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COVID-19 patients and survivors quite often experience depressive symptoms, which can increase risk for lower immune system response and poorer recovery. Vulnerability to depressive symptoms may be elevated in those patients who have the most severe COVID-19 course of illness, that is, patients who require supplementary oxygen therapy or even intubation. The current study involved a unique sample of patients who were hospitalized due to COVID-19 and who required respiratory support (N = 34, 10 women) in which we investigated depressive symptoms as well as psychopathological personality traits (PID5) as predictors. The majority of patients (76.5%) presented some degree of depressive symptoms. Although we expected severe levels of depressive symptoms to be most prevalent, more patients showed rather moderate levels. At the same time, Negative Affectivity was most predictive of depressive symptoms. We suggest that medical care for patients with greater emotional sensitivity and vulnerability to stress be supplemented with psychological support in order to address depressive symptoms and foster recovery.

BACKGROUND The genetic backgrounds of diabetic kidney disease (DKD) and end-stage kidney disease (ESKD) have not been fully elucidated. AIM To examine the individual and cumulative effects of single-nucleotide polymorphisms (SNPs) previously associated with DKD on the risk for ESKD of diabetic etiology and to determine if any associations observed were specific for DKD. METHODS Fourteen SNPs were genotyped in hemodialyzed 136 patients with diabetic ESKD (DKD group) and 121 patients with non-diabetic ESKD (NDKD group). Patients were also re-classified on the basis of the primary cause of chronic kidney disease (CKD). The distribution of alleles was compared between diabetic and non-diabetic groups as well as between different sub-phenotypes. The weighted multilocus genetic risk score (GRS) was calculated to estimate the cumulative risk conferred by all SNPs. The GRS distribution was then compared between the DKD and NDKD groups as well as in the groups according to the primary cause of CKD. RESULTS One SNP (rs841853; SLC2A1) showed a nominal association with DKD (P = 0.048; P > 0.05 after Bonferroni correction). The GRS was higher in the DKD group (0.615 ± 0.260) than in the NDKD group (0.590 ± 0.253), but the difference was not significant (P = 0.46). The analysis of associations between GRS and individual factors did not show any significant correlation. However, the GRS was significantly higher in patients with glomerular disease than in those with tubulointerstitial disease (P = 0.014) and in those with a combined group (tubulointerstitial, vascular, and cystic and congenital disease) (P = 0.018). CONCLUSION Our results suggest that selected SNPs that were previously associated with DKD may not be specific for DKD and may confer risk for CKD of different etiology, particularly those affecting renal glomeruli.

Background The secretion, distribution, and elimination of insulin in response to a bolus of glucose injected during regular hemodialysis was modeled to quantify the intra-dialytic mass balance of glucose and insulin in patients without (D0) and with type 2 diabetes (D1). Methods A two-compartment regional blood flow model with shared compartments and dynamics for glucose, insulin and c-peptide was used to identify parameters of insulin and c-peptide co-secretion, first- and second-pass hepatic insulin extraction, as well as insulin-independent and insulin-dependent glucose utilization. Experimental data from a previous study obtained in 21 D0 and 14 D1 were used to identify kinetic model parameters and the fractions of glucose and insulin removed by dialysis. Results Modeled gains for insulin secretion (β1 = 0.015 vs. 0.084 L/min, β2 = 0.004 vs. 0.666 L) were lower in D1, resulting in a lower total insulin secretion (Mi = 6.40 vs. 38.0 nmol). Hepatic insulin extraction was high (Eihep = 0.558 vs. 0.638) and only slightly smaller in D1. The fraction of insulin removed by dialysis (Fid = 0.07 vs. 0.05) was small and comparable between D1 and D0. Modeled gains for insulin-dependent glucose uptake (γ = 0.38 vs. 1.34 L2/nmol/min) were lower whereas those for insulin-independent glucose uptake (λ = 0.14 vs. 0.067 L/min) were higher in D1. The fraction of glucose removed by dialysis (Fgd = 0.31 vs. 0.28) was higher in D1. Conclusion Apart from expected differences in modeled secretion and glucose utilization in patients with and without diabetes an intravenous bolus of glucose causes only small differences in overall glucose and insulin balance during a typical hemodialysis treatment.

Nowadays, the high prevalence of kidney diseases and their related complications, including endothelial dysfunction and cardiovascular disease, represents one of the leading causes of death in patients with chronic kidney diseases. Renal failure leads to accumulation of uremic toxins, which are the main cause of oxidative stress development. The renal replacement therapy appears to be the best way to lower uremic toxin levels in patients with end-stage renal disease and reduce oxidative stress. At this moment, despite the increasing number of recognized toxins and their mechanisms of action, it is impossible to determine which of them are the most important and which cause the greatest complications. There are many different types of renal replacement therapy, but the best treatment has not been identified yet. Patients treated with diffusion methods have satisfactory clearance of small molecules, but the clearance of medium molecules appears to be insufficient, but treatment with convection methods cleans medium molecules better than small molecules. Hence, there is an urgent need of new more validated, appropriate, and reliable information not only on toxins and their role in metabolic disorders, including oxidative stress, but also on the best artificial renal replacement therapy to reduce complications and prolong the life of patients with chronic kidney disease.

