Chronic kidney disease (CKD) is an important factor that contributes to the increase of all-cause morbidity and mortality in the group of non-communicable diseases, and it is also recognized as a strong and independent risk factor that contributes to cardiovascular disease (CVD). CVDs are a consequence of the action of a large number of risk factors among which are traditional and non-traditional. These risk factors have been the subject of a large number of studies which partially explained the unfavorable cardiovascular (CV) outcome of CKD patients. Therefore, valid studies about clinical and biohumoral predictors are of particular importance, especially in the early stages of renal disease, that is, in patients with creatinine clearance below 60 ml/min/1.73 m² when preventive measures are most effective. Among potential predictors of adverse CV outcome are biomarkers of inflammation (Interleukin-18—IL-18), oxidative stress (ischemia-modified albumin—IMA; superoxide dismutase—SOD), acute kidney injury (kidney injury molecule -1—KIM-1; neutrophil gelatinase–associated lipocalin—NGAL), and microribonucleic acids (specific microRNA-133a). In this review, we tried to confirm the relationship between risk factors of CKD and CVD and newer, less frequently examined biomarkers with the occurrence of incidental CV events in renal patients.

Cardiovascular (CV) morbidity and mortality increase along with the progression of chronic kidney disease (CKD). The potential novel biomarkers of cardiotoxicity have been tested with the aim of the early detection of patients at high CV risk, and among them are markers of inflammation, oxidative stress, acute renal injury, and microRNAs. The study analyzed biomarkers in non-dialysis-dependent (NDD; stage 3a–4 CKD) and dialysis-dependent (DD) CKD patients. The prospective cohort study included 87 patients who were followed for 18 months, during which period newly occurred CV events were recorded. Cox regression analysis confirmed serum albumin, urea, interventricular septum thickness diameter (IVST), the use of calcium antagonist, and erythropoiesis-stimulating agent to be significant predictors of CV outcome. No significant difference was observed in biomarkers of inflammation, oxidative stress, acute kidney injury (IL-18, CRP, ferritin, IMA, SOD, NGAL, and KIM-1), and miR-133a, in regards to the presence/absence of CV event, CV death, and left ventricular hypertrophy. Serum albumin, urea, IVST, and the use of calcium antagonist and erythropoiesis-stimulating agents were confirmed to be factors associated with CV events in CKD patients. Apart from traditional risk factors, new research is needed to define novel and reliable biomarkers of cardiotoxicity in CKD patients.

Background and Aim: Long-term treatment with biologic therapy alongside immunomAfodulators in patients with inflammatory bowel disease (IBD) can be associated with severe side effects. The objective of this study was to determine whether discontinuing anti-TNF treatment after two years in patients who have achieved mucosal healing is associated with lower relapse rates. Materials and Methods: A total of 67 patients with IBD from a single tertiary IBD Center who had achieved mucosal healing were enrolled in this retrospective study. In this single-center retrospective study (January 2014–December 2022), we screened 67 IBD patients in deep remission (endoscopic mucosal healing after ≥2 years of anti-TNF therapy). After excluding three patients without histologic data, 64 patients (25 ulcerative colitis, 39 Crohn’s disease) were analyzed. Mayo endoscopic sub-score and SES-CD were used to evaluate endoscopic activity after two years of anti-TNF therapy. Histological activity was assessed using the GHAS (for CD) and Nancy index (for UC). Results: A total of 67 patients were screened, of whom 3 were excluded due to a lack of biopsies. Of the 64 included patients, 39.06% (25/64) had UC and 60.9% (39/64) had CD, with a mean disease duration of 11.6 ± 8.0 years. All patients were in endoscopic remission at the time of therapy de-escalation, and 60.9% (39/64) also achieved histological remission (“deep remission”). In the follow-up of 38.6 months (IQR 30–48) after biologic therapy was stopped, 57.8% (37/64) relapsed with a median time to relapse of 13.5 months (IQR 8–24) off anti-TNF—a total of 34 patients required a restarting of biologic therapy. Using Spearman’s correlation, a moderate connection was observed between histological activity at withdrawal and subsequent relapse (rho = 0.467, p < 0.001). The probability of relapsing within 4 years after anti-TNF cessation was significantly higher (OR 2.72) in patients with histologically active disease at the time of de-escalation. Conclusions: Achieving ‘deep remission’ (clinical, endoscopic, and histological healing) may be a suitable parameter for making decisions on when to de-escalate therapy; however, given that over half of patients in endoscopic remission relapse after discontinuation, any de-escalation should be approached with caution and individualized patient assessment.

