Patients with chronic kidney disease (CKD) are at a high risk for cardiovascular disease (CVD), and approximately half of all deaths among patients with CKD are a direct result of CVD. The premature cardiovascular disease extends from mild to moderate CKD stages, and the severity of CVD and the risk of death increase with a decline in kidney function. Successful kidney transplantation significantly decreases the risk of death relative to long-term dialysis treatment; nevertheless, the prevalence of CVD remains high and is responsible for approximately 20-35% of mortality in renal transplant recipients. The prevalence of traditional and nontraditional risk factors for CVD is higher in patients with CKD and transplant recipients compared with the general population; however, it can only partly explain the highly increased cardiovascular burden in CKD patients. Nontraditional risk factors, unique to CKD patients, include proteinuria, disturbed calcium, and phosphate metabolism, anemia, fluid overload, and accumulation of uremic toxins. This accumulation of uremic toxins is associated with systemic alterations including inflammation and oxidative stress which are considered crucial in CKD progression and CKD-related CVD. Kidney transplantation can mitigate the impact of some of these nontraditional factors, but they typically persist to some degree following transplantation. Taking into consideration the scarcity of data on uremic waste products, oxidative stress, and their relation to atherosclerosis in renal transplantation, in the review, we discussed the impact of uremic toxins on vascular dysfunction in CKD patients and kidney transplant recipients. Special attention was paid to the role of native and transplanted kidney function.

Anemia is a clinical feature of chronic kidney disease (CKD). Most common causes are iron and erythropoietin deficiency. The last two decades have yielded significant advances in understanding iron balance's physiology, including iron trafficking and the crosstalk between iron, oxygen, and erythropoiesis. This knowledge sheds new light on the regulation and disturbance of iron homeostasis in CKD and holds the promise for developing new diagnostic and therapeutic tools to improve the management of iron disorders. Hepcidin–ferroportin axis has a central role in regulating body iron balance and coordinating communication between tissues and cells that acquire, store, and utilize iron. Recent research has revealed a bidirectional relationship between fibroblast growth factor 23 (FGF23) and iron status, anemia, and inflammation, as well as the role of erythroferrone (ERFE) in iron homeostasis. However, ERFE concentrations and actions are not well-characterized in CKD patients. Studies on ERFE in CKD are limited with slightly conflicting results. Despite general interest in iron metabolism in kidney diseases, studies on the less prevalent renal replacement therapy mode, such as peritoneal dialysis or hemodiafiltration, are scarce. Slightly more was published on hemodialysis. There are several novel options on the horizon; however, clinical data are limited. One should be aware of the potential risks and benefits of the novel, sophisticated therapies. An inhibition of hepcidin on the different pathways might be also a viable adjunctive therapeutic option in other clinical situations.

Iron is the most abundant transition metal in the human body and an essential element required for growth and survival. Our understanding of the molecular control of iron metabolism has increased dramatically over the past 20 years due to the discovery of hepcidin, which regulates the uptake of dietary iron and its mobilization from macrophages and hepatic stores. Anemia and iron deficiency are common in chronic kidney disease. The pathogenesis of anemia of chronic kidney disease is multifactorial. Correction of anemia requires two main treatment strategies: increased stimulation of erythropoiesis, and maintenance of an adequate iron supply to the bone marrow. However, there are still many uncertainties in regard to iron metabolism in patients with chronic kidney disease and in renal replacement therapy. The aim of this review was to summarize the current knowledge on iron metabolism in this population, including new biomarkers of iron status. There is an area of uncertainty regarding diagnostic utility of both erythroferrone (ERFE) and hepcidin in end-stage renal disease (ESRD) patients. Higher concentration of hepcidin in oligoanuric patients may reflect decreased renal clearance. Furthermore, the hepcidin-lowering effect of ERFE in ESRD patients treated with erythropoiesis-stimulating agents (ESAs) may be blunted by underlying inflammation and concomitant iron treatment. Thus, future studies should validate the use of ERFE as a biomarker of erythropoiesis and predictor of response to iron and ESA therapy in dialysis-dependent patients.

Chronic kidney disease is a public health problem that, depending on the country, affects approximately 8–13% of the population, involving both males and females of all ages. Renal replacement therapy remains one of the most costly procedures. It is assumed that one of the factors influencing the course of chronic kidney disease might be oxidative stress. It is believed that the main mediators of oxidative stress are reactive oxygen species (ROS). Transiently increased concentrations of ROS play a significant role in maintaining an organism’s homeostasis, as they are part of the redox-related signaling, and in the immune defense system, as they are produced in high amounts in inflammation. Systemic oxidative stress can significantly contribute to endothelial dysfunction along with exaggeration of atherosclerosis and development of cardiovascular disease, the leading cause of mortality in patients with kidney disease. Moreover, the progression of chronic kidney disease is strictly associated with the atherosclerotic process. Transplantation is the optimal method for renal replacement therapy. It improves better quality of life and prolongs survival compared with hemodialysis and peritoneal dialysis; however, even a successful transplantation does not correct the abnormalities found in chronic kidney disease. As transplantation reduces the concentration of uremic toxins, which are a factor of inflammation per se, both the procedure itself and the subsequent immunosuppressive treatment may be a factor that increases oxidative stress and hence vascular sclerosis and atherosclerotic cardiovascular disease. In the current work, we review the effect of several risk factors in kidney transplant recipients as well as immunosuppressive therapy on oxidative stress.

Background. Cognitive impairment (CI) in patients with chronic kidney disease, including those treated with renal replacement therapy (RRT) is a growing problem worldwide. The study aimed to assess the prevalence of CI and associated factors in patients undergoing peritoneal dialysis (PD). Methods. In this cross-sectional study, 18 consecutive patients with PD therapy and 15 controls were evaluated for CI using the Addenbrooke's Cognitive Examination III (ACE III) test. Results. The prevalence of CI was 33% in patients and 27% in the control group and was not statistically significant. A higher prevalence of CI was found in subjects aged ≥65 years old than in those <65years old (p = 0.02), but only in the control group. The prevalence of CI in PD patients over and under 65 years of age did not differ statistically significantly (p = 0.12). Memory and verbal fluency were the most affected cognitive domain in PD patients with CI (p = 0.00, p = 0.04, respectively). There was a significant correlation between higher-educated PD patients and the ACE III test results. The duration of dialysis did not affect the results of the cognitive screening test. Conclusion. Cognitive impairment is a growing problem in the course of chronic kidney disease and dialysis therapy. It seems that cognitive problems may occur in patients undergoing peritoneal dialysis at a younger age than in the general population with particularly affected memory and verbal fluency. Higher-educated patients score better on the cognitive screening test.