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Background: Hemodialysis is one of the most resources consuming medical intervention. Due to its concept, the proper amount of dialysis fluid passed through dialyzer is crucial to obtain the expected outcomes. The most frequent source of dialysis fluid is production from liquid concentrate (delivered in containers or plastic bags) in dialysis machine. Alternatively, concentrates for dialysis may be produced in dialysis center by dilution in mixing devices dry or semidry premixed compounds connected with system of central dialysis fluid delivery system. Dialysate consumption depends on various factors like type of hemodialysis machine, session duration, prescribed flow, etc. Summary: Modern hemodialysis machines are equipped with the modules which automatically reduce flow rate of dialysis fluid to the patient blood flow and minimize dialysate consumption during preparation and after reinfusion. Smart using of available options offered by manufacturers allows to save additional portion of acid concentrate and water. The weight of concentrates to be delivered to the dialysis center is the major factor influencing the cost (financial and environmental) of transportation from the manufacturer to the final consumer. The crisis on the energy carriers market and extremely high fuel prices made the transportation cost one of the significant costs of the treatment, which must be bear by supplier and finally influence on the price of goods. Key Messages: The careful choice of the concentrate delivery system can improve cost-effectiveness of dialysis. Such solutions implemented in dialysis unit helps make significant savings and decrease the impact on natural environment by carbon footprint reduction. [ABSTRACT FROM AUTHOR]

Background: Cognitive impairment (CI) in patients with chronic kidney disease, including those treated with renal replacement therapy, is a growing problem worldwide. Objectives: 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 <65 years 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. Conclusions: CI is a growing problem in the course of chronic kidney disease and dialysis therapy. It seems that cognitive problems may occur in patients undergoing PD 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. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) affects the crosstalk between organs in the body and vast majority of studies were devoted to the interactions between the kidneys and the cardiovascular system. As of today, there is more evidence of the kidney and the central nervous system connections. Summary: Indeed, CKD and in particular dialysis therapy is linked to the increased prevalence of neurological complications, such as cerebrovascular disorders, movement disorders, cognitive impairment, and depression. Both traditional cardiovascular risk factors (such as diabetes, hypertension, and lipid disorders), nontraditional risk factors (such as uremic toxins, anemia, and secondary hyperparathyroidism) may predispose CKD patients to neurological disorders. Likewise, cognitive problems occur more commonly in kidney transplant recipients, regardless of age, than in the general population, but the prevalence is still understudied. Cognitive impairment is associated with a higher risk of hospitalization, mortality, decreased quality of life, or health care costs in kidney transplant recipients. Here, we review (i) the potential clinical impact of kidney transplantation on cerebrovascular and neurological complications, (ii) evaluation of patients with cognitive impairment for kidney transplantation (iii) the potential impact of cognitive impairment on waitlisted and transplanted patients on patient care, and (iv) unmet medical needs. Key Messages: Cognitive impairment in kidney transplant recipients is an underestimated, underrecognized but clinically relevant problem. The screening for cognitive declines after kidney transplantation is not yet a routine practice. Several prospective and cross-sectional studies reported improvement across some of the assessed cognitive domains after transplantation. [ABSTRACT FROM AUTHOR]

