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J Passlick-Deetjen

Publications and source records attributed to J Passlick-Deetjen.

At least 37 records · Page 2Linked to original sources
PubMed1997

LDL hemoperfusion--a new procedure for LDL apheresis: first clinical application of an LDL adsorber compatible with human whole blood.

To date, lipid apheresis procedures can remove low-density lipoprotein (LDL) cholesterol (LDL-C) only from plasma. Thus, initially plasma has to be separated from the blood cells, which increases the costs and complexity of the extracorporeal circuit. This paper describes the first clinical application of a new LDL adsorber that eliminates LDL directly from whole blood. The goal of this pilot study was to test the efficacy, safety, and feasibility of direct lipoprotein adsorption in patients. In a 2 center Phase II clinical trial, 12 hypercholesterolemic patients suffering from overt coronary or peripheral artery disease were treated once with LDL hemoperfusion. The new LDL adsorber (DALI, Fresenius, St. Wendel, Germany) contained 480 ml of polyacrylate coated polyacrylamide gel. The anticoagulation consisted of an initial heparin bolus followed by an acid citrate dextrose (ACD)-A infusion during the treatment. The processing of nearly 1 patient blood volume resulted in a reduction of LDL-C by 45 +/- 8% and triglycerides by 23 +/- 20%. HDL-C, fibrinogen, and cell counts were not significantly influenced. In a subgroup of 5 patients who exhibited elevated lipoprotein (a) (Lp[a]) levels, Lp(a) reduction was 43 +/- 15% (all results corrected for plasma volume shifts). The sessions were clinically uneventful; the system was technically safe and easily handled. In conclusion, short-term LDL hemoperfusion by the DALI proved to be a safe, effective, and simple procedure for the treatment of patients suffering from symptomatic recalcitrant hypercholesterolemia. The present study represents a solid basis for the clinical long-term evaluation of this new technique in the future.

Acrylic Resins↗
PubMed1997

Comparison of a lactate-versus acetate-based hemofiltration replacement fluid in patients with acute renal failure.

The objective of the study was to determine the impact of a lactate- and an acetate-based hemofiltration replacement fluid (HF) on the acid-base status in patients with acute renal failure (ARF) and continuous venovenous hemofiltration (CVVH). The prospective, cohort study was carried out in the intensive care unit of the Heinrich-Heine University Hospital, Düsseldorf, FRG. Subjects were 84 critically ill patients with ARF and CVVH. Fifty-two patients were subjected to lactate-based (group 1) and 32 to acetate-based hemofiltration (group 2). Thirty-eight patients had a septic, 46 a cardiovascular origin of the ARF. Creatinine, BUN, serum bicarbonate, arterial pH, lactate and APACHE II score were noted daily. Mean CVVH duration was 9.8 +/- 8.1 days; mortality was 65%. The groups did not differ with regard to the main clinical parameters. Lacate-based hemofiltration led to significantly higher serum bicarbonate and arterial pH values as compared to the acetate-based hemofiltration. Baseline serum bicarbonate values were 23.3 +/- 8.3 mmol/L in group 1 and 21.6 +/- 4.3 mmol/L in group 2 (NS); values at 48 h after initiating CVVH treatment were 25.7 +/- 3.8 mmol/L and 20.6 +/- 3.1 mmol/L, respectively (p < 0.001). Arterial pH prior to CVVH treatment was 7.36 +/- 0.1 in group 1 and 7.34 +/- 0.1 in group 2 (NS), and 7.43 +/- 0.07 versus 7.37 +/- 0.06 (p < 0.001) on day 2. These findings were maintained throughout therapy. While a lack of increase in serum bicarbonate and arterial pH was correlated to a poor prognosis in lactate-based hemofiltration, no such observation could be made in acetate-based hemofiltration. Septic patients did not differ in their acid-base status from nonseptic patients. Lactic acidosis occurred in 8 septic patients irrespective of the substitution fluid. All 8 patients died. There was a significant increase in HCO3 and arterial pH values in lactate-based as compared to acetate-based HF.

APACHE↗
PubMed1996

Correction of acidosis in CAPD decreases whole body protein degradation.

Correction of acidosis in CAPD decreases protein degradation and synthesis but has no effect on leucine oxidation. The effect of the correction of metabolic acidosis in CRF patients treated with CAPD was determined from the kinetics of infused L-[1-13C]leucine. Seven CAPD patients were studied before (acid) and after correction of acidosis (bicarbonate) (pH:acid 7.39 +/- 0.01, bicarbonate 7.41 +/- 0.01, P = 0.005). Leucine appearance from body protein (PD) [corrected] and leucine disappearance into body protein (PS) [corrected] decreased significantly with correction of acidosis. (PS: acid 211.7 +/- 9.8, bicarbonate 142.3 +/- 4.2 micromol x kg-1 x hr-1, P < 0.001; PD: acid 200.6 +/- 8.5, bicarbonate 132.4 +/- 3.7 micromol x kg-1 x hr-1, P < 0.001). There was no significant change in leucine oxidation or plasma amino acid concentrations. These results demonstrate that optimal correction of acidosis in CAPD is beneficial in terms of protein turnover.

