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Biomedical subjects

I Stefanidis

Publications and source records attributed to I Stefanidis.

At least 19 recordsLinked to original sources
PubMed2002

Filtration fluid for hemodialysis treatment.

Bacterial contamination of dialysis fluid has long been recognized as a problem in hemodialyis. Cytokines released as a consequence of contaminated dialysis fluid are believed to be responsible for many acute and chronic side effects in patients undergoing renal replacement therapy. For several years now, attempts have been made to eliminate pyrogenic substances and ensure a sterile and endotoxin-free dialysis fluid. A recent dialysis fluid filter known as DIASAFE, containing a membrane based on Polysulfone (Fresenius), was tested for a period of 1,000 hours (approx. 14 weeks). Dialysis fluid samples were collected once weekly before and behind the filter and cultivated for detection of microorganisms and endotoxins. Additionally, starting after the fourth week of the study, serum samples were collected weekly and the beta2-microglobulin concentration was determined. The filter reduced microorganisms at a rate of at least 10(5) and in the majority of cases (86% of samples) by more than 106. Under clinical conditions the stability and microbiological functionality of the filters could be demonstrated for more than 1,000 hours and 150 disinfecting cycles. In four cases of endotoxin burden (> 0.5 IU/ml) in the dialysis fluid in front of the filter the concentration behind the filter was lower than 0.1 IU/ml, indicating effective reduction of endotoxins. A tendency to a reduction of beta2-microglobulin in serum from 32.5+/-3.9 mg/L to 21.5+/-5.3 mg/L was observed. These results indicate that the dialysis fluid filter used was effective, dramatically reducing the bacterial contaminants in dialysis fluid, thus protecting patients from the potentially harmful acute and long-term life-threatening consequences of contaminated dialysis fluid.

Adolescent↗
PubMed2002

Sodium and body fluid homeostasis in profiling hemodialysis treatment.

Acute adverse side-effects of hemodialysis such as hypotension, muscle cramps, osmotic imbalance and thirst are induced by the interference with fluid and electrolyte balance occurring during treatment. Changes in osmolarity due to alterations of plasma sodium concentration during hemodialysis strongly influence fluid distribution between extracellular and intracellular fluid volume. Increased sodium dialysate concentration induces fluid shift from the intracellular to the extracellular compartment. This shift leads to a more efficient ultrafiltration by increasing plasma refilling volume but also to an increased thirst. Treatment of hypotension, cramps and nausea with hypertonic saline solution leads also to a considerable retention of sodium. Profiling hemodialysis consists in deliberately changing ultrafiltration and dialysate. sodium in order to combine an efficient ultrafiltration with a balanced sodium handling and to prevent side-effects during treatment. Continuous measurement and control of blood volume seems to be the best method to prevent hypotensive episodes. Profiling of sodium should not be the cause of a positive sodium balance. The clinical benefits of sodium profiling to the patients have still to be proven.

Biological Transport↗
PubMed2001

Influence of recombinant human erythropoietin therapy on plasma endothelin-1 levels during hemodialysis.

