Interleukin-6 and epidermal growth factor as noninvasive biomarkers of progression in chronic glomerulonephritis.

Several cytokines and chemokines are involved in the pathogenesis and progressive injury of renal tissues in patients with primary chronic glomerulonephritis (CGN). The objective of this study was to determine whether the urinary excretion of interleukin-6 (IL-6), transforming growth factor ß1 (TGFß1), monocytes chemoattractant protein (MCP-1), soluble tumor necrosis factor receptor 1 (sTNFR1), and epidermal growth factor (EGF) in patients with newly recognized CGN can serve as prognostic biomarkers in patients with newly recognized CGN and whether they can be effective in predicting a progressive reduction of renal function in prospective observation. The study included 150 Caucasian patients. UIL-6, UTGFß1, UMCP-1, UsTNFR1, and UEGF were measured using enzyme-linked immunosorbent assay (ELISA) methods (Quantikine R&D System). UIL-6, UTGFß1, UMCP-1, and UsTNFR1 were significantly higher, yet UEGF excretion was significantly lower in nephrotic patients, in patients with estimated glomerular filtration rate (eGFR) < 60/min/1.73 m2 at presentation, as well as in the progressor (PG) subgroup. In a multivariate regression analysis basal eGFR correlated with UsTNFR1, UIL-6, and UEGF excretion, although in the follow-up, ΔeGFR (delta estimated glomerular filtration rate) significantly correlated only with UEGF excretion. A logistic regression analysis showed that the most significant independent risk factors for the deterioration of renal function with time are initial high (>11.8 pg/mgCr) UIL-6 excretion, initial low (<15.5 ng/mgCr) urinary UEGF excretion, and male gender. In patients with newly diagnosed CGN, UIL-6, and UEGF can serve as prognostic biomarkers for the progression of the disease.NEW & NOTEWORTHY Baseline high urinary interleukin-6 (IL-6) excretion and low urinary epidermal growth factor (EGF) excretion and particularly high IL-6/EGF ratio were stronger predictive factors of the progression of the deterioration of the kidney function than initial estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 or proteinuria. In patients with newly diagnosed chronic glomerulonephritis, UIL-6 and UEGF can serve as prognostic biomarkers for the progression of the disease.

Can Low SHBG Serum Concentration Be A Good Early Marker Of Male Hypogonadism In Metabolic Syndrome?

INTRODUCTION: In men suffering from metabolic syndrome, accompanying insulin resistance may result in a lowering of sex hormone-binding globulin (SHBG) plasma levels and cause changes in their androgenic status. AIM: The objective of the research was to assess selected androgens and SHBG plasma levels in males meeting diagnostic criteria for MS compared to healthy males. PATIENTS AND METHODS: The group consisted of 65 men aged between 40 and 70 years old fitting IDF metabolic syndrome criteria and 84 controls. Dehydroepiandrosterone (DHEA) and its sulphate (DHEA-S), total and free testosterone and SHBG serum levels were evaluated. Calculated free and bioavailable testosterone were estimated using an algorithm proposed by the International Society for the Study of the Aging Male. RESULTS: Men diagnosed with MS showed a statistically significant decrease in plasma levels of DHEA in comparison to healthy ones: 11.579 (8.39-15.56) vs 14.014 (9.611-17.125) ng/mL; p = 0.0350, SHBG: 47.46 (35.78-62.83) vs 71.965 (54.45-91.56) nM/L; p<0.0001 and total testosterone: 5.2 (3.8-6.5) vs 6.3 (5.4-8.25) ng/mL; p = 0.0001 (values presented as a median with Q1-Q3). CONCLUSION: The results suggest that SHBG is a good early marker for metabolic dysregulation in MS, considering its strength of association and significance is comparable to, or better than, those of MS criteria.

Advanced Oxidation Protein Products and Carbonylated Proteins as Biomarkers of Oxidative Stress in Selected Atherosclerosis-Mediated Diseases.

