Hemolytic uremic syndrome (HUS), a thrombotic microangiopathy primarily affecting the kidneys, can also involve the central nervous system (CNS), often leading to significant morbidity and mortality. Neurologic manifestations are among the most severe extra-renal complications, particularly in children and during outbreaks of Shiga toxin-producing Escherichia coli (STEC)-associated HUS (typical (tHUS)). This review explores the clinical spectrum, pathophysiology, diagnostic workup, and age-specific outcomes of neurologic involvement in both typical (tHUS) and atypical (aHUS). Neurologic complications occur in up to 11% of pediatric and over 40% of adult STEC-HUS cases in outbreak settings. Presentations include seizures, encephalopathy, focal deficits, movement disorders, and posterior reversible encephalopathy syndrome (PRES). Magnetic resonance imaging (MRI) commonly reveals basal ganglia or parieto-occipital lesions, though subtle or delayed findings may occur. Laboratory workup typically confirms microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and kidney damage, with additional markers of inflammation or metabolic dysregulation. Eculizumab is the first-line treatment for aHUS with CNS involvement, while its utility in STEC-HUS remains uncertain. Although many children recover fully, those with early CNS involvement are at greater risk of developing epilepsy, cognitive delays, or fine motor deficits. Adults may experience lingering neurocognitive symptoms despite apparent clinical recovery. Differences in presentation and imaging findings between age groups emphasize the need for tailored diagnostic and therapeutic strategies. Comprehensive neurorehabilitation and long-term follow-up are crucial for identifying residual deficits. Continued research into predictive biomarkers, neuroprotective interventions, and standardized treatment protocols is needed for improving outcomes in HUS patients with neurological complications.

Increased peritoneal protein loss has been associated with the fast transport of small molecules, diabetes mellitus (DM), and a reduced survival in patients on peritoneal dialysis (PD), although some studies did not confirm the association with survival. In this single-center retrospective study, we investigated the relationship of baseline peritoneal albumin and protein loss with transport status, comorbidities including DM, and survival in 106 incident PD patients during the period of July 2005–June 2014. Five-year survival rate was determined using Cox-regression analysis. There were not significant differences in D/Pcr or peritoneal protein and albumin loss between diabetics and non-diabetics. In the group of 66 non-diabetics, high and high-average transporters for creatinine had higher values for both peritoneal protein (11.85 ± 6.77 vs. 7.85 ± 4.36 g/day; p = 0.002) and albumin (5.03 ± 2.32 vs. 3.72 ± 1.54 g/day; p = 0.016) loss as compared to slow transporters. However, in the group of 40 diabetics, this association was not observed. Upon multivariable regression analysis, the independent association of D/PCr with peritoneal albumin (β = 0.313; p = 0.008) and protein (β = 0.441; p = 0.001) loss was found only in non-diabetics in whom ultrafiltration also appeared as a significant predictor of peritoneal protein loss (β = 0.330; p = 0.000). A high comorbidity grade, older age, and low serum albumin were associated with mortality, but both peritoneal protein and albumin loss as well as D/Pcr were not determinants of survival. Baseline peritoneal protein and albumin loss was not associated with DM and did not predict survival. The clinical significance of the absence of association between fast peritoneal transport status and peritoneal protein flux in diabetics should be evaluated in a prospective study comprising a greater number of diabetics with evaluation of overhydration as a main inducing variable of protein leak.

Ischemic heart disease (IHD) remains a leading cause of global morbidity and mortality despite advances in prevention, diagnosis, and therapy. Traditional clinical risk scores and biomarkers often fail to fully capture the complex molecular processes underlying atherosclerosis, myocardial infarction, and ischemic cardiomyopathy, leaving substantial residual risk. MicroRNAs have emerged as promising regulators and biomarkers of cardiovascular disease, among which microRNA-21 (miR-21) has attracted particular attention. MiR-21 is deeply involved in key pathophysiological mechanisms of IHD, including endothelial dysfunction, vascular inflammation, vascular smooth muscle cell proliferation, plaque development and vulnerability, cardiomyocyte survival, and myocardial fibrosis. Accumulating clinical evidence suggests that circulating miR-21 holds diagnostic value across the ischemic continuum, from stable coronary artery disease to acute coronary syndromes, myocardial infarction, and ischemic heart failure. Moreover, miR-21 demonstrates prognostic relevance, correlating with plaque instability, adverse remodeling, heart failure progression, and long-term cardiovascular outcomes. Preclinical studies further indicate that miR-21 represents a double-edged therapeutic target, offering cardio protection in acute ischemic injury while contributing to fibrosis and maladaptive remodeling if dysregulated. This narrative review summarizes current evidence on the diagnostic, prognostic, and therapeutic utility of miR-21 in IHD, highlighting its clinical promise as well as key limitations and future translational challenges.