Background: Tumor lysis syndrome (TLS) is an oncologic emergency due to a rapid break down of malignant cells usually induced by cytotoxic therapy, with hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and serious clinical consequences such as acute renal injury, cardiac arrhythmia, hypotension, and death. Rapidly expanding knowledge of cancer immune evasion mechanisms and host-tumor interactions has significantly changed our therapeutic strategies in hemato-oncology what resulted in the expanding spectrum of neoplasms with a risk of TLS. Summary: Since clinical TLS is a life-threatening condition, identifying patients with risk factors for TLS development and implementation of adequate preventive measures remains the most critical component of its medical management. In general, these consist of vigilant laboratory and clinical monitoring, vigorous IV hydration, urate-lowering therapy, avoidance of exogenous potassium, use of phosphate binders, and – in high-risk cases – considering cytoreduction before the start of the aggressive agent or a gradual escalation of its dose. Key Messages: In patients with a high risk of TLS, cytotoxic chemotherapy should be given in the facility with ready access to dialysis and a treatment plan discussed with the nephrology team. In the case of hyperkalemia, severe hyperphosphatemia or acidosis, and fluid overload unresponsive to diuretic therapy, the early renal replacement therapy (RRT) should be considered. One must remember that in TLS, the threshold for RRT initiation may be lower than in other clinical situations since the process of cell breakdown is ongoing, and rapid increases in serum electrolytes cannot be predicted. [ABSTRACT FROM AUTHOR]

Background/Aims: Several studies have implicated atrial fibrillation (AF) as a contributing factor in chronic kidney disease (CKD) and cardiovascular events. The prevalence of coronary artery disease (CAD) in patients with AF varies substantially from 17% to 46.5%. There are only few studies concerning renal function in population with AF undergoing coronary angiography. The aim of the present study was to assess which type of AF is dominant in CKD population scheduled for coronary angiography and if it can influence patients' outcome, the association between renal impairment and the type of coronary procedures in AF patients and the influence of renal function on in-hospital mortality. Methods: We retrospectively studied 867 patients with AF hospitalized due to coronary angiography in two year time. The cut off value of CKD was eGFR ≤ 60 ml/min./1.73m2 evaluated by CKD-EPI formula. Results: A total of 867 patients with AF (44% women; mean age 72±10 years) were included in the analysis. The mean eGFR was 44±11ml/min./1.73m2 in patients with CKD and 89±18 ml/min./1.73m2 in patients with preserved renal function. Patients with CKD and AF were older (p< 0.001), had more often diabetes (p=0.009), heart failure (p< 0.001) and anaemia (p< 0.001). Patients with CKD and AF had more often permanent type of AF (p< 0.001). In CKD patients CHA2DS2VASc score was 4.3±1.5 and HAS-BLED score was 2.0±1.2 and it was significantly higher as compared to population with preserved renal function (p< 0.001, p=0.02, respectively). The use of oral anticoagulation was less frequent in CKD group (p< 0.001) although these patients had higher CHA2DS2VASc score. Patients with AF and CKD were more often admitted due to myocardial infarction (STEMI or NSTEMI) (p=0.02, p< 0.001, respectively) and more often underwent percutaneous coronary intervention (PCI) (p=0.01). Among coronary arteries the percutaneous coronary intervention (PCI) of left main artery was done more frequently in CKD patients (p=0.01). Among CKD population in-hospital mortality was significantly higher in patients with eGFR < 30 ml/min (p< 0.001). Conclusion: Patients with CKD had more often permanent type of AF. Percutaneous interventions of the left main coronary artery, the only elective procedures influencing patients' prognosis, were done more frequently in CKD patients with AF. In-hospital mortality was significantly higher in patients with severe renal impairment. Despite the higher risk of ischaemic stroke in CKD group the use of oral anticoagulation therapy was significantly less frequent and the patients were deprived of the confirmed benefits of such treatment. [ABSTRACT FROM AUTHOR]