OBJECTIVES: The main question of this study was to evaluate the intensity of oxidative protein modification shown as advanced oxidation protein products (AOPP) and carbonylated proteins, expressed as protein carbonyl content (C=O) in abdominal aortic aneurysms (AAA), aortoiliac occlusive disease (AIOD), and chronic kidney disease (CKD). DESIGN AND METHODS: The study was carried out in a group of 35 AAA patients and 13 AIOD patients. However, CKD patients were divided into two groups: predialysis (PRE) included 50 patients or hemodialysis (HD) consisted of 34 patients. AOPP and C=O were measured using colorimetric assay kit, while C-reactive protein concentration was measured by high-sensitivity assay (hsCRP). RESULTS: The concentration of AOPP in both AAA and AIOD groups was higher than in PRE and HD groups according to descending order: AAA~AIOD > HD > PRE. The content of C=O was higher in the PRE group in comparison to AIOD and AAA according to the descending order: PRE~HD > AAA~AIOD. CONCLUSIONS: AAA, AIOD, and CKD-related atherosclerosis (PRE and HD) contribute to the changes in the formation of AOPP and C=O. They may promote modification of proteins in a different way, probably due to the various factors that influence oxidative stress here.

iTRAQ-based proteomic analysis of plasma reveals abnormalities in lipid metabolism proteins in chronic kidney disease-related atherosclerosis.

Patients with chronic kidney disease (CKD) have a considerably higher risk of death due to cardiovascular causes. Using an iTRAQ MS/MS approach, we investigated the alterations in plasma protein accumulation in patients with CKD and classical cardiovascular disease (CVD) without CKD. The proteomic analysis led to the identification of 130 differentially expressed proteins among CVD and CKD patients and healthy volunteers. Bioinformatics analysis revealed that 29 differentially expressed proteins were involved in lipid metabolism and atherosclerosis, 20 of which were apolipoproteins and constituents of high-density lipoprotein (HDL) and low-density lipoprotein (LDL). Although dyslipidemia is common in CKD patients, we found that significant changes in apolipoproteins were not strictly associated with changes in plasma lipid levels. A lack of correlation between apoB and LDL concentration and an inverse relationship of some proteins with the HDL level were revealed. An increased level of apolipoprotein AIV, adiponectin, or apolipoprotein C, despite their anti-atherogenic properties, was not associated with a decrease in cardiovascular event risk in CKD patients. The presence of the distinctive pattern of apolipoproteins demonstrated in this study may suggest that lipid abnormalities in CKD are characterized by more qualitative abnormalities and may be related to HDL function rather than HDL deficiency.

Label-Free Quantitative Proteomics Reveals Differences in Molecular Mechanism of Atherosclerosis Related and Non-Related to Chronic Kidney Disease.

The major cause of mortality in patients with chronic kidney disease (CKD) is atherosclerosis related to traditional and non-traditional risk factors. However, the understanding of the molecular specificity that distinguishes the risk factors for classical cardiovascular disease (CVD) and CKD-related atherosclerosis (CKD-A) is far from complete. In this study we investigated the disease-related differences in the proteomes of patients with atherosclerosis related and non-related to CKD. Plasma collected from patients in various stages of CKD, CVD patients without symptoms of kidney dysfunction, and healthy volunteers (HVs), were analyzed by a coupled label-free and mass spectrometry approach. Dysregulated proteins were confirmed by an enzyme-linked immunosorbent assay (ELISA). All proteomic data were correlated with kidney disease development and were subjected to bioinformatics analysis. One hundred sixty-two differentially expressed proteins were identified. By directly comparing the plasma proteomes from HVs, CKD, and CVD patients in one study, we demonstrated that proteins involved in inflammation, blood coagulation, oxidative stress, vascular damage, and calcification process exhibited greater alterations in patients with atherosclerosis related with CKD. These data indicate that the above nontraditional risk factors are strongly specific for CKD-A and appear to be less essential for the development of "classical" CVD.

