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Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The progressive reduction in estimated glomerular filtration rate (eGFR) resulting in chronic kidney disease (CKD) is associated with increased risk of cardiovascular disease (CVD) (i.e. cardiorenal disease). Cardiorenal disease is associated with poor outcomes, mainly due to increased cardiovascular (CV) complications and CV death. Data from general population–based studies and studies of cohorts with CKD and/or CVD show that compared with creatinine-based eGFR, cystatin C–based eGFR and creatinine plus cystatin C–based eGFR detect higher risks of adverse CV outcomes and add predictive discrimination to current CVD risk scores. On the other hand, growing clinical evidence supports kidney and CV protective effects of sodium–glucose cotransporter-2 (SGLT2) inhibitors in cardiorenal patients. However, recent data suggest that some detrimental effects of SGLT2 inhibitors on skeletal muscle mass may lead to overestimation of creatinine-based eGFR and subsequent misinterpretation of associated CV risk in patients treated with these agents. Within this framework, we suggest the advisability of using cystatin C and/or creatinine plus cystatin C–based eGFR for routine clinical practice in cardiorenal patients to more accurately stratify CV risk and evaluate the kidney and CV protective effects of SGLT2 inhibitors. In this regard, we make a call to action to investigate the protective effects of these pharmacological agents using cystatin C–based eGFR. [ABSTRACT FROM AUTHOR]

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cardiorenal syndromes (CRS) are broadly defined as disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other. CRS are currently classified into five categories, mostly based on disease-initiating events and their acuity or chronicity. CRS types 3 and 4 (also called renocardiac syndromes) refer to acute and chronic kidney dysfunction resulting in acute and chronic heart dysfunction, respectively. The notion of renocardiac syndromes has broadened interest in kidney–heart interactions but uncertainty remains in the nephrological community's understanding of the clinical diversity, pathophysiological mechanisms and optimal management approaches of these syndromes. This triple challenge that renocardiac syndromes (and likely other cardiorenal syndromes) pose to the nephrologist can only be faced through a specific and demanding training plan to enhance his/her cardiological scientific knowledge and through an appropriate clinical environment to develop his/her cardiological clinical skills. The first must be the objective of the subspecialty of cardionephrology (or nephrocardiology) and the second must be the result of collaboration with cardiologists (and other specialists) in cardiorenal care units. This review will first consider various aspects of the challenge s that renocardiac syndromes pose to nephrologists and, then, will discuss those aspects of cardionephrology and cardiorenal units that can facilitate an effective response to the challenges. [ABSTRACT FROM AUTHOR]

Background Acute kidney injury (AKI) is associated with short- and long-term complications but the consequences of the AKI-to-CKD transition are still poorly understood. We aimed to evaluate the association between the AKI-to-CKD transition and the long-term risk of infection. Methods This retrospective study included patients admitted in a tertiary hospital with community-acquired AKI in 2013 and 2014 who had their estimated glomerular filtration rate (eGFR) assessed at 3 months (±2 weeks) after serum creatinine peaked in the AKI episode. Key exclusion criteria were baseline CKD or confounding factors (active neoplasia, primary immunodeficiency, human immunodeficiency virus, immunosuppressive drugs). The association between the AKI-to-CKD transition (defined as an eGFR <60 ml/min/1.73 m2 at 3 months) and long-term infections (defined using clinical features, blood/urine analysis, cultures and imaging) was assessed during a follow-up of 9 months (range 2–56). Results Among the 1731 patients admitted with AKI, 367 (21%) were included in the present analysis (64% male, 71 ± 15 years). Three months after AKI, 159 (43%) developed AKI-to-CKD transition. Baseline and post-AKI eGFR were independent predictors of AKI-to-CKD transition [hazard ratio (HR) 0.97, P  = .044 and HR 0.96, P  < .001, respectively]. During follow-up, 153 (42%) patients developed an infection. Factors associated with infection were older age, cognitive impairment, lower post-AKI eGFR, eGFR loss from baseline to 3 months and AKI-to-CKD transition. Adjusted Cox regression showed that baseline eGFR, 3-month eGFR, eGFR loss and AKI-to-CKD transition were independent predictors of the long-term risk of infection. Conclusions The AKI-to-CKD transition independently predicts the long-term risk of infection following an episode of AKI. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) is the most common arrhythmia in patients with chronic kidney disease (CKD), and its presence is associated with a higher risk of stroke and mortality. Material and Methods: The FAERC study performed a retrospective multicentre analysis of historical cohorts in which data were collected from arrhythmia diagnosis onwards. Results: We analysed a Spanish cohort of 4749 patients with CKD (mean eGFR 33.9 mL/min) followed up in the nephrology clinic, observing a 12.2% prevalence of non-valvular AF. In total, 98.6% of these patients were receiving anticoagulant treatment, mainly with coumarins (79.7%). Using direct-acting oral anticoagulants (DOACs) was associated with fewer cerebrovascular events than using acenocoumarol, but in contrast with other studies, we could not corroborate the association of risk of bleeding, coronary events, or death with a type of anticoagulant prescribed. Conclusions: Atrial fibrillation is highly prevalent in renal patients. Direct-acting anticoagulants seem to be associated with fewer ischemic-embolic complications, with no differences in bleeding, coronary events, or mortality rates. [ABSTRACT FROM AUTHOR]

