4.78% (p=0.003) in the OS group. Secondary analysis revealed significant increases in ferritin levels (p<0.001) and transferrin saturation (TSAT) levels (p=0.031) in the IV group. Post-treatment follow-up demonstrated stable hemoglobin levels in the OS group and a consistent increase in ferritin levels in the IV group. Adverse reactions predominantly included hypotension in the IV group (4 (30.7%)) and constipation in the OS group (4 (28.4%)). Discussion and conclusion Anemia remains a significant challenge in CKD patients. Our study compares oral liposomal iron to injectable iron for anemia treatment, aiming to minimize hospitalizations for iron infusion, preserve venous capital, and mitigate potential harmful side effects. We found oral liposomal iron to be a safe and effective option for correcting anemia in non-dialysis CKD patients, albeit with lower efficacy in replenishing iron stores compared to IV iron. Comparative analysis with similar studies supports the non-inferiority of oral liposomal iron, although IV iron retains superiority in replenishing iron reserves.

The kidney-skeletal muscle-heart axis in chronic kidney disease: implications for myokines.

Myokines are signalling moieties released by the skeletal muscle in response to acute and/or chronic exercise, which exert their beneficial or detrimental effects through paracrine and/or autocrine pathways on the own muscle and through endocrine pathways in many other organs (e.g. the heart). Interestingly, alterations in myokines have been described in patients with heart failure (HF) that are associated with adverse structural and functional left ventricular remodelling and poor cardiac outcomes. Recent experimental and clinical studies have shown that the muscle regulation of a number of myokines is altered in chronic kidney disease (CKD) thus representing a new molecular aspect of the pathophysiology of skeletal myopathy present in patients with CKD. Muscle dysregulation of myokines may contribute to a number of disorders in non-dialysis and dialysis patients with CKD, including the high risk of developing HF. This possibility would translate into a range of new diagnostic and therapeutic options. In fact, the measurement of circulating myokines opens their possible usefulness as biomarkers to personalize exercise training and pharmacological therapies for the prevetion and treatment of HF in patients with CKD and skeletal myopathy. This review will analyze information on some myokines that target the heart and are altered at the level of skeletal muscle and circulation in patients with CKD.

Estimated Glomerular Filtration Rate and Sleep Quality in Stage 3-5 Non-Dialysis Chronic Kidney Disease Patients: Is There a Correlation?

Background: Chronic kidney disease (CKD) is a growing health issue that significantly affects patients' quality of life. CKD patients are prone to sleep disturbances, which can lead to chronic fatigue and a decrease in their quality of life. The Pittsburgh Sleep Quality Index (PSQI) is a parameter that can be used to assess the sleep quality of CKD patients. Objective: This study aims to determine the relationship between estimated glomerular filtration rate (eGFR) and sleep quality in non-dialysis CKD patients. Methods: The research design is an observational analytic study with a cross-sectional approach. The research subjects were stage 3-5 non-dialysis CKD patients aged 18 to 60 years at Prof. Dr. R. D. Kandou Hospital Manado from March to May 2022. The sleep quality of CKD patients was assessed using the PSQI score. Data analysis was performed with a significance level of p &lt; 0.05. Results: A total of 30 patients with stage 3-5 non-dialysis CKD were found. They consisted of 20 males and 10 females, aged 38-59 years, with an average of 59.80 ± 9.86 years. In the normality test using Shapiro-Wilk, the patient samples were not normally distributed (p = .000). For statistical analysis using the Spearman test, a negative correlation was found between eGFR and PSQI scores (r = -0.554), which was statistically significant (p = 0.002). Conclusion: This study found a significant relationship between eGFR and PSQI scores, which shows that a decrease in eGFR worsens the sleep quality of non-dialysis CKD patients.

Hyperkalemia-Related RAASi Reduction and Estimated Number Needed to Treat to Avoid a First Hospitalization by Maintaining RAASi.

Renin-angiotensin-aldosterone system inhibitor (RAASi) therapy provides cardiorenal protection but is often down-titrated or discontinued following a hyperkalemia episode. This observational study describes the extent of hyperkalemia-related RAASi reduction in patients with chronic kidney disease (CKD) and/or heart failure (HF), and estimates the number needed to treat (NNT) to avoid a first hospitalization if RAASi had been maintained at the prior dose. Healthcare registers and claims data from Germany, Spain, Sweden, and the UK were used to identify non-dialysis patients with CKD and/or HF who had a hyperkalemia episode while on RAASi. Patients whose RAASi therapy was reduced (down-titrated/discontinued) after the hyperkalemia episode were propensity score (PS)-matched to those with maintained RAASi, and their risks of a hospitalization within 6 months were estimated using the Kaplan-Meier method. Based on the absolute difference in this 6-month risk, the NNT framework was applied to estimate the number of patients who needed to have maintained instead of reduced their RAASi to avoid a first hospitalization during this period. Overall, 40,059 patients from Germany, Spain, Sweden, and the UK were included. Presence of CKD at baseline was similar across countries (72%-92%), while HF was less common in Spain (18%) versus other countries (32%-71%). After the hyperkalemia episode, RAASi was reduced in 25%-57% of patients. Following PS matching, the 6-month risk of hospitalization was consistently higher in those with reduced versus maintained RAASi; the absolute risk difference ranged from 2.7% to 7.3%. Applying the NNT framework, these data suggest that a first hospitalization within 6 months could potentially have been avoided if 25 patients had maintained instead of reduced their RAASi. Our findings suggest a potential for avoiding a first hospitalization, even within a short time frame, by increasing adherence to guidelines to maintain instead of reduce RAASi after a hyperkalemia episode.