Introduction: The increasing number of patients with end-stage renal disease (ESRD) requires seeking new opportunities to improve their quality of life, not only because of kidney disease but also due to other disturbances, such as thyroid hormone disorders. The objective of the study was to evaluate the influence of coexisting hypothyroidism and thyroid hormone therapy in patients with ESRD on thyroid hormone conversion ratios and rT3 concentration. Material and methods: The study involved 85 patients aged 26 to 87 years, with a mean age of 59.62 ± 15.45 years. Four groups of patients were examined: G1 group — 25 persons without RF and hypothyroidism, G2 — 26 patients with ESRD treated with haemodialysis (HD), G3 — 12 patients with ESRD treated with HD and newly diagnosed hypothyroidism, and G4 — 22 HD patients with hypothyroidism treated with thyroid hormones substitution. The concentrations of TSH, T4, T3, fT4, fT3, and rT3 were measured and the fT3/fT4, T3/T4, and rT3/T4 conversion ratios and rT3/T3 ratio were calculated. Concentrations of protein, hsCRP, Hg, and blood gases were also checked; the anion gap was calculated. Results: Patients from group G1 through G2 to G3 were older (p trend = 0.002), with lower Hb level (p trend < 0.001), with lower pH (p trend < 0.001), with increased anion gap (p trend < 0.013) and CRP concentrations (p trend < 0.001), and decreased total protein level (p trend < 0.001). There were increased TSH values (p trend < 0.001) and lower T4 (p trend = 0.024), fT3 (p trend < 0.001), T3 (p trend < 0.001), and rT3 (p trend = 0.008) levels. rT3/T3 ratio did not change, the rT3/T4 ratio tended to decrease (p trend = 0.065) similarly to T3/T4 ratio (p trend = 0.063), and the fT3/fT4 ratio also decreased (p trend = 0.005). It seems that the treatment of thyroid disease in patients with renal failure, treated with haemodialysis, is not associated with change of rT3 and conversion factor levels. Conclusions: The concentration of rT3 in HD patients in relation to healthy persons tends to decrease, and hypothyroidism increases this tendency in these patients. Hormone substitution treatment does not eliminate the influence of RF on inhibition of rT3 production. In patients with ESRD, hypothyroidism additionally reduces the conversion of thyroid hormones examined by fT3/fT4 and to a lesser extent T3/T4 ratios.

Background and Aims Few studies have focused on the imbalance of the autonomic nervous system during hemodialysis (HD), although it seems to be an important factor for the maintenance of blood pressure. The aim of this work was to assess the impact of hemodialysis (HD) and glucose injection upon entropy of heart rate and blood pressure during HD session in end stage renal disease (ESRD) patients with and without diabetes mellitus (DM) type 2. Method 21 patients without DM (NDO), in age 54,95 +/-13,08 y.o., and 10 DM patients, in age 69,70 +/- 8,27 y.o., were studied during HD. 30 minutes after dialysis begins, 40% glucose solution was administered in the amount of 0.5g/kg body dry-weight (constant rate of 1 mL/s). The cardiovascular signals were extracted from the recordings using Portapres® system. The analysis was performed using Amplitude Aware Permutation Entropy (AAPE). The parameters of AAPE were set as d=7, A=0.5. All statistical analysis were performed on significance level α=0.05. The comparisons between groups were conducted with Mann-Whitney test with Holm corrections. The comparisons in time points were performed using Friedman test with post-hoc (Wilcoxon test with Holm corrections). The calculations of AAPE and all statistical analysis were performed with Matlab R2020a and R. Results The results are presented in table. It was found that AAPE(HR) tends to decrease during dialysis (NS) and increases only in the DM group after glucose injection (p=0.019); without difference between groups. There were no differences in AAPE of blood pressure between the groups, but hemodialysis reduces AAPE(fiSYS) in both groups (p Conclusion AAPE(HR)tends to decrease during HD, and glucose injections increase AAPE(HR) in DM patients. Hemodialysis reduce, and glucose injections increase AAPE of blood pressure especially in NDO. A weaker response to hemodialysis and glucose injection in diabetic patients may be caused by impairment of the autonomic system, and may have clinical impact – may leads to faint. Glucose administration does not prevent autonomic system disorders in patients with DM.