Usefulness of serum interleukin-18 in predicting cardiovascular mortality in patients with chronic kidney disease--systems and clinical approach.

The aim of this study was to check if serum interleukin-18 (IL-18) predicts 2-year cardiovascular mortality in patients at various stages of chronic kidney disease (CKD) and history of acute myocardial infarction (AMI) within the previous year. Diabetes mellitus was one of the key factors of exclusion. It was found that an increase in serum concentration of IL-18 above the cut-off point (1584.5 pg/mL) was characterized by 20.63-fold higher risk of cardiovascular deaths among studied patients. IL-18 serum concentration was found to be superior to the well-known cardiovascular risk parameters, like high sensitivity C-reactive protein (hsCRP), carotid intima media thickness (CIMT), glomerular filtration rate, albumins, ferritin, N-terminal prohormone of brain natriuretic peptide (NT-proBNP) in prognosis of cardiovascular mortality. The best predictive for IL-18 were 4 variables, such as CIMT, NT-proBNP, albumins and hsCRP, as they predicted its concentration at 89.5%. Concluding, IL-18 seems to be important indicator and predictor of cardiovascular death in two-year follow-up among non-diabetic patients suffering from CKD, with history of AMI in the previous year. The importance of IL-18 in the process of atherosclerotic plaque formation has been confirmed by systems analysis based on a formal model expressed in the language of Petri nets theory.

Deeper insight into chronic kidney disease-related atherosclerosis: comparative proteomic studies of blood plasma using 2DE and mass spectrometry.

BACKGROUND: Atherosclerosis is a major cause of cardiac events and mortality in patients suffering from chronic kidney disease (CKD). Moreover, the risk of cardiovascular disease (CVD) development in patients with CKD increases as kidney function declines. Although the close connection between atherosclerosis and kidney dysfunction is undeniable, particular risk factors and specific mechanisms that promote CVD in patients with CKD remain unclear. To gain insight into better recognition of the mechanisms of accelerated atherosclerosis in patients with CKD, we performed a comparative proteomic analysis of blood plasma from patients in various stages of CKD and thus distinct progression of atherosclerosis (n = 90), patients with advanced CVD and normal renal function (n = 30) and healthy volunteers (n = 30). METHODS: Plasma samples were depleted using affinity chromatography and divided into three fractions: high-abundant, low-abundant and low-molecular weight proteins. The first two fractions were analyzed by two-dimensional gel electrophoresis and mass spectrometry, the last one has been subjected to direct MS/MS analysis. A proteomic profiles for high-abundant, low-abundant and low-molecular weight proteins fractions were obtained. Differential accumulated proteins were confirmed by selected reaction monitoring analysis (SRM). The Gene Ontology (GO) function and the interaction networks of differentially expressed proteins were then analyzed. RESULTS: Forty-nine proteins (13 high- and 36 low-molecular mass) showed differences in accumulation levels. For eleven of them differential expression were confirmed by selected reaction monitoring analysis. Bioinformatic analysis showed that identified differential proteins were related to three different processes: the blood coagulation cascade, the transport, binding and metabolism of lipoproteins and inflammatory processes. CONCLUSIONS: Obtained data provide an additional line of evidence that different molecular mechanisms are involved in the development of CKD- and CVD-related atherosclerosis. The abundance of some anti-atherogenic factors revealed in patients with CKD suggests that these factors are not associated with the reduction of atherosclerosis progression in CKD that is typically observed in "classical" CVD. Moreover, obtained data also suggest that mechanism of CVD acceleration may be different in initial and advanced stages of CKD. Undoubtedly, in advanced stages of CKD inflammation is highly pronounced.

