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The management of patients with diabetic foot presents an important challenge for health services research. Since today there is no algorithm describingkind of diagnostic tests and treatment is the best for patients with different extremity ulcers. This article could be helpful for future decisions regarding the management of patients with lower extremity ulceration.

There is an increasing number of evidence of correlation between bacterial infection and atherosclerosis. Heat shock proteins as a possible factor connecting an inflammation reaction inducted by infection and development of the early atherosclerotic lesions is postulated.

The high risik of cardiovascular diseases in diabetes is connected with wide and premature atheromatosis. It is caused by systemic metabolic disorders like hyperglycaemia, insulin resistance, dyslipidaemia, endothelium dysfunction. This review will discuss the role of peroxisome proliferator-activated receptor gamma (PPARgamma) in the pathogenesis diabetes and atheromatosous injury of vessels. PPARgamma is a nuclear transcript factor with a very wide spectrum of biological activities. It influences important risik factors of atheromathosis, especially by patients with metabolic syndrome in diabetes type 2. Thiazolidinediones, which is activators PPARgamma, could be a turning-point in the treatment of diabetic angiopathy.

Background: [corrected] Etiology and pathogenesis of thromboangiitis obliterans, an uncommon disease, but connected with high risk of leg amputation, is still unknown. Genetic predisposition and inconvenient factors of environment, especially nicotine, could initiate an immunological process, which evokes endothelial dysfunction. In histological preparation inflammation and thrombus are observed. Endo-thelin-1 could affect these processes. It is a strong vasa-constrictor and has a wide spectrum of biological activity, often opposed to effect of prostacycline analogs. The aim of study was a role of endothelin-1, antielastin antibodies and selectin P, L, E in the pathogenesis Buerger's disease and influence of alprostadil on these parameters., Material and Methods: We examined 10 patients with Buerger disease in the active phase, which were divided in two subgroups. Four persons with necrosis of toes were in the first subgroup, and six patients with rest pain but without trophic changes in the second subgroup. 13 healthy persons composed the control group. Index of antielastin antibodies, concentration of endotehlin-1, selectin P, L and E were measured in venous and arterial serum. These parameters by patients were determined twice: before and after 10-days treatment with alprostadil 20-40 microg per day. Concentration of endothelin-1, selectins and index antielastin antibodies were measured by enzyme-linked immuno-sorbent assay., Results: We observe increase in endothelin-1 concentration by persons with necrosis of toes compared to patients without these changes (p=0.024) and to control (p=0.022). In the subgroup I index of antielastin antibodies IgA was higher than in control group (p=0.020). After alprostadil treatment endothelin-1 concentration, antielastin antibodies index was not statistically significant compared to results before treatment or control group. We observed correlation between concentration of endo-tehlin-1 before treatment and index of antielastin antibodies IgG (p=0.0475). We observed significant diffrance of concentration of selectin P, L and E compared to control (p=0.038). Especially we noticed higher concentration of selectin P (p=0.001) than in control group. The after treatment reduction of concentration was only for selectin L statistically significant (p=0.038)., Conclusion: 1. Plasma endothelin-1 level play a role in the exacerbation of clinical symtpoms of thromboangiitis obliterans. 2. Endothelial injury is connected with increase in concentration of selectin P in patient's serum. 3. Alprostadil didn't influence on concentration of endothelin-1 in these patients.

Diabetes causes the development of atherosclerotic vascular changes. Leukocytes, thrombocytes and also cytokines are involved in this process via endothelial activation. Estimation of interleukin 1 beta (IL-1 beta) and fibrinogen serum level of patients suffering from diabetes in context of endothelial damage is presented. The stage of vascular endothelium damage is based on the measurement of blood endothelial cells (EC) count and concentration of the plasmatic von Willebrand factor (vWF). Endothelial destruction level was established on the base of selectin L, P and E serum concentration. Activation of inflammatory proliferative mechanisms was indicated by IL-1 beta serum level. Serum haemostasis disorders were indicated by fibrinogen concentration. Patients with diabetes t. 1 and t. 2 differentiated by age and diabetes duration time with normal blood pressure and hypertension were included into the research. We showed that in both types of diabetes endothelium damage goes with significant increase of circulated EC count and vWF concentration. Increased serum level of IL-1 beta and fibrinogen in those patients shoulds significant correlation with vascular wall destruction, visibly marked in patients with diabetes t. 2. Hiperfibrinogenaemia and increased IL-1 beta concentration associate with significant engagement of SL and SE in inflammatory proliferative process of endothelium in young people suffering from diabetes t. 1 over 6 years. Hypertension coexisting with essential disease in both types of diabetes remains important progression factor in atheromatic vascular changes.