Low LCAT activity is linked to acute decompensated heart failure and mortality in patients with CKD

Chronic kidney disease (CKD) is often associated with decreased activity of lecithin-cholesterol acyltransferase (LCAT), an enzyme essential for HDL maturation. This reduction in LCAT activity may potentially contribute to an increased risk of cardiovascular mortality in patients with CKD. The objective of this study was to investigate the association between LCAT activity in patients with CKD and the risk of adverse outcomes. We measured serum LCAT activity and characterized lipoprotein profiles using nuclear magnetic resonance spectroscopy in 453 non-dialysis CKD patients from the CARE FOR HOMe study. LCAT activity correlated directly with smaller HDL particle size, a type of HDL potentially linked to greater cardiovascular protection. Over a mean follow-up of 5.0 ± 2.2 years, baseline LCAT activity was inversely associated with risk of death (standardized HR 0.62, 95% CI 0.50–0.76; P < 0.001) and acute decompensated heart failure (ADHF) (standardized HR 0.67, 95% CI 0.52–0.85; P = 0.001). These associations remained significant even after adjusting for other risk factors. Interestingly, LCAT activity was not associated with the incidence of atherosclerotic cardiovascular events or kidney function decline during the follow-up. To conclude, our findings demonstrate that low LCAT activity is independently associated with all-cause mortality and ADHF in patients with CKD, and is directly linked to smaller, potentially more protective HDL subclasses.

The Relationship between Circulating Kidney Injury Molecule-1 and Cardiovascular Morbidity and Mortality in Hemodialysis Patients.

The importance of identifying mortality biomarkers in chronic kidney disease (CKD), and especially in patients treated with hemodialysis (HD), has become evident. In addition to being a marker of tubulointerstitial injury, plasma kidney injury molecule-1 (KIM-1) has been mentioned in regard to HD patients as a risk marker for cardiovascular (CV) mortality and coronary artery calcification. The aim of this study was to assess the level of plasma KIM-1 as a marker of cardiovascular disease (CVD) and mortality in CKD5-HD patients (patients with CKD stage G5D treated with hemodialysis). We conducted a prospective case-control study that included 63 CKD5-HD patients (HD for 1-5 years) followed up for 48 months and a control group consisting of 52 non-dialysis patients diagnosed with CKD stages G1-G5 (ND-CKD). All patients had a CVD baseline assessment including medical history, echocardiography, and electrocardiography (ECG). Circulating plasma KIM-1 levels were determined with single-molecule counting immunoassay technology using an enzyme-linked immunosorbent assay. We obtained the following parameters: serum creatinine and urea; the inflammation markers CRP (C-reactive protein) and IL-6 (interleukin-6); and the anemia markers complete blood count, serum ferritin, and transferrin saturation (TSAT). The mean plasma KIM-1 level was 403.8 ± 546.8 pg/mL, showing a statistically significant correlation with inflammation (CRP, R = 0.28, p = 0.02; IL-6, R = 0.36, p = 0.005) and with anemia (hematocrit, R = -0.5, p = -0.0316; hemoglobin (Hb), R = -0.5, p = 0.02). We found that patients with left ventricular hypertrophy (LVH) on echocardiography (59.7%) had significantly lower mean levels of plasma KIM-1 than patients from the control group (155.51 vs. 432.12 pg/mL; p = 0.026). Regarding the patients' follow-up, we assessed all-cause mortality as an endpoint. After 24 months of follow-up, we found a mortality rate of 22.23%, while after 48 months, the mortality rate was 50.73%. A plasma KIM-1 level < 82.98 pg/mL was significantly associated with decreased survival in hemodialysis patients (p < 0.001). In patients treated with hemodialysis, low levels of plasma KIM-1 were associated with cardiovascular changes and an increased risk of mortality. Plasma KIM-1 levels were significantly higher in HD patients compared to ND-CKD patients.

Associations of 24-Hour Central Systolic Blood Pressure With Multiorgan Damage in Nondialysis Patients With Chronic Kidney Disease.