[Evaluation of relationships between plasma androgens level and clinical signs of hipoandrogenism according to age and comorbidity of metabolic syndrome in men]. / Ocena powiazan miedzy androgenemia oraz klinicznymi objawami andropenii u mezczyzn w zaleznosci od wieku i wspólwystepowania zespolu metabolicznego.

UNLABELLED: The prevalence of late-onset hipogonadism (LOH) in men is not accurately determined and may be overestimated. Androgen deficiency is causally linked to insulin resistance, regardless of age. Clinical signs of androgen deficiency are not uniquely specific for LOH. The aim of this study was to assess the correlations between androgen serum levels and clinical symptoms of andropenia depending on the age. We evaluated the relationships between the frequency of LOH and metabolic syndrome (MS) and compared different methods of androgen assessment in the context of their clinical relevance. MATERIAL AND METHODS: In 153 randomly selected men aged 40 to 70 years adrenal (DHEA and DHEAS) and gonadal (total-TT and free testosterone-FT) androgens were evaluated and compared with free (c-FT) and bioavailable testosterone (c-BAT) calculated with a mathematical algorithm. European Male Aging Study criteria for the diagnosis of LOH were used. RESULTS: TT concentration (r = -0.074, p = 0.363) and FT (r = -0.054, p = 0.505) did not correlate with age, in contrast to the c-FT (r = -0.280, p = 0.0005 ), c-BAT (r = -0.297, p = 0.0002) and both adrenal androgens: DHEA (r = -0.318, p = 0.00001) and DHEAS (r = -0.506, p < 0.00001). The clinical signs suggesting andropenia were found in 31.4% of participants and androgen deficiency in 28.8% of men. The incidence of these signs increased significantly with the age of respondents. In contrast, the criteria of LOH in the entire group were fulfilled by only 6.5% of men. Men diagnosed with MS showed significantly lower TT plasma levels: 5.05 (3.70-6.45) vs. 6.30 (5.40-8.30), p < 0.0001--contrary to the FT, c-FT, c-BAT as well as DHEA/DHEAS serum levels, regardless of age. Men meeting the full criteria for LOH (clinical symptoms and laboratory-confirmed hipoandrogenemia) revealed more than a five-fold higher risk of metabolic syndrome in relation to others (OR = 5.533, 95% CI: 1.134-27.+ 01). Total, free, calculated-free and calculated-bioavailable testosterone serum concentrations were strongly correlated with each other. Similarly, the plasma concentrations of both adrenal androgens were mutually positively correlated (r = 0.417, p < 0.0001), but any correlation between the gonadal androgens and DHEA/DHEAS were revealed. CONCLUSIONS: The prevalence of isolated hipoandrogenemia and clinical symptoms suggestive andropenia is clearly greater than the actual frequency of LOH. Fulfilling the criteria for LOH significantly increases the risk of MS.

The polymorphism of the ACE gene affects left ventricular hypertrophy and causes disturbances in left ventricular systolic/diastolic function in patients with autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequently occurring autosomal diseases inherited in the dominant manner. Due to this, lesions in the cardiovascular system of ADPKD patients have caught the attention of clinical investigators worldwide. The aim of the study was to analyse cardiovascular complications in ADPKD patients with a focus on left ventricular hypertrophy (LVH) and selected components of its systolic/diastolic function based on echocardiography. The study was conducted on 55 patients with ADPKD (24 males, 31 females), subdivided into three groups according to the stage of chronic kidney disease (CKD). The patient group with ADPKD and ESRD (group C) manifested an increased incidence of the D allele as compared to group A and group B (χ(2) = 4.217, P = 0.04). In all ADPKD patients with the DD genotype, left ventricular mass (LVM), posterior wall thickness (PWT), and interventricular septal thickness (IVS) were significantly higher compared to patients possessing the II and ID genotypes (P < 0.02, P < 0.003, and P < 0.009, resp.). The DD genotype exists more frequently in ADPKD patients with ESRD and is associated with a higher occurrence of LVH and disturbances in systolic-diastolic function when compared to ADPKD ESRD patients with the II and ID genotypes.