Background: Platelet thrombi play critical role in pathogenesis of cardiovascular complications in atherosclerotic peripheral arterial disease (PAOD). The aim of this study was to evaluate the concentration of platelets GP IIb/IIIa, GP I b/IX and plasma levels of their ligands (fibrinogen and vWF) and their relation to other atherosclerotic risk factors in the patients with intermittent claudication secondary to PAOD., Methods: Consecutive patients of the University Vascular Clinic were studied: 64 claudicants and 38 controls were enrolled. The concentration of platelets GPII b/IIIa and GP Ib/IX was estimated by ELISA method using monoclonal antibody against GPII b/IIIa (CD41a) and GPI b/IX (CD42a Immunotech). Plasma levels of vWF, fibrinogen, and platelets were measured by routine, Results: Plasma vWF (145+/-41%), fibrinogen (3.8+/-1 g/l) and platelet concentration of GP Ib/IX (121.1+/-23.39), GPIIb/IIIa (117.9 6 +/-32.7%), as well as plasma lipids and uric acid were statistically higher in claudicants than in controls (vWF: 103+/-42%, fibrinogen: 2.9+/-0.5 g/l, GP Ib/IX: 100+/-16.9%, GP IIb/IIIa: 100+/-29.4%). We have observed statistically higher concentration of GP IIb/IIIa and GP Ib/IX in smoking patients than in non-smoking patients with PAOD and significant correlation between the concentration of GP Ib/IX and GP IIb/IIIa and plasma fibrinogen in patients with PAOD and controls., Conclusions: Our results demonstrate higher platelet concentration of GP Ib/IX,GP IIb/IIIa and elevated plasma levels of ligands for platelets receptors-fibrinogen and vWF in patients with PAOD. This prothrombotic conditions may explain increased cardiovascular morbidity and mortality in this patient's group.

The aim of the study was an assessment of alpha 1-antitrypsin (alpha 1-AT) serum concentration in patients with abdominal aortic aneurysm and investigation the relationship between alpha 1-AT and parametric and non-parametric atherosclerosis risk factors. A statistically significant increase of alpha 1-AT concentration was demonstrated in the group of patients as compared to healthy subjects; the alpha 1-AT concentration demonstrated no correlation with aneurysm diameter. A positive correlation was found between alpha 1-AT level and the age of the studied patients; the alpha 1-AT concentration demonstrated no correlation with the remaining risk factors of atherosclerosis. alpha 1-AT may be regarded as a marker of inflammatory lesions in abdominal aortic aneurysms, directly independent of atherosclerosis risk factors.

Uric acid has been suggested as a risk factor in cardiovascular disease since the beginning of the twentieth century. While some clinical evidence have found a significant, specific and independent association between the uric acid serum level and cardiovascular morbidity and mortality, others came to an opposite conclusion. Hyperuricemia commonly coexists with hyperlipidaemia, hypertension, diabetes, obesity and others cardiovascular risk factors. This strong association makes the the role of risk factors difficult to separate out. Thus, the role of uric acid as an independent risk marker remains an open question.

Anti-endothelial cell antibodies (AECA) are a heterogeneous group of autoantibodies directed against antigens located on endothelial cells. AECA can be detected in a wide variety of clinically distinct diseases in which the common feature appears to be immune, inflammatory-mediated damage to the vessel wall. In in vitro studies it has been demonstrated that AECA possess functional properties, such as endothelial cell activation leading to the induction of a pro-inflammatory/pro-coagulant phenotype of the endothelial cells. Increasing evidence is accumulating on the possibility that AECA may play an important role in the development or progression of atherosclerotic lesions. Moreover, it has been suggested that AECA may contribute to the instability of angina and postangioplasty intimal proliferation, associated with the high restenosis rate after PTCA (percutaneous transluminal coronary angioplasty). In diabetes these autoantibodies seem to be involved in the complex pathogenesis of diabetic vascular complications.