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction. Patients on peritoneal dialysis (PD) present an impaired humoral response against SARS-CoV-2, at least after the initial vaccination and booster dose. Until now, the effect of a fourth dose has not been established. The aim of the present study is to evaluate the long-term dynamics of the humoral response of PD patients to multiple doses of SARS-CoV-2 vaccines, focusing on the effect of the fourth dose. Methods. This is an analysis of the prospective and multicentric SENCOVAC study. We included patients on PD without additional immunosuppression that had received at least 3 SARS-CoV-2 mRNA vaccine doses. We evaluated anti-spike antibody titers after the initial vaccination, third and fourth doses, using prespecified fixed assessments (i.e., baseline, 28 days, 3, 6, and 12 months after completing the initial vaccine schedule). Breakthrough infections were also collected. Results. We included 164 patients on PD (69% males, 62 ± 13 years old). In patients who had received only two doses, the rates of positive humoral response progressively decreased from 96% at 28 days to 80% at 6 months, as did with anti-spike antibody titers. At 6 months, 102 (62%) patients had received the third vaccine dose. Patients with the third dose had higher rates of positive humoral response (p = 0.01) and higher anti-spike antibody titers (p < 0.001) at 6 months than those with only 2 doses. At 12 months, the whole cohort had received 3 vaccine doses, and 44 (27%) patients had an additional fourth dose. The fourth dose was not associated to higher rates of positive humoral response (100 vs. 97%, p = 0.466) or to statistically significant differences in anti-spike antibody titers as compared to three doses (p = 0.371) at 12 months. Prior antibody titers were the only predictor for subsequent higher anti-spike antibody titer (B 0.53 [95%CI 0.27–0.78], p < 0.001). The 2 (1.2%) patients that developed COVID-19 during follow-up had mild disease. Conclusions. PD presents an acceptable humoral response with three doses of SARS-CoV-2 vaccines that improve the progressive loss of anti-spike antibody titers following two vaccine doses. [ABSTRACT FROM AUTHOR]

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Patients with chronic kidney disease (CKD) are at high risk for developing cardiovascular events. However, limited evidence is available regarding the use of aspirin in CKD patients to decrease cardiovascular risk and to slow renal disease progression.Study Design: Prospective, multicenter, open-label randomized controlled trial.Setting and Participants: One hundred eleven patients with estimated glomerular filtration rate (eGFR) 15-60 ml/min/1.73 m2 without previous cardiovascular events.Intervention: Aspirin treatment (100 mg/day) (n = 50) or usual therapy (n = 61). Mean follow-up time was 64.8 ± 16.4 months.Outcomes: The primary endpoint was composed of cardiovascular death, acute coronary syndrome (nonfatal MI, coronary revascularization, or unstable angina pectoris), cerebrovascular disease, heart failure, or nonfatal peripheral arterial disease. Secondary endpoints were fatal and nonfatal coronary events, renal events (defined as doubling of serum creatinine, ≥ 50% decrease in eGFR, or renal replacement therapy), and bleeding episodes.Results: During follow-up, 17 and 5 participants suffered from a primary endpoint in the control and aspirin groups, respectively. Aspirin did not significantly reduce primary composite endpoint (HR, 0.396 (0.146-1.076), p = 0.069. Eight patients suffered from a fatal or nonfatal coronary event in the control group compared to no patients in the aspirin group. Aspirin significantly reduced the risk of coronary events (log-rank, 5.997; p = 0.014). Seventeen patients in the control group reached the renal outcome in comparison with 3 patients in the aspirin group. Aspirin treatment decreased renal disease progression in a model adjusted for age, baseline kidney function, and diabetes mellitus (HR, 0.272; 95% CI, 0.077-0.955; p = 0.043) but did not when adjusted for albuminuria. No differences were found in minor bleeding episodes between groups and no major bleeding was registered.Limitations: Small sample size and open-label trial.Conclusions: Long-term treatment with low-dose aspirin did not reduce the composite primary endpoint; however, there were reductions in secondary endpoints with fewer coronary events and renal outcomes. ClinicalTrials.gov Identifier: NCT01709994. [ABSTRACT FROM AUTHOR]