Chronic kidney disease-related atherosclerosis - proteomic studies of blood plasma.

BACKGROUND: Atherosclerosis is considered the major cause of the dramatic increase in cardiovascular mortality among patients suffering from chronic kidney disease (CKD). Although the close connection between atherosclerosis and kidney dysfunction is undeniable, factors enhancing CKD-mediated plaque formation are still not well recognized. RESULTS: To increase our knowledge of this process we carried out a comparative proteomic analysis of blood plasma proteins isolated from 75 patients in various stages of renal dysfunction (CKD group), 25 patients with advanced cardiovascular disease (CVD group) and 25 healthy volunteers (HV group). The collected samples were subjected to 2D electrophoresis. Then, individual proteins were identified by mass spectrometry. The comparative analysis involving CKD and HV groups showed a differential accumulation of α-1-microglobulin, apolipoprotein A-IV, γ-fibrinogen and haptoglobin in patients with kidney disease. Exactly the same proteins were identified as differentially expressed when proteomes of CVD patients and HV were compared. However, a direct comparison of CKD and CVD groups revealed significant differences in the accumulation of two proteins: α-1-microglobulin and apolipoprotein A-IV. CONCLUSIONS: The obtained results indicate that at least two processes differentially contribute to the plaque formation in CKD- and CVD-mediated atherosclerosis. It seems that the inflammatory process is more intense in CKD patients. On the other hand, the down- and up-regulation of apolipoprotein A-IV in CVD and CKD groups, respectively, suggests that substantial differences exist in the efficacy of cholesterol transport in both groups of patients.

Urinary excretion of soluble tumour necrosis factor receptor 1 as a marker of increased risk of progressive kidney function deterioration in patients with primary chronic glomerulonephritis.

BACKGROUND: The effects of tumor necrosis factor α (TNF α), a potent proinflammatory cytokine, in the kidneys are mediated by two membrane receptors (TNFR), TNFR1 and TNFR2. The expression of both TNF and TNFRs increases in several kidney diseases and is associated with the shedding of the receptors out of the cell membranes. In an experimental model of glomerulonephritis (GN), elevated concentrations of TNFRs in serum and TNFRs excretion in urine were demonstrated. The aim of this study was evaluation of urinary excretion of TNFR1 and its relationship with the clinical markers of kidney injury in patients with GN. The value of basal urinary TNFR1 excretion as a prognostic indicator of the progression of kidney function impairment was also assessed. MATERIAL AND METHODS: Fifty-five patients with newly diagnosed, biopsy-proven primary GN were included in the study. In all patients, and in 20 healthy subjects, UTNFR1 was measured using an ELISA . In the patients, risk factors of the progression of impairment of kidney function (reduced eCcr, nephrotic syndrome, hypertension and intensity of morphological lesions in the kidneys) were evaluated. The appropriate treatment was then introduced and the patients were in follow-up for 4 years. The progression of kidney function impairment was defined as a reduction of eCcr > 5 mL/min/1.73 m2 /year during follow-up. The association of basal TNFR1 excretion with the progression was evaluated. RESULTS: Urinary excretion of TNFR1 in the patients with GN (4039.2 ± 3801.5 pg/mgCr) was greater than in the healthy subjects (1358.9 ± 927.8 pg/mgCr, P < 0,00002). A significant negative correlation between TNFR1 excretion and eCcr (Sr=0.464, P < 0.01) and a positive correlation between TNFR1 excretion and proteinuria (Sr = 0,463, P < 0.01) were found. In 13 patients, a marked reduction of eCcr was observed during follow-up. Logistic regression analysis revealed that TNFR1 excretion > 3863.3 pg/mgCr predicts progression of renal function impairment along with advanced interstitial fibrosis in the kidney biopsy specimens at presentation. CONCLUSION: Markedly elevated urinary TNFR1 excretion may be considered as a good marker of an activated TNFα-pathway in patients with newly diagnosed GN and as a potentially modifiable risk factor of progressive kidney function impairment.