The arterial platelet thrombus contribute to development of thrombotic complications of atherosclerosis: acute coronary syndrome, thrombotic strokes and exacerbations of peripheral arterial occlusive disease. Platelet adhesion and aggregation is mediated by interaction between platelet glycoprotein receptors GPI b/IX GPII b/III a and their ligands-adhesive proteins: von Willebrand factor (vWF) and/or fibrinogen. Pharmacological blockade of interaction between glycoproteins receptor and their ligands may offer an effective prevention of thrombotic complications.

This paper presents involvement of autoimmune mechanism, and especially the role of autoantibodies anti-dsDNA (double stranded DNA) in atherosclerosis. Authors on the basis of results from experimental models and human studies demonstrate contribution of antibodies anti-DNA in the pathogenesis of atherosclerosis. Antibodies anti-dsDNA may play a role in atherosclerosis by promoting accumulation of cholesterol in macrophages and smooth muscle cells, influence on dyslipoproteinemias, cytotoxicity and releasing cytocines.

Prostaglandin E1 because of its unique protective and repaired endothelial action is used in the treatment of many diseases. The aim of the study was the investigation of prostaglandin E1 influence on some adhesive molecules profile in the patients with thrombangitis obliterans. 21 patients, aged 31-49 years (mean 40.3 +/- 5.3), with thrombangitis obliterans were observed. The control group consisted of 22 healthy patients, aged 18-50 years (mean 34.6 +/- 12.25 years). In both groups as well the number of circulated endothelial cells and selectin L, P, E and vWF factor concentration were measured. In patients suffered from thrombangitis obliterans these parameters were measured before and after 21 days intraarterial 10 mg PGE1 (Alprostadil) infusion. No PGE1 influence on selectin E concentration was observed, the mean values as well before as after the treatment were equal to 66.56 +/- 8.92 ng/ml. The decrease in selectin P concentration was observed but the difference was not statistically significant. The statistically significant reduction was observed in selectin L (decrease from 799.88 +/- 104.79 ng/ml to 764.83 +/- 116.04 ng/ml) and vWF concentration (decrease from 195.04% +/- 26.2% to 187.69% +/- 22.83%). The final PGE1 therapeutic result was the circulating endothelial cells decrease (from 2.47 +/- 1.01 before to 2.36 +/- 0.97 cells/ml after treatment). Intraarterial PGE1 infusion in patients with thrombangitis obliterans results in significant selectin L, vWF factor concentration decrease less; this decrease is less marked in selectin P concentration. As the inhibition of the adhesive molecules activation effect the number of exfoliated circulated endothelial cells decrease is observed.

Although 75 years have passed since Buerger's disease was described as a separate nosological, its etiology and pathogenesis are not sufficiently elucidated. According to many authors the disease origin is significantly connected to genetic and environmental factors. Exposure of some patients with special genotype, mainly HLA-A9 and HLA-B5, to environmental factors, mainly nicotine, may be the base of etiology and pathogenesis of Buerger's disease. Discovery of antielastin, anticollagen I and III antibodies, antinicotine and antivascular antigen antibodies in blood of patients, allowed to put forward a theory of immunological character of TO. In Buerger's disease, defined in recent years as an inactive collagenosis, immunological complexes, cell toxins developing during phagocytosis, found in smokers, constitute the main agents responsible for vascular wall damage. Disturbance of prostacyclin I2/thromboxane A2 balance and accelerated platelet aggregation cause spasm of arterioles and in effect lead to higher procoagulant readiness. Some adhesive molecules, for example P and L selectins, play an important role in vascular endothelium damage. Prostaglandin treatment induces an improvement of vascular wall (endothelium) status, and simultaneously improvement of tissue perfusion, expressed by a decrease of selectin and vWF concentrations and of the number of desquamated endothelial cells.