The correction of anemia with human recombinant erythropoietin (rHuEPO) in end stage renal disease is associated with hypertension in about one third of hemodialysis patients. The pathogenesis of the rHuEPO-induced hypertension is still uncertain, though evidence of the involvement of endothelial cells has emerged. The aim of this study was to determine plasma endothelin-1 during hemodialysis and to compare the endothelin-1 levels in hemodialysis patients with and without rHuEPO substitution. Nineteen stable patients (13 male and 6 female, mean age 62 +/- 11 years) with end stage renal disease were studied. Cuprophan dialysers (GFS 12, Gambro, Lund, Sweden) were used for hemodialysis in all cases. rHuEPO (40 U/kg s.c.) was administered to 10 patients. Blood pressure (BP; RR mmHg) and blood volume changes (deltaBV; hemoglobinometry %) were serially measured. Samples were taken before and every hour during hemodialysis. Plasma endothelin-1 was measured by ELISA (R&D Systems, Minneapolis, USA) and corrected for hemoconcentration. Endothelin-1 concentration was elevated before commencement of hemodialysis (1.16 +/- 0.36 pg/ml) when compared to healthy controls (ref. 0.3-0.9) and increased to 1.47 +/- 0.51 pg/ml by the end of the session (p<0.05). In patients under rHuEPO-substitution plasma endothelin-1 was higher when compared to patients without substitution before (1.25 +/- 0.3 vs. 1.05 +/- 0.3 pg/ml) and at the end of HD (1.62 +/- 0.5 vs. 1.28 +/- 0.3 pg/ml, p<0.05). There was no difference in BP and deltaBV between the two groups during treatment. Plasma endothelin-1 was higher in hemodialysis patients and there was a continuous rise in plasma endothelin-1 during a session. Comparison of two groups of hemodialysis patients with and without s.c. rHuEPO-replacement treatment revealed a significantly higher plasma endothelin-1 concentration in patients with s.c. rHuEPO treatment. However, the elevated endothelin-1 levels were not accompanied by arterial hypertension.

Anemia↗
PubMed2000

Urinary thymidine glycol as a biomarker for oxidative stress after kidney transplantation.

Reactive oxygen species are generated during ischemia-reperfusion tissue injury. Oxidation of thymidine by hydroxyl radicals (HO*) causes formation of 5,6-dihydroxy-5,6-dihydrothymidine (thymidine glycol). Thymidine glycol excreted in urine can be used as a biomarker of oxidative DNA damage. The aim of this study was to investigate the oxidative DNA damage in patients showing immediate allograft function after kidney transplantation, and to find out whether this damage correlates with glomerular and tubular lesions. Time dependent changes in urinary excretion rates of thymidine glycol, but also of total protein, albumin, low molecular weight (alpha1-microglobulin, beta2-microglobulin) and high molecular weight proteins (transferrin, IgG, alpha2-macroglobulin) were analyzed quantitatively and by polyacrylamide-gel electrophoresis in six patients. Urinary thymidine glycol was determined by a fluorimetric assay in combination with affinity chromatography and HPLC. After kidney transplantation the urinary excretion rate of thymidine glycol increased gradually reaching a maximum within the first 48 hours (16.56+/-11.3 nmol/m mol creatinine, ref. 4.3+/-0.97). Severe proteinuria with an excretion rate of up to 7.2 g/mmol creatinine was observed and declined within the first 24 hours of allograft function (0.35+/-0.26 g/mmol creatinine). The gel-electrophoretic pattern showed a nonselective glomerular and tubular proteinuria. The initial nonselective glomerular proteinuria disappeared within 48 hours, changing to a mild selective glomerular proteinuria. In this period (12-48 hours) higher levels of thymidine glycol excretion were observed, when compared to the initial posttransplant phase (13.66+/-9.76 vs. 4.31+/-3.61 nmol/mmol creatinine; p<0.05). An increased excretion of thymidine glycol is seen after kidney transplantation and is explained by the ischemia-reperfusion induced oxidative DNA damage in the kidney. In the second phase higher levels of excretion were observed parallel to the change from a nonselective to a selective glomerular and tubular proteinuria. An explanation may be sought in the repair process of DNA in the glomerular and tubular epithelial cells, appearing simultaneously with functional recovery.

Adult↗
PubMed2000

The heterogeneous and delayed course of blood pressure normalization in hypertensive patients after bilateral nephrectomy with and without subsequent renal transplantation.