Multiple target-organ damages (TODs) in the same patient are common and further increase the risk of cardiovascular disease. However, the relationship between ambulatory central systolic blood pressure (SBP) and multiple TODs has yet to be explored. MobilO-Graph PWA was used to monitor the participants' ambulatory blood pressure, and the presence of left ventricular hypertrophy, carotid hypertrophy, and kidney injury were used to define TOD. Logistic regression analyses and receiver operating characteristic analyses were used to explore the correlation between SBP and TOD. Overall, 2018 nondialysis patients with chronic kidney disease were included and 580 (28.74%) had multiple TODs. Twenty-four-hour central SBP with c2 calibration exhibited a stronger correlation with the increasing number of TOD compared with 24-hour brachial SBP in ordinal logistic regression analyses. In the multivariable analyses with the presence of multiple TODs, the odds ratios were 1.786 (95% CI, 1.474-2.165; P<0.001) for 24-hour brachial SBP and 1.949 (95% CI, 1.605-2.366; P<0.001) for 24-hour central SBP with c2 calibration. The receiver operating characteristic analyses also showed that 24-hour central SBP with c2 calibration had higher discrimination than 24-hour brachial SBP regarding multiple TODs (P<0.001). In addition, using 130/135 mm Hg as the threshold for 24-hour brachial SBP/central SBP with c2 calibration to cross-classify, the prevalence of multiple TODs was greater in cases of concordant hypertension compared with cases of isolated brachial hypertension and concordant normotension, with no difference between the latter 2 conditions. Twenty-four-hour central SBP with c2 calibration was more associated with the presence of multiple TODs compared with 24-hour brachial SBP and was helpful in risk classification of multiple TODs among nondialysis patients with chronic kidney disease.

Reduced renal function is associated with faster loss of bone mineral density in patients with non-dialysis CKD

Abstract Background Bone mineral density (BMD) predicts fracture risk in patients with chronic kidney disease (CKD) and in the general population. However, few studies have investigated risk factors for bone loss in patients with CKD. The aim of this study was to investigate whether renal function is associated with the rate of BMD decline. Methods A prospective cohort study included 1 006 patients with CKD stages 2–4 between 2011 and 2016. BMD was measured using dual-energy X-ray absorptiometry at baseline and 4 years. The eGFR was measured 2–6 times during the 4-year follow-up. We analyzed the decline in bone mineral density according to CKD stage and further compared the rate of BMD decline according to eGFR trajectories at each stage. Results Advanced CKD stage was associated with a faster rate of decline in total hip BMD (stage 2: −0.23, stage 3A: −0.39, stage 3B: −0.80, stage 4: −1.23% change/year in men [p &amp;lt; 0.001]; stage 2: −0.86, stage 3A: −1.19, stage 3B: −1.20, stage 4: −1.58% change/year in women [p &amp;lt; 0.03]). Two distinct eGFR trajectories (Class 1: stable group; Class 2: rapid decline group) were observed. The rapid decline group showed a trend toward an increased rate of decline in total hip BMD. Subgroup analysis according to eGFR trajectories revealed a significant difference in BMD decline rate between stable and rapid decline groups. Conclusions Advanced CKD stage and accelerated decline in renal function were associated with rapid BMD decline in non-dialysis patients with CKD.

Myosteatosis: an underrecognized risk factor for mortality in non-dialysis chronic kidney disease patients.

Low muscle mass quantity and quality (myosteatosis) can be evaluated by computed tomography (CT)by measuring skeletal muscle area and muscular attenuation, respectively, at the third lumbar vertebra. We aimed to define cut-off points of skeletal muscle area and muscular attenuation to predict mortality in non-dialysis chronic kidney disease (CKD)patients. We conducted a retrospective study including non-dialysis CKD patients over two years, who underwent an opportunistic computed tomography within a two year period, and for whom creatinine was measured within 90days of CT. Skeletal muscle area was normalized for stature to calculate the skeletal muscle index. Area under the receiver operating characteristic (AuROC) curve and Youden's index were used, to identify the cut-point, separatelyaccording to sex. One hundred sixty-seven patients (50.9% male, mean age of 68.3 ± 16.4years) were included, most with CKD stages 3 and 4. During a median follow-up of 4.9 (4.2) years, 39 (23.4%) patients died. Muscular attenuation showed a better ability to predict mortality (AuROC curve 0.739 [95% CI 0.623-0.855] in women and 0.744 in men [95% CI 0.618-0.869]) than skeletal muscle index (AuROC curve 0.491 [95% CI 0.332-0.651] in women and 0.711 [95% CI 0.571-0.850] in men). For muscular attenuation, the best cut-off values to predict mortality were 27.56 Hounsfield units in women and 24.58 Hounsfield units in men. For skeletal muscle index, the best cut-off values were 38.47 cm2/m2 in women and 47.81 cm2/m2 in men. In univariable Cox-regression both low muscle mass and myosteatosis were associated with increased mortality. In multivariable Cox-regression models only myosteatosismaintained a significant association with mortality (Hazard Ratio 2.651 (95% CI 1.232-5.703, p = 0.013)). We found sex-specific cut-off values for muscle parameters using CT analysis in non-dialysis CKD patients that were associated with mortality. In this population, myosteatosis may be more closely associated with mortality than muscle quantity.