Background: In order to compare hemostasis in diabetic and non-diabetic claudicants we evaluated endothelial (von Willebrand factor, vWF), rheologic (fibrinogen, hematocrit), coagulation system (thrombin-antithrombin complex, TAT) and platelet (platelet factor 4, PF4, aggregation on thrombin, collagen and ADP stimulation) parameters in both groups and healthy controls., Methods: Twenty-five diabetic, 34 non-diabetic patients with claudication and 26 healthy individuals were enrolled into the study., Results: The severity of lower limbs ischemia was similar in two groups of claudicants but coronary heart disease and cerebral ischemia were significantly more common in diabetic than in non-diabetic claudicants. vWF level was significantly higher in diabetic than non-diabetic claudicants and healthy controls (184+/-43%, 147+/-43%, and 103+/-42%, respectively). Fibrinogen was significantly higher in diabetic and non-diabetic claudicants compared to controls (4.2+/-1.7, and 3.9+/-1.1, versus 2.9+/-0.5 g/l) and TAT plasma concentration was much higher in diabetic compare to non-diabetic patients and controls (9.8+/-4.4, 1.7+/-1.1, and 1.3+/-0.6 microg, respectively). PF4 concentration was significantly higher in non-diabetic patients with PAOD (34+/-29 UI/ml) when compare to healthy controls (14+/-9 UI/ml), but diabetic PAOD patients with the disease showed lower PF4 concentration (26+/-30 UI/ml). Platelet aggregation with all used activators was similar in all groups likewise hematocrit values, and platelet count., Conclusions: Complicated DM is linked with significant endothelial perturbation when compared with healthy, but also with PAOD individuals; rheologic parameters are not different from those found in PAOD patients; coagulation system activation but not platelet hyperactivity is associated with DM complicated by PAOD when compared to both control groups.

Studies in the recent years have provided numerous evidence of the inflammatory and immunological character of atherosclerosis. In the early stages of the adhesion of leucocytes and platelets to the blood vessel wall, and also in occurring intercellular interactions leading to creating the atherosclerotic lamina, the adhesive molecules from the selectine family ply the crucial role. Their expression, mainly selectines L, P and E on the endothelial surface and on the smooth muscles of the vessels, undergoes a distinct intensification under the influence of hypoxia. The begun cascade of molecular changes with the contribution of selectines leads inevitably to the development of atherosclerotic changes. The neutrophile and lymphocyte fixed to the endothelium show ability to its damage, both as a result of immediate response [release of free oxygen radicals, enzymes and cytoxic substances] and as a result of indirect action [release of cytocines which change the biological property of the endothelium--the so called endothelial activation]. In this work the role of diabetes and hypertension in the intensification of those processes has been noticed.

Based on literary data we carried out the analysis of the influence vascular endothelium on maintaining the haematological and circulatory balance in the organism. Particular attention was paid on its active metabolic and secretory role in this process.

Cardinal pathological mechanisms responsible for initiation and development of the Raynaud's phenomenon have been presented according to the current data from literature. The role of endothelin-1, cytokins and growth factor in pathophysiology of this phenomenon have been highlighted. According to own observations randomised results of investigation in these patients have shown that basic disease stimulate the development of the vasomotoric disturbances: idiopathic Raynaud's phenomenon and Raynaud's phenomenon which accompany connective tissue disease.

Endothelin is an endogenous vasoconstrictor and plays an important role in pathogenesis of Raynaud's phenomenon. Plasma endothelin-1 (ET-1) and von Willebrand factor (vWF) concentrations following cold exposure in 52 patients with Raynaud's phenomenon were measured. Statistically significant increase of ET-1 and vWF was found in the study group in compare to healthy volunteers. There was positive correlation between ET-1 and vWF in those cases. The dates suggest that ET-changes indicates a vasospastic effect on vascular injury. Treatment with endothelin-receptor antagonist may prevent structural changes in vessel well.