BACKGROUND: Controversy exists about the time course of blood pressure normalization following bilateral nephrectomy. We sought to evaluate the time course of blood pressure normalization following bilateral nephrectomy and after subsequent kidney transplantation. METHODS AND RESULTS: Clinical data from 14 hypertensive patients were retrospectively assessed. Baseline blood pressure was 175 +/- 33/109 +/- 9 mmHg. Ten patients firstly underwent unilateral nephrectomy, which resulted in a slight increase of blood pressure (185 +/- 22/110 +/- 5 mmHg). One month following bilateral nephrectomy, blood pressure was 167 +/- 23/104 +/- 17 mmHg, at 3 months 159 +/- 42/104 +/- 25 mmHg, and at 6 months 149 +/- 41/96 +/- 30 mmHg. Antihypertensive medication was necessary in 9/14 patients at a 2 year follow-up. Eight patients remained anephric (group I), 6 patients had subsequent kidney transplantation (group II). In group I, blood pressure was 159 +/- 42/93 +/- 17 mmHg and 129 +/- 34/75 +/- 14 mmHg at 3 and 6 months, respectively (p< 0.05 vs. baseline). In group II, blood pressure decreased from 188 +/- 42/ 128 +/- 46 mmHg to 167 +/- 48/113 +/- 32 mmHg at 3 months, but increased after transplantation to 186 +/- 39/118 +/- 33 mmHg. Antihypertensive medication was still necessary in 5 transplanted patients (83%) and in 3 anephric patients (38%). CONCLUSION: Adaptation of the blood pressure response following bilateral nephrectomy is a time requiring process, and long-term antihypertensive medication may still be necessary.

Adolescent↗
PubMed1999

Hirudin elimination by hemofiltration: a comparative in vitro study of different membranes.

BACKGROUND: Recombinant hirudin (r-hirudin) is a highly specific and selective thrombin inhibitor. Since 1997, it has been approved for the treatment of heparin-induced thrombocytopenia (HIT type II). Renal function impairment drastically prolongs the elimination half-life time. In cases of bleeding or overdosage, there is currently no antidote available. Hemofiltration has been reported to be useful in r-hirudin elimination. In this study, we determined sieving coefficients (SCs) and drug clearances for two different hemofilters currently used in clinical medicine and intensive care. METHODS: We developed an in vitro postdilution hemofiltration model using 500 ml heparinized (2 IU unfractionated heparin/ml) fresh human blood and bicarbonate substitution fluid. The investigated membranes were high-flux polysulfone F50 (1.0 m2, Fresenius) and AN69 Nephral 200 (1.05 m2, Hospal Cobe). After equilibration, a bolus of Lepirudin was injected into the postfilter port to achieve a r-hirudin blood level of approximately 15 microg/ml. Serial blood and ultrafiltrate samples were taken for the determination of hirudin levels (chromogenic assay) and control parameters. SC and clearances were calculated according to standard formulae. RESULTS: The observed SCs and clearances differed significantly between F50 and Nephral 200 (0.60+/-0.17 and 21.0+/-5.9 ml/min, respectively, vs. 0.44+/-0.09 and 15.5+/-3.0 ml/min, respectively; P = 0.001). The determination of prothrombin fragments showed no coagulation activation during the experiments. The hematocrit values remained stable. CONCLUSIONS: Our data show that r-hirudin can be eliminated by hemofiltration. The elimination obviously depends on the membrane material with high-flux polysulfone being more effective than AN69. These findings may be important in cases of overdosage and for r-hirudin dosage guidelines in continuous hemofiltration.

Adolescent↗
PubMed1999

Influence of hematocrit on hemostasis in continuous venovenous hemofiltration during acute renal failure.