Elevated urinary fibronectin excretion predicts poor outcome in patients with primary chronic glomerulonephritis.

BACKGROUND/AIMS: Fibronectin (FN) is one of the major matrix proteins in the kidney. The accumulation of FN fragments in inflamed glomeruli could contribute to the progression of renal injury. In the present study, the urinary FN excretion (UFN) was measured for evaluation of its possible role as a prognostic marker in patients with newly diagnosed chronic glomerulonephritis (GN). METHODS: In 55 patients with newly diagnosed biopsy-proven chronic GN, UFN was measured using an enzyme-immunossay kit. The progression of kidney disease was defined as a reduction of the estimated glomerular filtration rate (eGFR) >or=5 ml/min/year during the 4-year follow-up. RESULTS: The mean UFN in patients with GN (245.0 +/- 229.2 ng/mmol creatinine) was higher than in the 19 healthy subjects (100.7 +/- 87.3 ng/mmol creatinine; p < 0.002). No correlations between the initial UFN and eGFR and proteinuria were found. We did not find any association between UFN and the severity of glomerular sclerosis or the intensity of interstitial fibrosis. The progressive fall of eGFR was recorded in 13 patients (progressors). The mean initial UFN was significantly higher in progressors than in nonprogressors (p < 0.01). In logistic regression analysis, the initial high UFN was identified as independent factor predicting kidney function deterioration. CONCLUSION: These results indicate that UFN measured before treatment could serve as an additional prognostic marker of a poor outcome in patients with newly diagnosed primary GN.

[Combined therapy with L-carnitine and erythropoietin of anemia in chronic kidney failure patients undergoing hemodialysis]. / Skojarzone leczenie niedokrwistosci L-karnityna i erytropoetyna u chorych na przewlekla niewydolnosc nerek poddanych hemodializoterapii.

OBJECTIVES: The aim of this study was to analyze the influence of combined therapy with L-carnitine and erythropoietin on selected blood morphology parameters in patients treated with hemodialysis and to assess whether combined therapy could decrease the requirement for exogenous erythropoietin. PATIENTS AND METHODS: The results of anemia treatment were compared in three groups of patients: 27 patients treated with L-carnitine and erythropoietin, 15 patients treated with erythropoietin and 9 patients treated only with L-carnitine. The patients were treated for 6 months. L-carnitine was given orally at a dose of 4 x 250 mg daily. Erythropoietin was administered intravenously after each hemodialysis session and the mean dose of erythropoietin at the beginning of observation was 5642 +/- 2134 units/week. Before treatment serum concentrations of free and total carnitine, parathormone (PTH), aluminium, lead were determined and basic laboratory examinations were performed. The blood morphology was evaluated once a month. RESULTS: Combined therapy resulted in the improvement of blood morphology parameters (hemoglobin [Hb] before treatment 9.9 +/-1.4 g/dl, during treatment 10.7 +/- 1.6 g/dl), compared to treatment with erythropoietin (Hb before treatment 9.5 +/- 1.2 g/dl, during treatment 9.9 +/- 1.4 g/dl) or L-carnitine alone (Hb before treatment 11.3 +/- 1.0 g/dl, during treatment 12.0 +/- 1.1 g/dl). Combined therapy was associated with the reduction of erythropoietin dosage during treatment from 6287 +/- 1987 units/week to 2286 +/- 1684 units/week. The correlation between serum carnitine concentration and erythrocyte osmotic resistance indicates indirectly the beneficial effect of L-carnitine administration on erythrocyte cell membrane stabilization.

[Cardiac troponin I (cTnl) serum concentration in patients with chronic renal failure treated by hemodialysis]. / Stezenie sercowej izoformy troponiny I (cTnl) w surowicy chorych z przewlekla niewydolnoscia nerek leczonych hemodializami.