Diabetes mellitus (DM) type 2 is a very strong risk factor for atherosclerosis. The final event of atherosclerosis is the vessels occlusion by platelet riche thrombus. Platelets adhesion and aggregation is mediated by interaction between platelets glycoproteins: GPIb-IX, GPIIb-IIIa and adhesive proteins: von Willebrand factor or fibrinogen. The expression of platelets GPIb-IX, GPIIb-IIIa, plasma vWF, fibrinogen concentrations were evaluated in 40 patients with diabetes type 2 (22 patients with PAOD stage II and IV according to Fontain, 18 diabetics without paod) and 32 healthy individuals. The expression of platelets glycoproteins GPIIb-IIIa and GPIb-IX was estimated by ELISA using monoclonal antibody against GPIIb-IIIa (CD41a) and GPIb-IX (CD 42a Immunotech). Plasma vWf (189.7 +/- 53.6%), fibrinogen (4.5 +/- +/- 1.3 g/l) level and expression of platelets GPIb-IX (63.2 +/- 19.6% in platelets concentration 125,000/mm3, 104.5 +/- 28.1% in platelets concentrations 250,000/mm3) and GPIIb-IIIa 50.8 +/- 10.1% in platelets concentrations 125,000/mm3, 95.3 +/- 21.3% in platelets concentrations 250,000/mm3 were statistically higher in patients with diabetes type 2 than in controls (vWf: 94.9 +/- 27.1%, fibrinogen: 2.8 +/- 0.4 g/l, GPIb-IX in platelets concentration 125,000/mm3: 43.8 +/- 9.3%, in concentration 250,000/mm3: 83.9 +/- 18.3%, GPIIb-IIIa in platelets concentration 125,000/mm3: 33.7 +/- 10.1%, in platelets concentration 250,000/mm3: 63.2 +/- 15.4%). We found significant correlation between the expression of GPIIb-IIIa, GPIb-IIIa, GPIb-IX and plasma adhesive proteins: vWF, fibrinogen in controls and both subgroups of diabetic patients. The correlation between plasma vWF and fibrinogen level and degree of arterial insufficiency in diabetic patients was also found. We can assume that higher vWf, fibrinogen plasma level in diabetic patients with and without PAOD could account for high expression of platelets GPIIb-IIIa and GPIb-IX.

Systemic lupus erythematodes is a disease commonly associated with peripheric circulation disturbances. The goal of the study was the evaluation of the role of the following nuclear antibodies: anti-Ro (SS-A), anti-La (SS-B) and anti-Sm in the endothelium damage process in the SLE patients with symptoms of microcirculation disturbances. The concentration of plasma thrombomodulin was used as a marker of the endothelium destructive changes intensity. Twenty-four patients with SLE (22 women and 2 man) aged of 18-57 (the average age 40.50 +/- 9.72 years) in which occurred: the Raynauds symptom (16 patients), fingers cyanosis (5 patients) and fingers and/or toes necrosis (3 patients) were investigated. Antinuclear antibodies and thrombomodulin level was estimated with the ELISA method. In all patients, the concentration of anticardiolipin antibodies in serum was determined (ELISA-method, cardiolipin was used as an antigenes, Sigma USA). Higher titers of ANA antibodies in 83%, anti-SM antibodies in 30%, anti-Ro in 42% and anti-La in 42%, examined patients and higher titer of anti-Ro and anti-La antibodies together in 29% of examined patients were stated. Statistical significant correlation between the increased level of thrombomodulin and anti-La antibodies concentrations in serum of patients with the disease lasting over 6 years was found out. The significant statistical correlation of thrombomodulin concentration increasing and anti-La antibodies in serum was proved. The dynamism of limbs circulation disorders depends on the disease duration.

Lipoprotein(a) [Lp(a)] is the specific lipoprotein which physiological role has not been explained. Similarity between apolipoprotein(a) and plasminogen structure suggests, that Lp(a) can be the bridge connecting the lipid metabolism and the coagulation system. The aim of the study was to evaluate if there is any correlation between Lp(a) and plasminogen serum concentrations in patients with diabetes t.2. 20 males and females with diabetes t.2 in the age 19-75 years (mean: 54.9 years). The control group consisted of 15 healthy men and woman in the age of 23 years (medical students). Lp(a) was estimated by ELISA, plasminogen by turbidimetric methods. Lp(a) serum level in the examined group was: 40.06 + 59.45 mg%. In 7 patients it was over 30 mg%. In the control group: Lp(a) concentration was: 13.23 + 10.5 mg%, no one was above 30 mg%. The different was significant. Plasminogen concentration was: in patients: 94.08 + 53.08%, in the control group: 89.08 + 40.7%. There was no significant difference. Correlation index between Lp(a) and plasminogen concentrations was in the patient's group: 0.3, in the control group: 0.2. In patients with diabetes we can find increased Lp(a) commentation in serum and normal plasminogen concentration. Concentration of Lp(a) didn't demonstrate significant correlation with plasminogen serum level.