Glycemic assessment in patients with chronic kidney disease (CKD) Stage V on hemodialysis (HD) is limited by the inaccuracy of hemoglobin A1c (HbA1c), mainly due to anemia, shortened erythrocyte lifespan, and erythropoiesis-stimulating agent (ESA) therapy. Glycated albumin (GA), independent of erythrocyte turnover, may better reflect glycemic exposure. We evaluated the diagnostic performance and clinical utility of GA as a biomarker of poor glycemic control and cardiovascular risk in patients with diabetes mellitus (DM). A cross-sectional analysis and five-year prospective follow-up were conducted in three subgroups: HD+DM+ (n = 40), HD- DM+ (n = 15), and HD+DM– (n = 22). Glycemic markers (mean plasma glucose over 3 months (PG₃m), GA, and HbA1c) were compared between groups. GA levels were significantly higher in HD+DM+ patients (p < 0.001) and showed the strongest correlation with PG₃m. GA independently predicted poor glycemic control (OR 3.23; 95% CI 1.54–6.77; p = 0.002) and demonstrated high diagnostic accuracy (AUC 0.873; optimal cut-off 10%). During the five-year follow-up, CV mortality was 35%, and 85% of deceased patients had GA > 10%. Although Cox regression did not reach statistical significance, GA showed a consistent trend toward higher CV mortality risk after adjustment for age and HD duration (HR 2.56; 95% CI 0.57–11.44; p = 0.21), whereas HbA1c was not prognostic (HR 1.39; 95% CI 0.49–3.91; p = 0.28). GA appears to be a clinically useful marker of glycemic control in diabetic patients with CKD Stage V receiving maintenance hemodialysis. In this cohort, GA showed high diagnostic accuracy and a more balanced sensitivity/specificity profile compared with HbA1c, with a consistent trend toward association with cardiovascular mortality. In this regard, the wider use of this marker in clinical practice is worth considering. Nevertheless, larger prospective studies are warranted to validate these observations.

Background: Obesity has reached epidemic proportions and represents a challenge in selecting the optimal renal replacement therapy for patients with end-stage renal disease (ESRD). This study aimed to evaluate the outcomes of peritoneal dialysis (PD) patients according to baseline body mass index (BMI) and to assess the impact of BMI changes during follow-up on PD-related complications and patient outcomes. Methods: This retrospective, single-center study included 53 incident PD patients treated between June 2006 and August 2015. Based on baseline BMI, patients were classified as normal weight (18.5–24.9 kg/m²; n = 17), overweight (25.0–29.9 kg/m²; n = 25), or obese (≥30.0 kg/m²; n = 11). PD adequacy, mechanical and infectious complications, technique survival, and patient survival were assessed over a 48-month follow-up. The effect of BMI changes during follow-up was also analyzed. Results: At PD initiation, total weekly Kt/V was significantly lower in the obese compared with the normal-weight patients (2.0 ± 0.4 vs. 2.3 ± 0.5; p = 0.038), although values remained within the ISPD targets. The normal-weight patients had lower urine output compared with the overweight patients (p = 0.038). Exit-site infections were the most frequent, whereas peritonitis incidence was the lowest in the obese patients, without statistically significant differences. The obese patients demonstrated poorer technique survival and overall survival, again without statistical significance. Mean BMI change after one year was 1.65 ± 2.08 kg/m², and after 4 years, it was 2.07 ± 3.18 kg/m². The BMI change was not associated with complications or survival. Conclusions: No significant association during the 48-month follow-up period was observed between baseline nutritional status or weight gain assessed by body mass index and adverse peritoneal dialysis outcomes; therefore, overweight and obese patients can achieve adequate PD performance and may defer or avoid transition to hemodialysis.