Background Resolution of inflammation is regulated by endogenous lipid mediators, such as lipoxins and their epimers, including 15-epi-lipoxin A4 (15-epi-LXA4). However, there is no information on 15-epi-LXA4 and its in vivo regulation in chronic kidney disease (CKD) patients. Study design Open label randomized clinical trial. Setting and participants 50 participants with chronic kidney disease (CKD) stage 3 and 4 without prior cardiovascular disease (25 in the aspirin group and 25 in the standard group) followed for 46 months. Intervention Aspirin (100 mg/day) or standard treatment. Aim To analyze the effect of aspirin on plasma 15-epi-LXA4 levels and inflammatory markers in CKD patients. Results Baseline plasma15-epi-LXA4 levels were lower in diabetic (1.22 ± 0.99 ng/ml) than in non-diabetic CKD patients (2.05 ± 1.06 ng/ml, p < 0.001) and inversely correlated with glycosylated hemoglobin levels (r = −0.303, p = 0.006). In multivariate analysis, diabetes was associated with lower 15-epi-LXA4 levels, adjusted for age, inflammatory markers and renal function (p = 0.005). In the whole study population, 15-epi-LXA4 levels tended to increase, but not significantly (p = 0.45), after twelve months on aspirin (from mean ± SD 1.84 ± 1.06 to 2.04 ± 0.75 ng/ml) and decreased in the standard care group (1.60 ± 1.15 to 1.52 ± 0.68 ng/ml, p = 0.04). The aspirin effect on 15-epi-LXA4 levels was more striking in diabetic patients, increasing from 0.94 ± 0.70 to 1.93 ± 0.74 ng/ml, p = 0.017. Conclusions Diabetic patients with CKD have lower circulating 15-epi-LXA4 levels than non-diabetic CKD patients. Low dose aspirin for 12 months increased 15-epi-LXA4 levels in diabetic patients. Given its anti-inflammatory properties, this increase in 15-epi-LXA4 levels may contribute to the beneficial effects of low dose aspirin. [ABSTRACT FROM AUTHOR]

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background. Increased interarm systolic blood pressure difference (IASBPD) is associated with mortality and cardiovascular (CV) events both in the general population and in patients at high CV risk. The aim of the present study was to assess the value of IASBPD ≥ 10 mmHg for predicting CV events in patients with chronic kidney disease (CKD). Methods. The study sample comprised 652 patients with CKD (age 67 ± 15 years, 58.1% men). Follow-up was 19 ± 5 months. We recorded increased IASBPD and related factors and assessed the predictive value of this variable for CV events. Results. We recorded diabetes mellitus in 136 patients (20.8%), history of CV disease in 213 (32.6%) and dyslipidaemia in 327 (50.1%). The mean glomerular filtration rate was 45.9 ± 18.9 mL/min/1.73 m², and the median albumin/creatinine ratio was 26(0-151) mg/g. IASBPD was ≥10 mmHg in 184 patients (28.1%). The factors associated with IASBPD ≥10 mmHg were age, systolic blood pressure levels, history of congestive heart failure, lower levels of high-density lipid cholesterol and higher use of hypertensive drugs. Fifty-eight patients (8.5%) developed a CV event during the follow-up. IASBPD ≥10 mmHg [HR, 1.802, 95%CI (1.054-3.079); P = 0.031] was an independent predictor of CV events. Conclusions. Increased IASBPD is an independent predictor of CV events in CKD patients. [ABSTRACT FROM AUTHOR]

In chronic kidney disease (CKD) patients on dialysis, plasma interleukin (IL)-6 levels predict mortality better than other markers. Impact of intraindividual changes of inflammatory markers on cardiovascular (CV) events in CKD patients is unknown. The aim of this study is to demonstrate the relation between CV outcomes and variations of C-reactive protein (CRP), IL-6, IL-1 β, and tumor necrosis factor (TNF)- α in CKD. Ninety patients (mean age: 68.5 ± 12.8 years) at different stages (1-4) of CKD were evaluated. Serum CRP, IL-6, IL-1 β, and TNF- α were measured basally and after taking statins or angiotensin II receptor blockers. Three patterns were defined for each marker (baseline, mean of two measurements, and variation of the marker: increase or decrease after 6 months). During follow-up (mean time: 72.7 ± 19.8 months), 14 patients died, 11 were included on dialysis program, and 29 suffered a CV event. Patients with persistently elevated IL-6 values had higher risk to develop CV events [OR = 1.21 (1.11-1.32), p = 0.001]. Mean of two measurements of IL-6 was a better predictor for events than a single measurement of IL-6, CRP, TNF- α, and IL-1 β. A mean of two determinations of plasma IL-6 greater than 6 pg/mL and previous peripheral vascular disease was related to an increased risk for CV events [2.34 (1.05-5.22), p = 0.037 and 2.95 (1.27-6.93), p = 0.011, respectively] in an adjusted Cox regression model. IL-6 is a better inflammatory marker than CRP, TNF- α, and IL1 β at predicting CV events in CKD nondialysis patients. Mean of two measurements is better than simple determinations at predicting CV outcome. [ABSTRACT FROM AUTHOR]