IntroductionThe prognostic factors in autotransplanted multiple myeloma (MM) patients with concomitant advanced chronic kidney disease (CKD) are poorly understood, limited, and controversial.Material and methodsWe retrospectively analysed 44 patients with MM and CKD (eGFR < 40 ml/min), present both at diagnosis and at autologous stem cell transplantation (ASCT), with no improvement of renal function in-between.ResultsPatients exhibiting deeper paraprotein responses to pre-transplant treatment predicted better response post ASCT (odds ratio (OR) = 11.6, p = 0.028) and longer progression-free survival (PFS) (hazard ratio (HR) = 0.23, p = 0.017). Higher albumin concentration (per increase of 1 g/dl) (HR = 0.41, p = 0.03) and melphalan 140 mg/m2 versus higher melphalan doses (HR = 0.86, p = 0.008) were associated with longer PFS. Performance status (ECOG 0-1 versus ≥ 2) (HR = 0.28, p = 0.0036), higher albumin concentration (HR = 0.43, p < 0.037), and melphalan 140 mg/m2 versus higher melphalan doses (HR = 0.48, p = 0.081) decreased the risk of death. Three of 32 dialysis-dependent patients became dialysis independent (DID), and 5 of 12 in the DID group had eGFR improvement post ASCT. The median PFS was 2.3 years, which was shorter for DID compared to DD patients (0.7 vs. 3.3 years, respectively). The median overall survival (OS) was 3.6 years, there was no difference in median OS between the groups (4.0 vs. 3.5 years, respectively).ConclusionsOptimal patient selection including good performance status and higher albumin concentration (with every increase of 1 g/dl), chemotherapy-responsive disease pre-ASCT, melphalan dose adjusted to CKD, and intensive post-transplant supportive care are crucial to achieve acceptable results of treatment of MM patients with CKD.

AIMS The disposal of a glucose bolus was studied to identify glucose metabolism in patients with and without type 2 diabetes mellitus (T2DM) during their regular hemodialysis (HD) treatment. METHODS Plasma glucose, insulin, and c-peptide concentrations were measured during a 60 min observation phase following a rapid glucose infusion (0.5 g/kg dry weight). Glucose disposition and elimination rates were determined from kinetic analysis, and insulinogenic index was calculated. Insulin resistance (RHOMA) was determined by homeostatic model assessment (HOMA). RESULTS 35 HD patients (14 with T2DM) distinguished by a higher age (median: 70 vs. 55 y, p

This study was designed to investigate the biocompatibility of hemodialysis procedures, largely depending on the contact of patient's blood with the dialysis membranes. We addressed the issue by comparing the content of the proteolytic enzymes collagenase and cathepsin B and that of neutrophil myeloperoxidase (MPO) and C-reactive protein (CRP) in the blood before and after a single session treatment and a full course of successive 8-week-long therapies with three types of hemodialysis: low-flux (lfHD), high-flux (hfHD), and post-dilution hemodiafiltration (HDF). The study included 19 patients with chronic nephropathy. We found that collagenase significantly increased after a single session of each type of hemodialysis. Cathepsin B tended to decrease after single sessions; the decrease reached significance only after hfHD. CRP increased significantly after single hfHD and HDF treatments. These changes were meager, with no differences depending on the dialysis type, and their significance was lost after 8-week-long therapy, except the persisting increase in CRP after HDF. Neutrophil MPO apparently was not activated during any type of dialysis, as its content was below the detection threshold. We conclude that all three types of hemodialysis are compatible with the biological system, so that they would rather unlikely lead to clinically harmful effects in chronically hemodialyzed patients. Nonetheless, proteolytic enzymes and myeloperoxidase seem hardly appropriable estimators of hemodialysis biocompatibility due to meager and variable changes. Upregulation of C-reactive protein, on the other hand, expresses a general pro-inflammatory propensity of hemodialysis and is not a suitable estimator of biocompatibility either.

Genetic factors play a key role in the pathogenesis of atrial fibrillation (AF). We would like to establish an association between previously described single-nucleotide polymorphisms (SNPs) and AF in haemodialysed patients with end-stage kidney disease (ESKD-HD) as well as to assess the cumulative effect of all genotyped SNPs on AF risk. Sixteen SNPs were genotyped in 113 patients with AF-ESKD-HD and in 157 controls: without AF (NAF) and with ESKD-HD. The distribution of the risk alleles was compared in both groups and between different sub-phenotypes. The multilocus genetic risk score (GRS) was calculated to estimate the cumulative risk conferred by all SNPs. Several loci showed a trend toward an association with permanent AF (perm-AF): CAV1, Cx40 and PITX2. However, GRS was significantly higher in the AF and perm-AF groups, as compared to NAF. Three of the tested variables were independently associated with AF: male sex, history of myocardial infarction (MI) and GRS. The GRS, which combined 13 previously described SNPs, showed a significant and independent association with AF in a Polish population of patients with ESKD-HD and concomitant AF. Further studies on larger groups of patients are needed to confirm the associations.