Background/Aims: There are no data concerning renal function in population with valvular and non-valvular atrial fibrillation (AF). To assess renal function in patients with AF, the association between eGFR and AF perpetuation, in-hospital mortality. Methods: We studied 1523 patients with AF. Patients with chronic kidney disease (CKD) were compared to population with preserved renal function. Results: CKD was more frequently observed in patients with valvular AF(p=0.009). In non-valvular AF patients eGFR <60ml/min./1,73m2 had more often permanent AF(p<0.0001). In patients with CKD CHA2DS2VASc score was 4.1±1.5 and HAS-BLED score was 2.1±1.2 and it was higher as compared to population with preserved renal function (p<0.0001 vs p<0.0001). The odds of permanent AF in patients with non-valvular AF and CKD were increased 1.82 times(OR=1.82,p<0.0001,95%CI:1.46-2.27). The odds of permanent AF in patients with valvular AF and CKD were not significantly increased(OR=1.46,p=0.2,95%CI:0.86-2.5). In non-valvular AF, if eGFR decrease by 10ml/min, odds of permanent AF are increased by 10%(OR=1.1p<0.0001,95%CI1.05- 1.15). In multivariate logistic regression, in non-valvular AF, odds of in-hospital death were higher for patients >75 years old(OR=3.70,p=0.01,95%CI1.33-10.28), with CKD (OR=2.61,p=0.03,95%CI1.09-6.23). The type of AF had no significant influence on in-hospital mortality(OR=0.71,p=0.45,95%CI0.30-1.70). Conclusions: CKD is more often observed in patients with valvular AF. In population with non-valvular AF decreased eGFR is associated with permanent type of AF and with higher CHA2DS2VASc and HAS-BLED score. Among valvular AF patients there are no differences in type of AF between patients with and without CKD. There is the correlation between CKD and AF perpetuation but only in non-valvular population. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Neutrophil gelatinase-associated lipocalin (NGAL), a widely accepted diagnostic marker of acute renal injury (AKI) may be involved in the development of atherosclerosis. Purpose: To assess the prognostic significance of serum and urinary NGAL and serum cystatin C in patients with stable angina undergoing percutaneous coronary intervention (PCI) on a 3-year follow-up. Methods: We included patients with stable angina undergoing PCI. Serum NGAL and cystatin C were evaluated before and 4h, 8h after PCI. Urinary NGAL was evaluated before and 12h and 24h after the procedure. The primary end-point was all-cause mortality on a 3-year follow-up. Results: Among 132 patients there were 63% of males (mean age 64,5±9,8 years). Mean eGFR was 86.2±28.5 ml/min. During follow-up 8% of the patients died. All-cause mortality was significantly higher in patients with increased urinary NGAL concentration 12h after PCI (p=0.04). Urinary NGAL 12h after PCI correlated with eGFR (p<0.05), with serum NGAL evaluated before and 4h and 8h after PCI (p<0.05) and with increased serum cystatin C evaluated 4 hours after PCI (p<0.05). Conclusions: Increased urinary NGAL concentration is a strong predictor of mortality in patients with stable angina who undergo PCI and may be used for the risk stratification in this population. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background/Aims: VAP-1 (vascular adhesion protein-1) is a copper-containing SSAO (semicarbazide sensitive amine oxidase) secreted by vascular smooth muscle cells, adipocytes, endothelial cells with functional monoamine oxidase activity. The oxidation process generates harmful products that may be involved in atherosclerosis and vascular damage. Elevation of SSAO activity is observed in atherosclerosis, diabetes mellitus and obesity. On the other hand, renalase, with possible monoamine oxidase activity, which breaks down catecholamines like SSAO, is also expressed in the endothelium as well as in the kidney. The aim of the study was to assess VAP-1 levels and its correlations with endothelial injury markers and renalase in 50 kidney allograft recipients. Methods: Hemoglobin, urea, creatinine, rate were studied by standard laboratory method in the hospital central laboratory. We assessed markers of endothelial function/injury: vWF, thrombomodulin, ICAM, VCAM, CD40L, CD44, CD146, inflammation: hsCRP, and IL-6 and adipocytokines: leptin, adiponectin, visfatin, apelin with commercially available assays. Results: The mean serum VAP-1 in Tx was significantly higher comparing to the control group. In kidney transplant recipients VAP-1 correlated with BMI (r=0.39, p<0.01), CD44 (r=0.27, p<0.05), hsCRP (r=0.28, p<0.05), serum creatinine (r=0.29, p<0.05), eGFR (CKD-EPI formula r=-0.27, p<0.05, MDRD r=-0.27,p<0.05, Cockcroft-Gault r=-0.35,p<0.01), serum urea (r=0.27, p<0.05), CD146 (r=0.49, p<0.001), CD40L (r=0.26, p<0.06), and renalase (r=0.34, p<0.05). In multiple regression analysis VAP-1 was predicted 80% by serum creatinine (beta value 0.33, p=0.01), and CD146 (beta value 43, p=0.0005). Conclusion: VAP-1, elevated in kidney transplant recipients, is predominantly dependent on endothelial damage and kidney function, which deteriorated with time after kidney transplantation. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Renalase, secreted by the kidney, degrades catecholamines and may play a role in the regulation of sympathetic tone and blood pressure. The aim of this study was to assess serum renalase levels in hemodialysis patients and their relationship to blood pressure control, type of antihypertensive therapy and the presence of residual renal function. Results: The mean serum renalase in the study cohort was significantly higher than in the control group (27.53 ± 7.18 vs. 3.86 ± 0.73 p,g/ml,p< 0.001).The serum renalase concentration was significantly lower in patients with residual renal function when compared to the anuric patients. The type of hypotensive treatment ((3-blockers, ACE inhibitors or AT1 receptor blockers) did not affect renalase levels. There was a significant inverse correlation between the serum renalase and age (r = -0.28, p = 0.023) and residual renal function (r = -0.327, p = 0.001). Renalase was not related to blood pressure, heart rate or hemodialysis vintage. Conclusion: Elevated renalase levels in HD patients may be due to impaired kidney function. Further studies are needed to prove or disprove the possible role of renalase in the pathogenesis of hypertension in patients with kidney diseases. [ABSTRACT FROM AUTHOR]

The aim of the study was to collect retrospective data on renal anemia management, comorbidities and prospective data on 12-month standard care erythropoiesis-stimulating agent (ESA) therapy used in 398 hemodialyzed patients in selected Central and Eastern European countries (50 centers in 3 countries). Patients were divided into three groups according to ESA therapy start: group A-ESA (after start of hemodialysis, HD), B-ESA (within 3 months from start of HD), C-ESA (more than 3 months before HD). At the chronic kidney disease diagnosis, hemoglobin in all patients was 10.3 ± 2.3 g/dl; however, ferritin, iron, TSAT were within reference limits. Early ESA therapy (C) was administered to 10% of patients only. 47% of patients received ESA after start of dialysis. Before study, the mean weekly ESA dose in group C was statistically lower than in groups B and A (p < 0.001). At baseline visit, hemoglobin in group A patients was slightly lower than in group B and C patients (p = 0.025). In conclusion, in Central and Eastern European countries renal anemia therapy with ESA starts shortly before or after start of HD. This highlights important differences in standard care in Eastern Europe. However, paradoxically, due to the tight reimbursement policy we foresee the clinical implications of the TREAT trial for the chronic kidney disease population. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background/Aims: To assess the impact of diabetes mellitus (DM) on clinical outcome in patients with end-stage renal disease (ESRD) on a 3-year follow-up. Methods: 58 ESRD patients were divided into 2 groups according to the presence of DM. We analyzed following end points: death, cardiac arrest, myocardial infarction, stroke, hospitalizations due to cardiovascular causes, revascularization, and combined end point. Results: Among diabetics, 14 (77.8%) had significant atherosclerotic changes, in the group without DM only 8 (38.1%), p = 0.01. In the group without DM, 14 (46.7%) patients reached combined end point, while in the group with DM 16 (53.3%) patients, p = 0.0013. There were no statistical differences in mortality (p = 0.423). Conclusion: Survival of hemodialyzed diabetic patients is not inferior to nondiabetics; however, morbidity is significantly higher due to adverse cardiac events. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Acute kidney injury (AKI) is diagnosed in 5% of all hospitalized patients and in up to 50% of all ICU patients. In the last years a dramatic rise in the prevalence of AKI has been observed with virtually no change in mortality, reaching up to 50-80% in all dialyzed ICU patients. AKI may progress to end-stage renal disease, and even subclinical episodes of AKI, which are common, may also progress to end-stage renal disease. The early detection of AKI may enable timely intervention and prevention of progression; however, in animal models and in human studies the 'window of therapeutic intervention' is narrow. Different urinary and serum proteins have been intensively investigated as possible biomarkers for the early diagnosis of AKI. There are promising candidate biomarkers with the ability to detect an early and graded increase in tubular epithelial cell injury and distinguish pre-renal disease from acute tubular necrosis. In this review, new emerging biomarkers of AKI are presented and described in some clinical settings, such as cardiac surgery, contrast-induced nephropathy, delayed graft function and ICU/emergency departments, where biomarkers are urgently needed to diagnose, make prognoses and differentiate. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Iron is the fourth most common element in the Earth’s crust and is crucial for life. Over the last few years, our understanding of iron metabolism has dramatically increased due to the discovery of hepcidin, which is produced by hepatocytes and modulated in response to anemia, hypoxia and inflammation. It has been found that anemia upregulates lipocalin 2 (NGAL; neutrophil gelatinase-associated lipocalin) in the liver and serum. The aim of this review is to summarize the current knowledge dealing with a possible role of hepcidin and NGAL in iron metabolism and its regulation, particularly in kidney disease. Elevated NGAL a few days after insult is a possible preventive or protective mechanism limiting renal injury. NGAL is an innate antibacterial factor as well as hepcidin. NGAL binds siderophores, thereby preventing iron uptake by bacteria. Hepcidin, an antibacterial defensin, prevents iron absorption from the gut and iron release from macrophages, leading to hypoferremia and anemia. Both proteins sequester iron, but by different mechanisms. However, these proteins involved in iron metabolism do not seem to be independently related. Taking into account the antimicrobial moieties of NGAL, further studies are needed to address the role of NGAL in iron metabolism and inflammation in renal failure. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Neutrophil gelatinase-associated lipocalin (NGAL) has recently been proved useful in the quantitation of chronic kidney disease. A cross-sectional study was performed to assess NGAL in serum, urine and ultrafiltrate in relation to the type of renal replacement therapy and NGAL correlations with renal function and markers of inflammation. Methods: NGAL, hsCRP, TNFα, and IL-6 were measured using commercially available kits in 200 patients on hemodialysis (HD), 17 on hemodiafiltration (HDF). Results: Patients on HDF had lower serum NGAL than those on HD. In hemodialyzed patients with residual renal function, serum NGAL was significantly lower than in anuric patients. NGAL was significantly higher in patients dialyzed on modified cellulose dialyzers versus polysulphone dialyzers. NGAL correlated with age, residual renal function, hsCRP, IL-6, TNF-α, time on HD, ferritin, TSAT, creatinine, urea, urea reduction ratio, and Kt/V in hemodialyzed patients. In multiple regression analysis, residual renal function and hsCRP were predictors of NGAL in hemodialyzed patients. NGAL correlated with hsCRP and creatinine in HDF patients. Conclusions: Residual renal function seems to play a pivotal role in NGAL levels in dialyzed patients. Low-grade inflammation, more pronounced in anuric patients may also contribute to elevated NGAL. Removal of NGAL with ultrafiltrate may also partially explain its lower concentration after dialysis. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Hepcidin is the predominant negative regulator of iron absorption in the small intestine, iron transport across the placenta, and iron release from the macrophages. Iron supplementation is often introduced in dialyzed patients to replete or to maintain iron stores, particularly in patients treated with erythropoietin-stimulating agents. The aim of this study was to assess hepcidin levels in 12 hemodialyzed (HD) patients (6 females, 6 males, mean age 64 years, mean time on HD 36 months) before and after intravenous iron therapy. Prohepcidin and hepcidin were studied using commercially available kits from DRG Instruments GmbH, Marburg, Germany (ELISA method), and Bachem, St. Helens, UK (RIA