BACKGROUND: Hematocrit plays a major role in primary hemostasis by influencing blood viscosity and platelet adhesion. During continuous venovenous hemofiltration (CVVH), it is suspected that an increased hematocrit is accompanied by an activation of hemostasis and frequently leads to thromboses in the extracorporeal system. In order to examine this hypothesis, we studied the influence of hematocrit on hemostasis during CVVH. METHODS: Fourteen patients (8 men and 6 women, mean age 65+/-10 years) with acute renal failure undergoing CVVH were prospectively enrolled. Polysulfone hemofilters (AV 600; Fresenius, Oberursel, Germany) were used in all of the patients; blood flow rates were adjusted to 120 ml/min. No blood products and coagulation-related medication, except unfractionated heparin, were applied. Study exclusion criteria included a history of thromboembolism and artificial heart valves. Hemostasis activation markers (fibrinopeptide A, thrombin-antithrombin III complex, beta-thromboglobulin, platelet retention) and hematocrit values were determined before and at three-day intervals during the course of CVVH treatment. RESULTS: The mean hematocrit value (mean +/- SEM) was 29+/-1% (range, 22 to 35%). Patients with hematocrit values of less than 30% (N = 7) were compared with patients with higher hematocrit values (>30%, N = 7). The patients with a lower hematocrit (<30%) showed a stronger activation of hemostasis during CVVH when compared with those with a higher hematocrit (>30%), as indicated by a tendency toward higher values for fibrinopeptide A (25+/-8 vs. 14+/-5 ng/ml, P = 0.35), thrombin-antithrombin III complex (15+/-4 vs. 10+/-2 ng/ml, P = 0.66), and a higher beta-thromboglobulin/creatinine ratio (0.62+/-0.17 vs. 0.48+/-0.12, P = 0.8). CONCLUSION: Contrary to our hypothesis, hematocrit values of more than 30% are not accompanied by an increased hemostasis activation during CVVH. Concerning hemostasis activation, hematocrit values between 30 and 35% may be suitable for patients on CVVH.

Acute Kidney Injury↗
PubMed1998

Hemostasis activation markers in acute renal failure.

Fibrinopeptide A and thrombin-antithrombin III complex were used respectively as markers for in vivo thrombin formation and beta-thromboglobulin as a marker for platelet activation. In cases of acute renal failure (ARF) a heightened plasma concentration in the hemostasis activation markers may occur, because of a renal elimination disturbance, without a previous activation of the hemostasis. In order to check the validity of fibrinopeptide A, thrombin-antithrombin III complex and beta-thromboglobulin as markers for the hemostasis activation in cases of ARF we examined 32 patients prior to renal replacement therapy. A significant rise in fibrinopeptide A (x +/- SD: 34 +/- 22 ng/mL, ref < 3.0), thrombin-antithrombin III complex (19 +/- 15 ng/mL, ref 1.0-4.0) and beta-thromboglobulin (149 +/- 58 U/mL, ref 10-40) was found. None of the parameters examined showed a correlation to the serum creatinine. A correlation was observed respectively between fibrinopeptide A (r = 0.34, p < .05), beta-thromboglobulin (r = 0.39, p < .05) and the beta-thromboglobulin/creatinine coefficient (0.50 +/- 0.30, r = 0.72, p < .001) on the one side and the thrombin-antithrombin III complex on the other. A greater rise in the concentration of all parameters in patients with disseminated intravascular coagulation (DIC) was established, in contrast to patients without DIC (fibrinopeptide A: 44 +/- 31 vs. 32 +/- 20 ng/mL, beta-thromboglobulin: 169 +/- 57 vs. 144 +/- 60 U/mL, thrombin-antithrombin III complex 40 +/- 21 vs. 14 +/- 7 ng/mL, p < .05). Fibrinopeptide A and beta-thromboglobulin/creatinine coefficient in combination with the thrombin-antithrombin III complex can be employed as markers for the activation of hemostasis in cases of ARF there is no direct relationship between restricted kidney function in ARF and the plasma concentration of these markers, which behave similarly in spite of their varying elimination patterns.

Acute Kidney Injury↗
PubMed1997

Selenium deficiency and thyroid function in acute renal failure.