Based on the present literature data we have confronted the clinical parameters and some pathogenetic mechanisms of the syndrome X. Especially we stressed the danger of the accelerated development of the atherosclerotic changes in the vessels and the cardiologic complications.

DNA metabolism in lymphocytes was evaluated in patients suffering from the nephrotic syndrome decompensation, basing on measurement of endonucleases (DNases) activity in these cells. The examination involved 17 patients, aged 27.7 +/- 7.11 with clinical and biochemical active disease, all with the nephrotic syndrome decompensation and erythrocytes in urine. A significant rise in the enzyme activity was observed in T and B lymphocytes (p < 0.001) in all the patients, with a distinct 3-fold increase in enzyme activity in B lymphocytes, when compared with the other cell populations. To elucidate the nature of the observed changes in DNases activity in systemic lupus erythematosus, nucleus proteins of the cells were separated electrophoretically in acrylamide gradient with immobilized DNA. Degradation processes in nucleic acids were considerably more efficient than the DNA synthesis in B lymphocytes of these cells. A smaller increase in the enzyme activity in T cells than in B lymphocytes results exclusively from more intense catabolism of nucleic acids not parallel to the intensified DNA synthesis in these cells.

The nuclease activity in T and B lymphocytes isolated from patients with chronic renal failure and control subjects was studied. The data obtained show a slight increase in nuclease activity in T and B cells isolated from uraemic patients as compared to the control cells. The increase in enzyme activity was limited to the group of relatively small nucleases with molecular weights ranging from 14 kDa to 18 kDa. It was documented previously that these nucleases are among the cleavage products of the largest subunit of DNA-dependent RNA polymerase I, which is responsible for ribosomal RNA synthesis. Thus, we suggest that the characteristic feature of lymphocytes isolated from uraemic patients is lowering of their metabolic activity. Amongst toxins increasing catabolism of the active enzyme, a significant correlation with the rise of lymphocyte Mg2+ and Mn2+ ions was disclosed.

The calcium pathway of Cyclosporine A (CyA) action on peripheral blood lymphocytes was assessed with regard to the literature data and self observations of kidney graft recipients. A significant relation between the immunosuppressive action of the drug and intracellular concentrations of Ca2+ is intimately linked with the regulatory potential of calmodulin. Because of the widespread clinical use of calcium channel blockers also considered influence of these drugs on immunosuppression by CyA and their importance in reducing its nephrotoxicity.

The activity and quantity of deoxyribonucleases in T and B lymphocyte cells isolated from peripheral blood of patients with transplanted kidney were investigated. Twenty three patients with transplanted organ, aged 35 +/- 9.7, treated with cyclosporin A and thirteen individuals after renal transplantation in age 34.8 +/- 6.3 treated conservatively were studied. The enzyme activity was defined as resting DNase activity (DNase 0). Where specifiel the reaction mixture was supplied either with 5 mM MgCl2 (DNaseMg2+) or 1 mM MnCl2 (DNase1 x Mn2+) or 2 mM MnCl2 (DNase2 x Mn2+). Two enzyme groups with molecular mass 32 kDa and 14 to 18 kDa were analyzed. It was evidenced that the nuclease activity in B lymphocyte isolated from patients treated with cyclosporin A after organ transplantation was quite close to the control subjects. On the contrary, the nucleases activity and quantity increased in T lymphocyte of the same patients and increasing in enzymes activity was depending upon haemodialysis period of time prior to organ transplantation. Enzymes activity correlate with clinical parameters typical for kidney transplant rejection. The activity and quantity of nucleases was slightly reduced in both T and B lymphocytes isolated from patients treated conservatively after organ transplantation. The useful of nuclease assay for monitoring of kidney transplant rejection is discussed.

