Anemia is one of the most common chronic kidney disease (CKD) complications. It negatively affects patients’ quality of life and clinical outcomes. The pathophysiology of anemia in CKD involves the interplay of various factors such as erythropoietin (EPO) deficiency, iron dysregulation, chronic inflammation, bone marrow dysfunction, and nutritional deficiencies. Despite recent advances in understanding this condition, anemia still remains a serious clinical challenge in population of patients with CKD. Several guidelines have been published with the aim to systematize the diagnostic approach and treatment of anemia; however, due to emerging data, many recommendations vary between publications. Recent studies indicate a potential of novel biomarkers to evaluate anemia and related conditions such as iron deficiency, which is often present in CKD patients. Our article aims to summarize the pathophysiology of anemia in CKD, as well as the diagnosis and management of this condition, including novel therapeutic approaches such as hypoxia-inducible factor-prolyl hydroxylase inhibitors (HIF-PHI). Understanding these complex subjects is crucial for a targeted approach to diagnose and treat patients with anemia in CKD effectively.

Primary electrical heart diseases, often considered channelopathies, are inherited genetic abnormalities of cardiomyocyte electrical behavior carrying the risk of malignant arrhythmias leading to sudden cardiac death (SCD). Approximately 54% of sudden, unexpected deaths in individuals under the age of 35 do not exhibit signs of structural heart disease during autopsy, suggesting the potential significance of channelopathies in this group of age. Channelopathies constitute a highly heterogenous group comprising various diseases such as long QT syndrome (LQTS), short QT syndrome (SQTS), idiopathic ventricular fibrillation (IVF), Brugada syndrome (BrS), catecholaminergic polymorphic ventricular tachycardia (CPVT), and early repolarization syndromes (ERS). Although new advances in the diagnostic process of channelopathies have been made, the link between a disease and sudden cardiac death remains not fully explained. Evolving data in electrophysiology and genetic testing suggest previously described diseases as complex with multiple underlying genes and a high variety of factors associated with SCD in channelopathies. This review summarizes available, well-established information about channelopathy pathogenesis, genetic basics, and molecular aspects relative to principles of the pathophysiology of arrhythmia. In addition, general information about diagnostic approaches and management is presented. Analyzing principles of channelopathies and their underlying causes improves the understanding of genetic and molecular basics that may assist general research and improve SCD prevention.

Hepatorenal syndrome (HRS) is a disorder associated with cirrhosis and renal impairment, with portal hypertension as its major underlying cause. Moreover, HRS is the third most common cause of acute kidney injury, thus creating a major public health concern. This review summarizes the available information on the pathophysiological implications of HRS. We discuss pathogenesis associated with HRS. Mechanisms such as dysfunction of the circulatory system, bacterial infection, inflammation, impaired renal autoregulation, circulatory, and others, which have been identified as critical pathways for development of HRS, have become easier to diagnose in recent years. Additionally, relatively recently, renal dysfunction biomarkers have been found indicating renal injury, which are involved in the pathophysiology of HRS. This review also summarizes the available information on the management of HRS, focusing on vasoconstrictive drugs, renal replacement therapy, and liver transplant together with currently being investigated novel therapies. Analyzing new discoveries for the underlying causes of this condition assists the general research to improve understanding of the mechanism of pathophysiology and thus prevention of HRS.

Myocarditis is a non-ischemic condition with a heterogeneous etiology, clinical course and prognosis. The most common etiology of myocarditis are viral infections, whereas the most severe complications are acute and chronic heart failure and sudden cardiac death. The heterogeneous clinical course of the disease, as well as the availability and costs of diagnostic tools such as cardiac magnetic resonance and endomyocardial biopsy, hinder the diagnosis of myocarditis and its underlying cause. Non-coding RNAs such as micro-RNAs (miRNAs; miR) have been shown to be involved in the disease’s pathophysiology; however, their potential in disease diagnosis and treatment should also be considered. Non-coding RNAs are RNAs that are not translated into proteins, and they have the ability to regulate several intracellular pathways. MiRNAs regulate gene expression by binding with their targets and inhibiting protein synthesis by interfering with the translation of coding genes or causing the degradation of messenger RNA. Several miRNAs, such as miR-1, -133, -21, -15, -98, -126, -155, -148, -203, -208, -221, -222, -203 and -590, have been shown to be involved in the pathophysiology of viral myocarditis (VMC), and some of them have been shown to have diagnostic abilities. This article summarizes the available data on miRNAs and their associations with VMC.

Acute coronary syndromes (ACS) are a leading cause of death and impairment in the adult population. Precise identification and modification of risk factors is crucial for a favorable clinical outcome. In this review, we aim to provide a comprehensive overview of the significance of iron deficiency (ID) in patients with ACS, particularly myocardial infarction (MI). The paper evaluates the impact of ID on the prognosis of ACS patients, highlighting its potential influence on myocardial healing, regeneration and cardiovascular events during the follow-up period. The findings suggest that iron deficiency may have a negative impact on the prognosis of patients with MI, resulting in worse quality of life, physical capacity and higher rehospitalization rates in comparison to patients with normal iron status. Iron supplementation in patients with MI could be beneficial and may have an effect on myocardial healing and left ventricular remodeling.

Background/Objectives: Fetal lower urinary tract obstruction (LUTO) is a rare congenital anomaly that often leads to pulmonary hypoplasia and kidney dysfunction, which contribute to increased mortality. Prenatal estimation of the severity of LUTO is challenging due to the lack of specific diagnostic tools, which may guide clinical decisions. The aim of this analysis was to assess the role of fetal urinary concentrations of neutrophil gelatinase-associated lipocalin (NGAL), β2-microglobulin (B2M) and Cystatin C (CysC) in the prediction of unfavorable outcomes, such as postnatal renal dysfunction and death, among LUTO patients. Methods: A total of 38 women carrying fetuses with suspected LUTO (based on ultrasound features) were included in the study. Fetal urine was collected from the bladder of the fetus under ultrasound guidance, and measurements of NGAL, CysC and B2M were performed using an enzyme-linked immunosorbent assay. We analyzed the role of NGAL, CysC and B2M in the prediction of renal dysfunction or death within 30 days after birth. Results: Fetal urinary NGAL, CysC and B2M corrected for fetal urinary creatinine (FuCr) were significant predictors of impaired postnatal renal function or death within 30 days after birth. AUCs of ROC curves for NGAL/FuCr, CysC/FuCr and B2M/FuCr as predictors of renal dysfunction or death within 30 days after birth were: 0.793 (95% CI: 0.614–0.972, p = 0.001), 0.857 (95% CI: 0.7–1.0, p < 0.0001), 0.764 (95% CI: 0.562–0.966, p = 0.01), respectively. Among assessed biomarkers, only CysC/FuCr corrected for creatinine (p = 0.02) was associated with decreased eGFR on day 30 of postnatal life, whereas NGAL (p = 0.07) and B2M (p = 0.12) were not. AUCs of ROC curves for NGAL/FuCr, CysC/FuCr and B2M/FuCr as predictors of renal dysfunction on day 30 after birth were: 0.756 (95% CI: 0.535–0.976, p = 0.02), 0.833 (95% CI: 0.649–1.0, p = 0.0004), 0.722 (95% CI: 0.482–0.963, p = 0.07), respectively. Conclusions: Fetal urinary NGAL, CysC and B2M may constitute a promising tool in early prediction of impaired renal function and mortality in fetuses with LUTO. Accurate prediction of renal function decline after birth is crucial for proper pre- and postnatal counseling and may support prenatal intervention decision making. Further studies are required to establish the role of the studied biomarkers in the prediction of adverse outcomes.