This study was designed to investigate the biocompatibility of hemodialysis procedures, largely depending on the contact of patient's blood with the dialysis membranes. We addressed the issue by comparing the content of the proteolytic enzymes collagenase and cathepsin B and that of neutrophil myeloperoxidase (MPO) and C-reactive protein (CRP) in the blood before and after a single session treatment and a full course of successive 8-week-long therapies with three types of hemodialysis: low-flux (lfHD), high-flux (hfHD), and post-dilution hemodiafiltration (HDF). The study included 19 patients with chronic nephropathy. We found that collagenase significantly increased after a single session of each type of hemodialysis. Cathepsin B tended to decrease after single sessions; the decrease reached significance only after hfHD. CRP increased significantly after single hfHD and HDF treatments. These changes were meager, with no differences depending on the dialysis type, and their significance was lost after 8-week-long therapy, except the persisting increase in CRP after HDF. Neutrophil MPO apparently was not activated during any type of dialysis, as its content was below the detection threshold. We conclude that all three types of hemodialysis are compatible with the biological system, so that they would rather unlikely lead to clinically harmful effects in chronically hemodialyzed patients. Nonetheless, proteolytic enzymes and myeloperoxidase seem hardly appropriable estimators of hemodialysis biocompatibility due to meager and variable changes. Upregulation of C-reactive protein, on the other hand, expresses a general pro-inflammatory propensity of hemodialysis and is not a suitable estimator of biocompatibility either.

Indoxyl sulfate (IS) and p-cresol sulfate (p-CS) are protein-bound solutes that accumulate in the blood serum in chronic kidney disease and have a detrimental effect on the kidney and other organs’ function. This study seeks to define the effectiveness of IS and p-CS clearance after single dialysis sessions and after 8-week-long cycles of hemodialysis using the following different dialysis modalities in succession: low-flux hemodialysis (lfHD), high-flux hemodialysis (hfHD), and post-dilution hemodiafiltration (HDF). We also investigated to what extent IS and p-CS serum content would associate with some other biochemical indices in patients with chronic kidney diseases. The study included 21 uremic patients. We found that a single session of each modality effectively decreased the content of both IS and p-CS, with the predominance of p-CS decrease. There were no appreciable differences depending on the modality of hemodialysis chosen. However, the leaching effect tended to wear off with the weeks’ long dialysis cycles. We further found that a greater inflammation-prone level of hsCRP evoked by dialysis led to a greater removal of solutes, and thus their decrease in the serum, during a single dialysis session. Reversely, a greater protein level might result in a greater solute binding and a decrease in removal. We conclude that there are no major differences in the serum clearance of IS and p-CS depending on the dialysis modality. These protein-bound toxins are significantly cleared from the serum already during the first dialysis session, but their level tends to revert during weeks’ long dialysis sessions.

Renal perfusion, which depends on cardiac function, is a factor conditioning the work of kidneys. The objective of the study was to assess the influence of cardiac function, including left ventricular contractility and relaxation, on renal cortical perfusion in patients with hypertension and chronic kidney disease treated pharmacologically. There were 63 patients (7 F and 56 M; aged 56 ± 14) with hypertension and stable chronic kidney disease enrolled into the study. Serum cystatin C, with estimated glomerular filtration rate (eGFR), ambulatory blood pressure monitoring, carotid intima-media thickness (cIMT), echocardiography with speckle tracking imaging and the calculation of global longitudinal strain (GLS), diameter of vena cava inferior (VCI), and an ultrasound dynamic tissue perfusion measurement of the renal cortex were performed. We found that the renal cortical perfusion correlated significantly with age, renal function, cIMT, GLS, left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI), diastolic peak values of early (E) and late (A) mitral inflow velocities ratio (E/A) and E to early diastolic mitral annular tissue velocity (E/E'), but not with VCI, or the right ventricle echocardiographic parameters. In multivariable regression analysis adjusted to age, only eGFR, E/E', and GLS were independently related to renal cortical perfusion (r

Plasma content of copeptin increases with the advancement of chronic kidney disease (CKD). The purpose of this study was to evaluate copeptin content as a potential marker of CKD, as a single pathology or with coexisting heart failure. Seventy-six patients were divided into the following groups: Group 1 (control), without CKD and heart failure; Group 2, CKD stage 3a; Group 3, CKD stage 3b; Group 4, CKD stage 4; Group 5, CKD stage 5; and Group 6, CKD stage 3b and heart failure. For all patients, plasma concentrations of copeptin, creatinine, urea, cystatin C, sodium, C-reactive protein (CRP), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), and blood pH were assessed. We found that plasma content of creatinine, urea, CRP, cystatin, NT-proBNP, and copeptin increased with CKD progression. Heart failure in CKD patients was not the cause of an appreciable increase of copeptin level. Copeptin/creatinine, copeptin/cystatin C ratios, and especially copeptin/eGFR ratio enhanced copeptin prognostic sensitivity concerning renal failure in CKD, compared with copeptin alone. The copeptin×NT-proBNP ratio decreased along CKD progression, reaching a nadir in the accompanying heart failure. In contradistinction, copeptin×NT-proBNP/creatinine ratio increased along CKD progression, reaching a peak in the accompanying heart failure. We conclude that copeptin is an important marker in CKD, but not so concerning heart failure in the disease. A decrease in copeptin×NT-proBNP and an increase in copeptin×NT-proBNP/creatinine ratio are useful markers of cardiac function decline in CKD.