UNLABELLED: Elevated serum concentration of cardiac troponin I (cTnl) is a highly sensitive and specific marker of myocardial damage. Patients with chronic renal failure (crf) treated by hemodialysis often have increased serum cTnl level without evidence of acute myocardial ischemia. In chronic HD patients, elevated serum concentration of endothelin-1 (ET-1) and angiotensin II have been reported which may be associated with ischemic heart disease. The aim of the present study was to investigate possible association between cTnl serum level, ET-I, angiotensin II, other cardiac markers and the structural changes of myocardium assessed by echocardiographic (ECHO) method. Fifty nine patients with crf treated by HD were studied. ECHO and ECG examinations were performed in all patients and serum levels of cTnl, endothelin-1 (ET-1), angiotensin II were evaluated. In all patients left ventricular mass (LVM) was increased, and in 78% of patients was found concentric hypertrophy of the heart while in 22% excentric hypertrophy was found. In 54 patients there was no ECG changes and ST segment depression in V4-V6 leads, less than 1 mm was found in 5 patients. Arterial hypertension was found in 44 patients (75%), systolic and diastolic pressure was significantly higher (p<0.05) than in a control group. Increased serum level of cTnl was found in 12.0% of HD patients, increased serum level of endothelin-1 and angiotensin II were found in all patients. LVM in HD patients with elevated cTnl levels was significantly higher than in patients with normal cTnl concentration. There was a positive correlation between LVM and cTnl levels, and between angiotensin II serum concentration and cTnl levels and between ET-1 serum level and RWT. IN CONCLUSION: our findings suggest that elevated cTnl serum level reflect left ventricular hypertrophy and/or myocardial ischemia in HD patients, and indicate that ET-1 and angiotensin II might be associated with these conditions.

Prolongation of rat kidney graft survival after inoculation of allogeneic spleen cells: the effect of various routes of cell transfer.

OBJECTIVES: It has been clearly demonstrated that after donor-specific cell transfer the prolongation of allograft survival can be obtained, but the problem of how to inoculate cells remains unresolved. In this study, the effect of either portal venous (PV) or systemic intravenous (i.v.) inoculations of rat donor-specific spleen cells on subsequent renal graft survival was evaluated. METHODS: LEW recipients received 10(6) of spleen cells from allogeneic Fischer or syngeneic donors 30 days before kidney transplantation by either PV or i.v. routes. Animals from the control group obtained buffered saline by the same routes. RESULTS: Fischer grafts in nonimmunized LEW recipients were rejected after 9.6 +/- 1.3 days. In contrast, the immunization of the recipients by the pretreatment with donor spleen cells prolonged renal allograft survival significantly (p < 0.002). However, no difference in the graft survival was observed between animals inoculated with cells either by PV or by i.v. routes. In each studied group, long-time graft survival (> 100 days) was achieved in one case. CONCLUSIONS: These observations suggest that the effect of the various routes of allogeneic cell inoculations on subsequent organ graft survival time depends on the interval between the cell transfer and organ transplantation. Intravenous route seems to be as effective as PV route when transplantation is performed several days after donor-specific cell transfusion.

[Dermatosis bullosa in patient with chronic renal failure under hemodialysis treatment--case report]. / Porfiria skórna pózna u chorej na przewlekla niewydolnosc nerek leczonej zabiegami hemodializ--opis przypadku.

A case of 45-year-old patient with chronic renal failure treated by hemodialysis associated with skin changes typical for porphyria cutanea tarda is reported. The diagnosis was based on clinical manifestations and on histopathologic examination of the skin segment. The skin was low sensitive for UVA rays, serum levels of aluminium and lead were significantly elevated. We did not find porphyrins in the urine (24-hour collection 100 ml) as well as in the dialysis fluid.