The pandemic caused by the SARS-CoV-2 virus had a great impact on the population of patients treated with peritoneal dialysis (PD). This study demonstrates the impact of infection and vaccination in 66 patients treated with PD and their outcomes during a 6-month follow-up. This is the first research that has studied the dynamics of anti-SARS-CoV-2 IgG in serum and effluent. In our research, 57.6% of PD patients were vaccinated, predominantly with Sinopharm (81.6%), which was also the most frequently administered vaccine in the Republic of Serbia at the beginning of immunization. During the monitoring period, the level of anti-SARS-CoV-2 IgG antibodies in the PD patients had an increasing trend in serum. In the group of vaccinated patients with PD, anti-SARS-CoV-2 IgG antibodies had an increasing trend in both serum and effluent, in contrast to non-vaccinated patients, where they decreased in effluent regardless of the trend of increase in serum, but statistical significance was not reached. In contrast to vaccinated (immunized) patients who did not acquire infection, the patients who only underwent the COVID-19 infection, but were not immunized, were more prone to reinfection upon the outbreak of a new viral strain, yet without severe clinical presentation and with no need for hospital treatment.

Optimized glycemic management is crucial for controlling atherosclerosis and consequent cardiovascular morbidity in patients with diabetes. Due to the continuous glucose burden from glucose-containing peritoneal dialysis (PD) solutions, PD patients with diabetes experience difficulties in glucose level regulation with glucose hypervariability and worsening dyslipidemia. Even in non-diabetic PD patients, glucose-containing PD solutions aggravate insulin resistance and cause overweight. Additionally, glucose degradation products (GDP) from glucose-based PD solutions provoke oxidative stress and complex inflammatory processes, leading to chronic deleterious and fibrotic peritoneal membrane changes. In this narrative review, we searched the literature using PubMed, MEDLINE, and Google Scholar over the last three decades to summarize the most important facts relevant to the presented issues, aiming to inform both endocrinologists and nephrologists in providing the best currently available care for people with diabetes on PD. We not only focus on adequate tailoring of insulin therapy adapted at the time of PD exchange with hypertonic glucose solution., but also emphasize the use of continuous glucose monitoring (CGM) that allows assessment of mean glucose values and time spent in normal, hypo, and hyperglycemia. However, the routine use of CGM in PD patients is limited due to high cost, and hemoglobin A1c (HbA1c) analysis is still recommended as a basic clinical tool for the assessment of glycemic control. Possible choices of antidiabetic drugs were considered given the narrowed choice due to contraindications for metformin and sulfonylurea. The other important therapeutic approach in PD patients with diabetes is using glucose-sparing PD regimens based on icodextrin and amino acid PD solutions with the addition of just one or two bags of low glucose concentration PD solution daily. This glucose-sparing approach not only reduces the glucose load and improves glycoregulation with correction of the lipid profile but also maintains the viability of the peritoneal membrane by reducing the harmful effects of GDPs.

An increase in dietary protein intake (DPI) carries a risk with respect to increased sodium intake, which further leads to the development of cardiovascular morbidity in peritoneal dialysis (PD) patients. Dialytic (DSR) and urinary sodium removal (USR) are potential indicators of sodium intake. In this single-center cross-sectional study with 60 prevalent PD patients, we analyze the correlation of DPI with sodium intake and the association between residual renal function (RRF) and comorbidity grade, expressed as the Davies score with sodium removal and protein metabolism indices such as normalized protein catabolic rate (nPCR) and lean body mass (LBM). The value of RRF < 2 mL/min/1.73 m² is significantly associated with lower USR (p = 0.000) and lower %LBM (p < 0.001). The greatest USR is detected in patients with low Davies comorbidity grade (p = 0.018). Compared to patients with DPI < 0.8 g/kg/day, patients with DPI > 0.8 g/kg/day have a greater sodium intake (3.69 ± 0.71 vs. 2.94 ± 0.86; p < 0.018) and a greater nPCR (p < 0.001). Protein intake is significantly correlated with sodium intake (p = 0.041), but not with total sodium removal (TSR). A strong correlation is observed between sodium intake and TSR (p = 0.000), although single TSR values are not the same as the corresponding sodium intake values. An increasing protein intake implies the necessity to determine both sodium intake and sodium removal. Preservation of RRF has a beneficial role not just in sodium removal, but also in the increase of LBM.