In the article, the authors discuss proliferation signal inhibitors (PSI), a group of medicines used in immunosuppressive therapy after renal transplantation. They present the mechanism of action of this class, side effects and drug interactions important in clinical practice. In addition, they present the available drugs and their practical application.

Kidney dysfunction is a common complication of hematopoietic cell transplantation (HCT) with proven negative impact on early and long-term mortality. Causes of this complication are diverse, usually overlapping, and poorly understood. Therefore, management implicates multidirectional investigations and simultaneous treatment of suspected causes. The etiology is frequently unconfirmed due to a lack of specific markers and prevalence of contraindications to renal biopsy among HCT recipients. Herein, we provide a summary of etiology and propose an algorithm for evaluation of kidney injury after HCT. We also map out the most urgent areas for research that aim to identify patients at risk of severe renal injury and develop nephroprotective strategies. Keywords: Acute kidney injury, Chronic kidney disease, Hematopoietic cell transplantation

It is believed that the vasopressinergic system plays an important role in the pathogenesis of chronic kidney disease (CKD). The aim of this study was to evaluate the effect of CKD on changes in vasopressin system expression in the kidney cortex in rats with nephrectomy. The study was performed on 4 groups of Sprague Dawley (SPRD) rats: a control group (CN), 1/2 nephrectomy (N1/2), 2/3 nephrectomy (N2/3), and 5/6 nephrectomy (N5/6). Blood and the kidney cortex were collected to evaluate plasma copeptin concentrations and mRNA expressions of V1a vasopressin receptors (V1aR) and V2 vasopressin receptors (V2R) and V1aR, V2R, and aquaporin 2 (AQP2) protein levels. V1aR and V2R mRNA expression in the kidney cortex was significantly lower in the CN group compared with the other groups. In contrast, the V1aR, V2R, and AQP2 protein levels were significantly higher in the CN group compared with all of the nephrectomized groups. Plasma copeptin concentration was significantly lower in the CN group than in the nephrectomized groups. CKD caused significant changes in the expression of the vasopressinergic system. Further research is needed to explain the mechanisms of the impact of the vasopressinergic system on the kidney in CKD.

Renal perfusion, which depends on cardiac function, is a factor conditioning the work of kidneys. The objective of the study was to assess the influence of cardiac function, including left ventricular contractility and relaxation, on renal cortical perfusion in patients with hypertension and chronic kidney disease treated pharmacologically. There were 63 patients (7 F and 56 M; aged 56 ± 14) with hypertension and stable chronic kidney disease enrolled into the study. Serum cystatin C, with estimated glomerular filtration rate (eGFR), ambulatory blood pressure monitoring, carotid intima-media thickness (cIMT), echocardiography with speckle tracking imaging and the calculation of global longitudinal strain (GLS), diameter of vena cava inferior (VCI), and an ultrasound dynamic tissue perfusion measurement of the renal cortex were performed. We found that the renal cortical perfusion correlated significantly with age, renal function, cIMT, GLS, left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI), diastolic peak values of early (E) and late (A) mitral inflow velocities ratio (E/A) and E to early diastolic mitral annular tissue velocity (E/E′), but not with VCI, or the right ventricle echocardiographic parameters. In multivariable regression analysis adjusted to age, only eGFR, E/E′, and GLS were independently related to renal cortical perfusion (r2 = 0.44; p < 0.001). In conclusion, the intensity of left ventricular strain and relaxation independently influence renal cortical perfusion in hypertensive patients with chronic kidney disease. A reduction in left ventricular global longitudinal strain is superior to left ventricular ejection fraction in the prediction of a decline in renal cortical perfusion.