method). Soluble receptor of transferrin was studied using a kit from R&D, Abington, UK. We found a significant rise in hemoglobin concentration, hematocrit, ferritin, serum iron, transferrin saturation and a fall in soluble receptor of transferrin. Serum hepcidin and prohepcidin as well as urinary prohepcidin increased significantly after the therapy. In conclusion, hepcidin levels are influenced by iron supplementation in HD patients. Further examinations of hepcidin as a marker of iron deficiency using new validated measurement techniques are required. It remains to be seen if assay of hepcidin will be of help in identifying patients unresponsive to oral iron or requiring intravenous iron supplementation. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Hemojuvelin (HJV) is a membrane protein that is responsible for the iron overload condition known as juvenile hemochromatosis. HJV, highly expressed in the liver, skeletal muscle and heart, seems to play a role in iron absorption and release from cells and has anti-inflammatory properties. HJV is a bone morphogenetic protein (BMP) co-receptor and signals via the SMAD (human homolog of Drosophila mad – mother against decapentaplegic) pathway to regulate hepcidin expression. HJV acts as a BMP co-receptor. Moreover, HJV plays an essential role in the regulation of hepcidin expression, specifically in the iron-sensing pathway, although through unknown mechanisms. Dietary iron sensing and inflammatory pathways converge in the regulation of the key regulator hepcidin, but how these two pathways intersect remains unclear. Inflammation, through downregulation of hepatic HJV, might induce temporary elimination of iron sensing. Despite enormous scientific achievements in explaining the pathogenetic mechanisms of iron metabolism, many questions still remain unanswered: What is the functional role of HJV in iron metabolism? How it is related to hepcidin expression in different settings? How do iron-sensing and inflammatory pathways cooperate in hepcidin gene expression? Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Heart failure and chronic kidney disease share a number of risk factors and pathophysiological pathways. Renal insufficiency is common in patients with chronic heart failure (CHF). The aim of the study was to assess whether neutrophil gelatinase-associated lipocalin (NGAL) could represent a novel, sensitive marker of kidney function in adult patients with chronic heart failure and normal serum creatinine. The study was performed on 150 patients with chronic heart failure due to coronary artery disease. Serum and urinary NGAL as well as serum cystatin C were measured using commercially available kits. Serum NGAL was related, in univariate analysis, to serum creatinine, urinary NGAL, hemoglobin, hematocrit, leukocyte count, eGFR, cystatin C. Urinary NGAL correlated with age, hemoglobin, hematocrit, serum creatinine, eGFR. In multiple regression analysis predictors of serum NGAL were NYHA class, cystatin C, and eGFR. Taking into consideration the fact that the recent DOQI states that individuals with a reduced GFR is at greater risk for cardiovascular disease and cardiac deaths, precise evaluation of renal function is important in order to select the appropriate strategy to reduce the cardiovascular risk. NGAL should be investigated as a potential early and sensitive marker of kidney impairment/injury. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Maintaining the correct iron balance is crucial for health. Our understanding of the molecular control of iron metabolism has increased dramatically over the past 5 years due to the discovery of hepcidin. This is a circulating antimicrobial peptide mainly synthesized in the liver, which has been recently proposed as a factor regulating the uptake of dietary iron and its mobilization from macrophages and hepatic stores. Inflammation causes an increase of production of hepcidin, which is a potent mediator of anemia of chronic diseases. Anemia in chronic kidney disease is mainly due to erythropoietin deficiency but these patients often have a chronic inflammatory state. The aim of this review is to summarize the current knowledge dealing with a possible role of hepcidin in iron metabolism and its regulation, particularly in kidney disease. In addition, current methods of determination of hepcidin are reviewed. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]