The lethality of acute renal failure exceeds 50% due to multiorgan dysfunction. In such critically ill patients a reduction of thyroid hormone concentrations without clinical symptoms or laboratory evidence of hypothyroidism frequently occurs. Selenium has recently been shown to play a major role in thyroid hormone metabolism. The aim of this study was to investigate the possible influence of selenium on thyroid hormone metabolism in acute renal failure. Changes in thyroid metabolism were related to the severity of multiorgan failure and to the clinical course. Thyroxine (T4), tri-iodothyronine (T3), free-T4, free-T3, thyrotropin (TSH), serum creatinine, and plasma selenium concentrations in 28 patients (mean age 60 +/- 13) with acute renal failure and multiple-organ dysfunction syndrome were determined initially, and every 3 days after hospital admission. The plasma selenium concentration was found to be reduced compared to normal controls (32 +/- 14 vs. 70-120 micrograms/L). T4 (56 +/- 15 nmol/L, normal range 64-148), T3 (1.31 +/- 0.38 nmol/L, normal range 1.42-2.46), free-T3 (3.1 +/- 1.0 pmol/L, normal range 4.7-9.0), and free-T4 (10.8 +/- 4.0 pmol/L, normal range 10.3-25.8) values were low in 50-70% of the patients at the time of presentation. Plasma TSH concentrations were within the normal range (0.59 +/- 0.79 mU/L, normal range 0.25-3.1), and no clinical symptoms of hypothyroidism were observed. T4 concentration was higher in patients who survived acute renal failure compared to nonsurvivors (62 +/- 22 vs. 51 +/- 16 nmol/L, p < 0.05). Plasma selenium concentration was lower in patients with a severe organ dysfunction syndrome (36 +/- 10 vs. 29 +/- 19 micrograms/L) and correlated with the number of organ failures in these patients (r = -0.247, p < 0.05). T4 and free-T4 values paralleled decreasing selenium concentrations (r = 0.35, p < 0.05). Thyroid hormone levels were reduced in patients with acute renal failure without an increase in TSH. An increase in T4 concentrations became apparent during treatment and may be related to a favorable outcome in acute renal failure. Thyroid hormone concentrations paralleled plasma selenium levels, indicating a possible influence of selenium on thyroid function in acute renal failure.

Acute Kidney Injury↗
PubMed1996

Association between heparan sulfate proteoglycan excretion and proteinuria after renal transplantation.

The aim of the study presented here was to investigate whether, in patients showing immediate graft function after renal transplantation, cold-ischemia and reperfusion lead to damage of the glomerular basement membrane and consequently to a loss of heparan sulfate proteoglycans. Loss of these heparan sulfate proteoglycans is a major cause of proteinuria. Time-dependent changes in urinary excretion rates of heparan sulfate proteoglycans but also of total protein, albumin, low- and high-molecular-weight proteins were analyzed quantitatively and by polyacrylamid-gel-electrophoresis in eight patients. Immediately after renal transplantation, severe proteinuria with an excretion rate of up to 251 +/- 108 mg/min was apparent and rapidly declined within 24 h to 4.11 +/- 2.80 mg/min. The gel-electrophoretic pattern showed a nonselective glomerular and tubular proteinuria. The excretion rate of heparan sulfate proteoglycan was increased in this initial reperfusion phase (up to 7 h), most probably because of ischemia- and reperfusion-induced damage of the glomerular basement membrane. The initial nonselective glomerular proteinuria disappeared within 48 h, changing to a mild selective glomerular proteinuria. In this second phase (7 to 48 h), lower levels of heparan sulfate proteoglycan excretion were observed (0.54 +/- 0.54 microgram/min versus 1.66 +/- 1.93 micrograms/min, P < 0.05). However, during the repair process of the glomerular basement membrane, heparan sulfate proteoglycan is synthesized de novo, leading to an increasing heparan sulfate proteoglycan content of the glomerular basement membrane. This second phase is paralleled by the change from a nonselective to a selective glomerular proteinuria. In the third phase, when the heparan sulfate proteoglycan content of the glomerular basement membrane normalizes, glomerular proteinuria was abolished in most of the patients.

Adult↗
PubMed1996

Hemostatic alterations during continuous venovenous hemofiltration in acute renal failure.