Plasma content of copeptin increases with the advancement of chronic kidney disease (CKD). The purpose of this study was to evaluate copeptin content as a potential marker of CKD, as a single pathology or with coexisting heart failure. Seventy-six patients were divided into the following groups: Group 1 (control), without CKD and heart failure; Group 2, CKD stage 3a; Group 3, CKD stage 3b; Group 4, CKD stage 4; Group 5, CKD stage 5; and Group 6, CKD stage 3b and heart failure. For all patients, plasma concentrations of copeptin, creatinine, urea, cystatin C, sodium, C-reactive protein (CRP), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), and blood pH were assessed. We found that plasma content of creatinine, urea, CRP, cystatin, NT-proBNP, and copeptin increased with CKD progression. Heart failure in CKD patients was not the cause of an appreciable increase of copeptin level. Copeptin/creatinine, copeptin/cystatin C ratios, and especially copeptin/eGFR ratio enhanced copeptin prognostic sensitivity concerning renal failure in CKD, compared with copeptin alone. The copeptin×NT-proBNP ratio decreased along CKD progression, reaching a nadir in the accompanying heart failure. In contradistinction, copeptin×NT-proBNP/creatinine ratio increased along CKD progression, reaching a peak in the accompanying heart failure. We conclude that copeptin is an important marker in CKD, but not so concerning heart failure in the disease. A decrease in copeptin×NT-proBNP and an increase in copeptin×NT-proBNP/creatinine ratio are useful markers of cardiac function decline in CKD.

Background Lowered testosterone level in CRF patients is associated with elevated risk of death due to cardiovascular reasons, and is influenced by many factors, including acid-base balance disorders. Aims: evaluation of testosterone concentration (TT) and free testosterone concentration (fT) in pre-dialysis and dialysis patients; assessment of TT and fT relationships with biochemical parameters; evaluation of prognostic importance of TT and fT in predicting patient survival. Material/Methods 4 groups of men: 14 – on hemodialysis (HD), 13 – on peritoneal dialysis (PD), 9 – with chronic renal failure (CRF) and 8 – healthy (CG), aged 56±17, 53±15, 68±12, 43±10 years, respectively. TT and biochemical parameters were measured; fT was calculated. Results The lowest TT and fT were observed in HD and CRF, the highest – in CG (p=0.035 for TT; p=0.007 for fT). fT in CRF and CG were different (p=0.031). TT and age was associated in HD (p=0.026). Age and fT was strongly associated in PD (p

Hypothyroidism in patients with renal failure (RF) causes many metabolic and clinical problems, and both these diseases can mutually exacerbate their disturbances.The aim of this study was to evaluate the effect of hypothyroidism, and end-stage renal disease (ESRD) on conversion of thyroid hormones (TH) in patients with ESRD treated with chronic hemodialysis (HD).The study was performed in 74 patients, including 41 women (K) and 33 men (M) aged 28-83 y.o. in 4 groups: G1 - 12 people with ESRD treated with HD and with newly diagnosed hypothyroidism without substitution (6 K and M 6) aged 66,83±12,90 y.o., G2 - 26 patients with ESRD treated with HD without hypothyroidism (10 F, 16 M) aged 58,85±15,52 y.o., G3 - 11 hypothyroid patients without RF (9 K, 2 M) aged 54,73±21,26 y.o., G4 - 25-persons from control group of healthy subjects (16 M, 9 M) aged 51,24±12,58 y.o. In all subjects the concentration of TSH and TH (T4, T3, fT4, TSH, FT3, rT3) were measured and values of conversion factors (T3/T4, FT3/ fT4, rT3/fT4 and rT3/fT3) and binding TH to protein factors (fT4/T4 and fT3/T3) were calculated.Lower concentration of T3 (p=0.012), fT3 (p0.001) i fT4 (p=0.014) was found in patients without hypothyroidism than in healthy subjects. Renal failure with concomitant hypothyroidism intensify the disturbances of T4 to T3 conversion (p=0.034) and hypothyroidism with concomitant renal failure disrupts binding of T3 to proteins (p=0.001). FT3 to fT4 ratio in renal failure with concomitant hypothyroidism group was significantly lower than in each other group. rT3 concentrations were the highest in healthy subjects.Concomitance of hypothyroidism and end-stage renal disease reduces the conversion of thyroxine to triiodothyronine, but does not increase the production of rT3. Hypothyroidism significantly increases the disorders of thyroid hormones in end-stage renal disease. There is decreased tendency to bind of thyroid hormone to protein in hypothyroidism in patients with end-stage renal disease.

Acute tubule-interstitial nephritis is a heterogeneous group of inflammatory diseases which affect renal parenchyma and tubules, mostly as a result of the immune-mediated injury. They are the important cause of acute kidney injury accounting for 5-15% of all its causes. In subsequent years, with the development of pharmacotherapy, the incidence of drug-induced nephrotoxicity has been increasing. The other causes of the acute tubule-interstitial nephritis are autoimmune and inflammatory diseases, infections, neoplasms and electrolyte abnormalities. The diagnostics are complex and treatment of the disease is not always easy. The following overview provides a summary of causes of acute tubule-interstitial nephritis, clinical picture of the disease, the diagnosis and treatment.

