Effective biomarkers for early diagnosis, prognostication, and monitoring in renal diseases (in general) comprise an unmet need. Urinary retinol-binding protein 4, which is the most sensitive indicator of renal tubular damage, holds great promise as a universal biomarker for renal pathologies, in which tubular injury is the driving force. Here, we summarize the most important existing data on the associations between urinary retinol-binding protein 4 and renal diseases and highlight the untapped potential of retinol-binding protein 4 in clinical use.

Augmented peripheral chemoreceptor sensitivity (PChS) is a common feature of many sympathetically mediated diseases, among others, and it is an important mechanism of the pathophysiology of heart failure (HF). It is related not only to the greater severity of symptoms, especially to dyspnea and lower exercise tolerance but also to a greater prevalence of complications and poor prognosis. The causes, mechanisms, and impact of the enhanced activity of peripheral chemoreceptors (PChR) in the HF population are subject to intense research. Several methodologies have been established and utilized to assess the PChR function. Each of them presents certain advantages and limitations. Furthermore, numerous factors could influence and modulate the response from PChR in studied subjects. Nevertheless, even with the impressive number of studies conducted in this field, there are still some gaps in knowledge that require further research. We performed a review of all clinical trials in HF human patients, in which the function of PChR was evaluated. This review provides an extensive synthesis of studies evaluating PChR function in the HF human population, including methods used, factors potentially influencing the results, and predictors of increased PChS.

Primary membranous nephropathy is a leading cause of nephrotic syndrome in adults, characterized by immune complex deposition in the glomerular basement membrane. Predicting proteinuria remission is essential for guiding treatment decisions, optimizing immunosuppressive therapy, and improving renal outcomes. Traditional prognostic markers, such as anti-PLA2R antibody status and baseline proteinuria levels, offer valuable insights into disease progression. However, recent research has identified additional biomarkers that may enhance risk stratification and refine individualized treatment strategies. Serum-based markers, such as uric acid and inflammatory indices, may indicate systemic changes that impact disease progression. Urinary biomarkers, including microhematuria, α1-microglobulin, and CXCL13, have been proposed as potential predictors of disease activity and remission likelihood. Furthermore, histopathological features, such as glomerular basement membrane thickness, tubulointerstitial injury, and acute kidney injury, provide structural correlates that may inform prognosis. This review explores both established and emerging prognostic indicators across various biological domains. Understanding these predictors can aid in developing personalized therapeutic strategies, optimizing disease management, and improving patient outcomes in primary membranous nephropathy.

The majority of recently published studies indicate a greater incidence rate and mortality due to Clostridioides difficile infection (CDI) in patients with chronic kidney disease (CKD). The aim of this study was to assess the clinical determinants predicting CDI among hospitalized patients with CKD and refine methods of prevention. We evaluated the medical records of 279 patients treated at a nephrological department with symptoms suggesting CDI, of whom 93 tested positive for CDI. The survey showed that age, poor kidney function, high Padua prediction score (PPS) and patients’ classification of care at admission, treatment with antibiotics, and time of its duration were significantly higher or more frequent among patients who suffered CDI. Whereas BMI, Norton scale (ANSS) and serum albumin concentration were significantly lowered among CDI patients. In a multivariate analysis we proved the stage of CKD and length of antibiotics use increased the risk of CDI, whereas higher serum albumin concentration and ANSS have a protective impact.

The majority of recently published studies indicate a greater incidence and mortality due to Clostridioides difficile infection (CDI) in patients with chronic kidney disease (CKD). Hospitalization, older age, the use of antibiotics, immunosuppression, proton pump inhibitors (PPI), and chronic diseases such as CKD are responsible for the increased prevalence of infections. The aim of the study is to identify clinical indicators allowing, in combination with artificial intelligence (AI) techniques, the most accurate assessment of the patients being at elevated risk of CDI.

Background: The ability of hemoglobin to bind and dissociate oxygen is crucial in delivering oxygen to tissues and is influenced by a range of physiological states, compensatory mechanisms, and pathological conditions. This may be illustrated by the oxyhemoglobin dissociation curve (ODC). The key parameter for evaluating the oxygen affinity to hemoglobin is p50. The aim of this study was to evaluate the impact of hemodialysis on p50 in a group of patients with chronic kidney disease (CKD). An additional goal was to assess the correlation between p50 and the parameters of erythropoiesis, point-of-care testing (POCT), and other laboratory parameters. Methods: One hundred and eighty patients (106 male, 74 female), mean age 62.5 ± 17 years, with CKD stage G4 and G5 were enrolled in this cross-sectional study. Patients were divided into two groups, including 65 hemodialysis (HD) patients and 115 patients not receiving dialysis (non-HD). During the standard procedure of arteriovenous fistula creation, blood samples from the artery (A) and the vein (V) were taken for POCT. The causes of CKD, as well as demographic and comorbidity data, were obtained from medical records and direct interviews. Results: The weekly dose of erythropoietin was higher in HD patients than in non-HD patients (4914 ± 2253 UI vs. 403 ± 798 UI, p < 0.01), but hemoglobin levels did not differ between these groups. In the group of non-HD patients, more advanced metabolic acidosis (MA) was found, compared to the group with HD. In arterial and venosus blood samples, the non-HD group had significantly lower pH, pCO₂ and HCO₃⁻. This group had a higher proportion of individuals with MA with HCO₃⁻ < 22 mmol/L (42% vs. 24%, p < 0.01). The absolute difference of p50 in arterial and venous blood was determined using the formula Δp50 = (p50-A) − (p50-V). Δp50 was significantly higher in the HD group in comparison to non-HD (0.08 ± 2.05 mmHg vs. −0.66 ± 1.93 mmHg, p = 0,02). There was a negative correlation between pH and the p50 value in arterial (pH-A vs. p50-A, r = −0.56, p < 0.01) and venous blood (pH-V vs. p50-V, r = −0.45, p < 0.01). In non-HD patients, hemoglobin levels correlated negatively with p50 (r = −0.29, p < 0.01), whereas no significant relation was found in HD patients. Conclusions: The ODC in pre-dialysis CKD (non-HD) patients is shifted to the right due to MA, and this is an additional factor influencing erythropoiesis. Hemodialysis restores the natural differences in hemoglobin’s dissociation characteristics in the arterial and venous circulation.