In order to determine changes in hemostasis occurring during continuous venovenous hemofiltration (CVVH), we made a prospective study of 14 patients with acute renal failure. Fibrinopeptide A, thrombin-antithrombin III complex, beta-thromboglobulin and platelet retention were determined serially. Fibrinopeptide A (x +/- SD: 33 +/- 20 ng/ml, ref. < 3.0) and thrombin-antithrombin III complex (11 +/- 5 ng/ml, ref. 1.0-4.0) were enhanced prior to commencement of treatment but showed no further increase during therapy. Platelet retention (Hellem II, ref. 60-99%) fell from 39 +/- 32% before treatment to 16 +/- 15% after treatment, while the beta-thromboglobulin/creatinine ratio (ref. 0.23-0.41) rose from 0.39 +/- 0.20 to 0.64 +/- 0.44. Via platelet activation, CVVH leads to a reinforcement of the existing platelet dysfunction (thrombocytopathy), without influencing plasmatic coagulation. In order to analyze the influence of pre-existing hemostatic alterations on filter running time during CVVH, 60 patients were examined retrospectively in a second study. Filter running time, global coagulation tests, fibrinogen, antithrombin III, platelet count and hematocrit were registered daily. There was no significant correlation between filter running time and fibrinogen concentration, thrombin time, platelet count or hematocrit. Apart from filter occlusion, no thrombotic complications were observed. The frequency of filter occlusion increased with falling activated clotting time (ACT) (p < 0.05). Rising platelet count led to an increase in heparin dose (p < 0.05), primarily due to the anti-heparin effect of platelet factor 4.

Acute Kidney Injury↗
PubMed1995

Influence of recombinant human erythropoietin on hematological and hemostatic parameters with special reference to microhemolysis.

Twenty chronic hemodialysis patients with renal anemia (hematocrit < 25%) received recombinant human erythropoietin (40 IU/kg body weight 3 x weekly) intravenously after each dialysis. Prior to and at 4, 8 and 12 weeks after commencement of erythropoietin therapy, hematocrit together with hemostasis and microhemolysis parameters were determined. There were significant increases in hematocrit, platelet count and platelet retention, but a significant fall in the initial clearly prolonged bleeding time. Free plasma hemoglobin likewise increased. Conversely, lactate dehydrogenase, prothrombin time, fibrinogen, antithrombin III activity, protein C activity and protein S concentration were all unaltered. The positive effect on bleeding time and platelet retention is most probably caused by an increase in adenosine diphosphate due to the hematocrit-dependent rise in the blood shear stress via physiologic microhemolysis (raised free plasma hemoglobin).

Adult↗
PubMed1992

[Toxic myopathy with kidney failure as a colchicine side effect ifn familial Mediterranean fever].

A 24-year-old woman with familial Mediterranean fever (FMF) had for one year been treated with colchicine, 1 mg daily, for repeated bouts of fever, abdominal pain and arthritis. She was also known to have renal amyloidosis. Lately she had developed gastrointestinal symptoms, muscle pain and obvious, predominantly proximal muscular weakness in both legs. The cause of the symptoms was rhabdomyolysis with an increased creatinine activity of 1000 U/l and marked myoglobinuria (1600 micrograms/l), as well as renal failure with normal uric acid and a creatinine clearance of 3 ml/min per 1.73 m2. Serum creatinine concentration was 970 mumol/l, urea 34 mmol/l. Muscle biopsy corresponded to a subacute necrotizing myopathy with vacuole formation, signs typical of toxic damage. Renal biopsy confirmed advanced amyloidosis. The colchicine dose was reduced to 0.5 mg/d. The renal failure responded to conservative treatment. The myopathy symptoms receded within 4 weeks, creatinine clearance rising to 25 ml/min per 1.73 m2. 12 months after reduction of the colchicine dose the patient was without any FMF-related symptoms.

Acute Kidney Injury↗