Anemia is one of the most common problems of patients with advanced chronic kidney disease (CKD). Its main causes in this population are: iron deficiency and a decreased renal synthesis of erythropoietin. Up to the 80's of the twentieth century, treatment of anemia in CKD was limited to blood and red blood cells transfusions. However during last three decades there has been a huge progress in the field, starting with introduction into clinical practice of human recombinant erythropoietin (rHuEPO), followed by an appearance of agents with a longer duration of action, darbepoetin alfa and methoxy polyethylene glycol-epoetin beta, all of which are shortly reviewed in this paper.

Recent epidemiological studies show significant prevalence of chronic kidney disease (CKD) in the general population. Diuretics are critical in therapy ofvolume overload and hypertension commonly encountered in these patients. However, they frequently demonstrate relevant diuretic resistance, and from the other hand diuretic overdose may lead to dehydratation and worsening of kidney function. In this paper the main principles of diuretic treatment in CKD are described, including the diuretic agent and its dose selection, as well as adverse effects of the therapy.

Thyroid hormone disorders in patients with chronic kidney disease (CKD) are a result of impaired conversion of T4 to T3. The importance of kidneys in thyroid hormones conversion is not fully understood. The activities of different types of iodothyronine deiodinases in the kidney structures have not been determined yet. The aim of this study was to determine the activity of deiodinase type 1 (D1) and type 2 (D2) in renal cortex and medulla in renal cancer patients.Samples of renal cortex and medulla (ten patients) or renal cortex alone (13 patients) were taken from kidneys resected because of malignant cancer, from a site opposite to the cancer. Resections were performed in the 23 patients (seven female and 16 male) who were 52-82 years old. The material was stored at -72 oC.Activity of D1 in renal cortex was 3.785 ± 2.041 fmol 125I/mg protein/minute and activity of D2 was 0.236 ± 0.125 fmol 125I/mg protein/minute. There was a strong positive correlation between D1 and D2 activities in renal cortex (r = 0.890, p 〈 0.001). Activity of D1 in renal medulla was 2.157 ± 2.176 fmol 125I/mg protein/minute, and activity of D2 was 0.168 ± 0.095 fmol 125I/mg protein/minute. A positive correlation between D1 and D2 in renal medulla (r = 0.661, p = 0.038) was observed as well. Activities of D1 in cortex and medulla were strongly and positively associated (r = 0.794, p = 0.006), whereas there was no correlation between the activities of D2 in cortex and medulla (r = 0.224, p = 0.553).Results presented in this study suggest that both cortical and medullary D1 and D2 may be involved in thyroid hormone metabolism. This finding could be of clinical relevance in patients with impaired renal function.

The authors discussed disorders in adipocytokines' function in chronic renal failure (CRF) and their clinical implications. Adipocytokines' concentrations in CRF are in most cases elevated, which is associated with decreased level of their excretion. This may cause number of clinical implications such as inflammation, loss of appetite, development of protein energy wasting (PEW) syndrome and the progress of artherosclerosis, what leads to increased mortality in a group of patients with end-stage renal disease (ESRD). Disturbances in sexual hormones function are also characteristic for CRF. Disorders in fertility, sexual life and decreased quality of life are observed in patients with CRF. Therapeutic procedure is complicated and not fully effective.

Melkersson-Rosenthal syndrome (MRS) is a disease of unknown etiology, usually restricted to the orofacial region, characterized by reccurent orofacial swelling, relapsing facial palsy and plicated tongue. We report case of MRS associated with psoriasis in a 25-year-old woman. The patient has been treated with satisfying results with a combination of Cetirizine, Cefuroxime axetil and Mupirocin ointment; psoriatic eruptions were successfully treated with 10 % salicylic-sulphuric ointment twice a day. MRS syndrome is a rare disease and should be considered in the differential diagnosis of labial swelling and facial palsy.

Evaluation of metoclopramide (MTC) test values in end-stage renal disease patients undergoing hemodialysis with different level of hyperprolactinemia was aim of the study. Clinical value of application of the MTC test and influence of different laboratory and clinical factors including erytropoietin treatment were examined. Sixty-eight hemodialysed patients (31 male and 37 female) aged 20-74 yr. (medium 48 +/- 13 yr.) underwent the MTC test, the control group consisted of 8 healthy volunteers (4 male and 4 female). 10mg of MTC was given i.v. and serum level of PRL was determined in 0, 30 and 60 min. after injection. Significant suppression of PRL stimulation in the patients was shown as compared with the controls after 30 min and delayed decrease of the curve values was found. An increase in the PRL level after 60 min in investigated group was lower than in control. Lower relative enhance of PRL level in 30 min was found and slower decrease after 60 min. Despite the slower decrease PRL level was lower in the patients than in the controls after 60 min. The highest relative increase in PRL level after 30 min was observed in the patients with lowest initial level of PRL (r=-0.471; p0.001). Erytropoietin administration improved the response in the test (p=0.005) without relationship to the duration of erytropoietin treatment. There was influence of hemoglobin level on the results of the test.Results of the MTC test in end-stage renal disease patients is inadequate and the PRL response is diminished. Diagnostic value of the test in end-stage renal disease patients is low. Erytropoietin administration improves although not to the normal values the results of the MTC test.