The activity of three classes DNA-dependent RNA polymerases in T and B lymphocyte cells nuclei isolated from peripheral blood of patients with transplanted kidney were investigated. Twenty three patients with transplanted organ in age 35 +/- 9.7 treated simultaneously with cyclosporin A and small doses of prednisone and thirteen persons after renal transplantation in age 34.8 +/- 6.3 treated conservatively (azathioprine plus prednisone) were studied. The enzymes activity was assayed by the measurement of [3H] UTP incorporated into acid insoluble product in the presence of alpha-amanitin when specified. Both, "bound" and "free" enzymes activity was analysed. "Bound" polymerase is defined by the ability to transcribe endogenous template in the absence of exogenous DNA. "Free" enzyme was determined by the additional transcription on exogenous, calf thymus DNA as template. The quantity of polymerase I subunits by Western blotting was also analysed. It was shown that the polymerizing enzymes activity strongly depend upon haemodialysis period of time prior to organ transplantation as well as upon the treatment after transplantation. Characteristically in case of T lymphocyte isolated from patients treated with cyclosporin A, the transplant rejection process was accompanied by large increasing in polymerase activity especially in polymerase I. The correlation in polymerase activity and transplant rejection time was clearly observed. In case of lymphocyte cells isolated from patients with renal transplant treated conservatively, the polymerase activity in both T and B cell was slightly reduced. The useful of polymerase assay for monitoring of patients with renal transplant is considered.

We investigated the activity of some enzymes of the transcriptive DNA system to assess lymphocyte metabolic potential in patients with proliferative glomerulopathies. This study included analysis of the activity of three classes DNA-dependent RNA polymerases, before and 6 months after immunosuppressive therapy (Azathioprine + Prednisone). The enzyme activity was measured in nuclear extracts of T and B lymphocytes by estimation of the uptake of 3/H/UTP in the presence of alpha-amanitine. The immunoblotting technique using anti-polymerase I antibodies and nuclear proteins separation with immobilized exogenous DNA were employed to assess a type of the increase of the DNA-dependent RNA polymerase activity in lymphocytes populations (enhancement of the synthesis or limited depolymerization and degradation of the active enzyme). We found that the RNA polymerizing activity was increased in both lymphocyte populations. In T lymphocytes the increase was caused by an enhanced activity of transcript DNA enzymes, secondary to increased gene expression. In B lymphocytes an increase in enzyme activity was rather due to large stability RNA-polymerases in these cells. DNA-dependent RNA polymerase I in T and B cells was not modified by immunosuppression, while reduction in enzymatic activity of the remaining RNA-polymerase classes in T lymphocytes depends on partial limitation of their gene expression. Our study indicates that profound and various lymphocyte metabolic changes occur in patients with proliferative glomerulonephritis resulting from modifications in a gene expression and initiation of DNA synthesis in these cells.

On the basis of a retrospective assessment of aluminium content in the bones and morphometric findings in spongy bones of patients maintained on long-term dialyses a trial was undertaken of demonstration of a possible causative effect of this metal on the development of osteomalacia. The analysis included also the role of aluminium in the development of intravitally occurring fractures of bones in these patients. A biopsy specimen was taken from the iliac ala with a modified Bartelheimer's needle. The study comprised two groups of patients. The first one included 10 patients in a mean age of 38.2 +/- 6.6 years remaining, on the average, since 72.3 +/- 33.6 month who had previously evidence of fractures demonstrated clinically and radiologically. In the second group 12 patients of a mean age of, 41.9 +/- 6.8 years on dialyses since 40.3 +/- 12.2 months with demonstrated subperiosteal resorption, and patients with normal radiological appearance of the skeleton were studied. The patients were dialysed using a dialysate prepared from water not previously adapted and containing Al in a concentration of 0.135 +/- 0.102 mg/l. The diagnosis of osteomalacia was based on the morphometric method of Bordier (6). In both studied groups a highly significant rise was demonstrated in the concentration of Al in the spongy bone, and pathological fractures were closely related to the morphometric markers of osteomalacia. Aluminium cumulation in the bone tissue of patients with fractures exerted a significant effect on an increase of osteoid volume and reduction of mineralization fronts, and demonstrated a directly proportional relationship with the time of treatment with dialyses and overall exposure to aluminium in the dialysing fluid. In the group with osteomalacia a linear trend was observed in the increase of osteoid volume related to aluminium retention in spongy bone.

The authors describe a rare case of Richter's syndrome (transition of chronic lymphatic leukaemia into reticulosarcoma) developing during rheumatoid arthritis in a women aged 53 years. Chronic antigenic stimulation and disturbances of interaction between lymphocytes T and B are suggested as a cause of Richter's syndrome.