Determination of circadian of prolactine (PRL) profile and its relationship to selected clinical and laboratory indices in end-stage renal disease (ESRD) patients undergoing hemodialysis, peritoneal dialysis as well as those in predialysis period was the aim of the study. Investigations were carried out in 38 patients with ESRD aged 36 to 79 yr. (medium 59 +/- 11 yr.), (20 male, 18 female, 7 treated with peritoneal dialysis, 25 undergoing hemodialysis, 6 in predialysis period) and the control group consisting of 7 healthy volunteers (4 male and 3 female). Serum concentration of PRL was evaluated at 3:00, 7:00, 12:00, 18:00, 22:00. The influence of different dialysis methods, blood concentration of parathormone, hemoglobin, total protein, erytropoietin (EPO), C-reactive protein, EPO therapy and duration of dialysis therapy on the PRL profile was analyzed. Results were analyzed according to medium obtained values of daily PRL profiles and individual indexes of variation of the daily concentration. Impaired circadian PRL profile was found in the all of followed groups comparing to the control, which was based on flatting of the curve and decreasing of the nightly pick of secretion PRL. None of analyzed factors had normalized the PRL profile curve.The PRL profile in ESRD patients treated with hemodialysis, peritoneal dialysis and in predialysis period is changed. The PRL profile curve is flatted and there was no night pick of PRL secretion in the patients. PRL level was shown to increase with progress of the disease, and the highest levels were in hemodialysed patients. EPO treatment, general appearance improvement, increased hemoglobin level and any of studied different dialysis method did not normalize the altered PRL profile.

We analysed medical documentation of 65 patients with alcoholic cirrhosis admitted to the Internal Diseases Department with Dialysis Ward in the hospital in Wolomin between 2002 and 2004 year. Patients were divided into 3 groups according to renal disfunction: patients with HRS-1, patients with HRS-2 and patients with cirrhosis without renal failure. Each diagnosis was established basing on criteria of International Ascites Club. Different factors, which may influence a development of HRS, such as large--volume paracentesis without plasma expansion, bacterial infections, gastrointestinal bleeding and nephrotoxic drugs were analysed. Patients were treated with terlipressin and intravenous albumin infusions, antibiotics, diuretics, dopamine, haemodialysis and paracentesis. 10 patients (3 with HRS-1.5 with HRS-2 and 2 without renal failure) died, which is 15.4% of the all group. The mortality in the group of patients with HRS is high but complex treatment may be effective. Nowadays liver transplantation is the most effective method.

Due to a high frequency of autoimmune diseases in patients with ESRF we observed for 4 years 8 patients treated with HD with high level of TPOAb and 8 patients without TPOAb. Aim of the study was to estimate the role of TPOAb as a prognostic factor of hypothyreosis. We observed in a 4-years follow-up significant increase of TSH (p0.05) in patients with high TPOAb level. fT3 and fT4 did't change in this time. In the group without TPOAb we observed significant (p0.01) decrease of fT3 probably due to the disturbances in T4 to T3 conversion. Our results don't permit us to draw a final conclusions but induce us to further observation of hypothyreosis development in patients with ESRF.

Indoxyl sulfate (IS) and p-cresol sulfate (p-CS) are protein-bound solutes that accumulate in the blood serum in chronic kidney disease and have a detrimental effect on the kidney and other organs' function. This study seeks to define the effectiveness of IS and p-CS clearance after single dialysis sessions and after 8-week-long cycles of hemodialysis using the following different dialysis modalities in succession: low-flux hemodialysis (lfHD), high-flux hemodialysis (hfHD), and post-dilution hemodiafiltration (HDF). We also investigated to what extent IS and p-CS serum content would associate with some other biochemical indices in patients with chronic kidney diseases. The study included 21 uremic patients. We found that a single session of each modality effectively decreased the content of both IS and p-CS, with the predominance of p-CS decrease. There were no appreciable differences depending on the modality of hemodialysis chosen. However, the leaching effect tended to wear off with the weeks' long dialysis cycles. We further found that a greater inflammation-prone level of hsCRP evoked by dialysis led to a greater removal of solutes, and thus their decrease in the serum, during a single dialysis session. Reversely, a greater protein level might result in a greater solute binding and a decrease in removal. We conclude that there are no major differences in the serum clearance of IS and p-CS depending on the dialysis modality. These protein-bound toxins are significantly cleared from the serum already during the first dialysis session, but their level tends to revert during weeks' long dialysis sessions.