Acidosis↗
PubMed1996

Biocompatibility of bicarbonate buffered peritoneal dialysis fluids: influence on mesothelial cell and neutrophil function.

The present study compares the effects of lactate and bicarbonate buffered PDF on human neutrophil (PMN) and human peritoneal mesothelial cell (HPMC) viability and function. Acute exposure of PMN to lactate buffered PDF at pH 5.5 (CAPD 2, 1.5% and CAPD 3, 4.25% glucose) resulted in significant reductions in cellular ATP levels, the phagocytosis of serum treated zymosan (STZ) and respiratory burst activation (CL). Exposure of PMN to bicarbonate buffered PDF (BIC 20, 1.5% glucose and BIC 30, 4.25% glucose both at pH 7.2) had no significant effect on cell viability or the CL response. Phagocytosis was, however, depressed significantly more following exposure to BIC 30 than BIC 20. PMN cellular ATP levels and phagocytosis were significantly better in cells exposed to BIC 30 than to CAPD 3 at pH 7.4 (P = 0.043 for both). Pre-exposure of HPMC to CAPD 2, CAPD 3 or BIC 30 for 30 minutes resulted in a significant reduction in cellular ATP content compared to control medium. Pre-exposure to BIC 20 did not result in a reduction in HPMC ATP levels. HPMC synthesis of IL-6 was unaffected by 15 or 30 minutes pre-exposure to BIC 20 or BIC 30, in contrast pre-exposure to CAPD 2 or CAPD 3 for 15 or 30 minutes resulted in a significant reduction in stimulated IL-6 synthesis (24.5 +/- 3.01 and 32.3 +/- 5.0 vs. 43.9 +/- 10 pg/microgram cell protein in M199, N = 6; P = 0.02). Neutralization of the pH of CAPD 2 and CAPD 3 resulted in normalization of HPMC IL-6 secretion. Analysis of IL-6 mRNA expression in control, BIC 20 and 30 pre-treated HPMC subsequently stimulated with IL-1 beta revealed no differences in the expression of the IL-6 specific 465 base pair transcripts. The improved cellular function in bicarbonate buffered PDF indicates potentially improved host defence status and preservation of the peritoneal membrane in CAPD patients.

Adenosine Triphosphate↗
PubMed1996

What is the appropriate dialysate calcium concentration for the dialysis patient?

Recently, there has been a trend to lower dialysate calcium concentrations because of the frequent occurrence of hypercalcaemia with the use of calcium-containing phosphate binders. No single dialysate calcium concentration is available which suits all dialysis patients. The risk of hypercalcaemia depends on intradialytic (diffusive and convective) calcium transport and interdialytic calcium balance (negative or positive intestinal balance). Low dialysate calcium concentrations expose the patient to the risks of negative calcium balance and increase in parathyroid hormone concentration, particularly if patients are non-compliant with the intake of calcium-containing phosphate binders.

Calcium↗
PubMed1996

Bicarbonate: the alternative buffer for peritoneal dialysis.

For a long time bicarbonate, the physiological buffer of the body, was suggested to be the best buffer for peritoneal dialysis. However, since the production of bicarbonate-containing solutions is associated with technical problems, lactate was favored. To avoid the well-known disadvantages of lactate solution concerning biocompatibility and possible metabolic side effects, different attempts have been made to use bicarbonate as a buffer in peritoneal dialysis. One of the major approaches was the total replacement of lactate by bicarbonate combined with storage of the fluid in a specially designed double-chamber bag. Further solutions of the above-mentioned problem were the on-line preparation of bicarbonate fluids for intermittent peritoneal dialysis, the addition of bicarbonate just before use, the combination of bicarbonate with organic acids, or its combination with the dipeptide glycylglycine as a stabilizing agent. By now, the beneficial effect of the neutral bicarbonate fluid, for example, on cell viability and cell functions, has been demonstrated in many different in vitro and animal studies. However, only few reports on clinical experience have been published. These investigations demonstrated independently that bicarbonate fluids diminish inflow pain, are well tolerated by the patients, and may correct metabolic acidosis of uremic patients. A controlled randomized multicenter trial using 34 mmol/L bicarbonate for at least three months confirmed that bicarbonate is as efficacious as lactate in equimolar concentrations. Concomitant investigations on energy metabolism and redox state of red blood cells and phospholipid secretion of mesothelial cells additionally demonstrated the improvement of cell function with bicarbonate solutions. For some patients with severe metabolic acidosis the bicarbonate concentration used in the multicenter trial seemed to be too low. Thus, a fluid containing a higher bicarbonate concentration was tested in a pilot study resulting in the expected significant increase of arterial bicarbonate levels. In summary, bicarbonate-containing peritoneal dialysis solutions are a promising alternative to lactate, especially if bicarbonate concentrations are adjusted individually to the patient's need.

Acid-Base Equilibrium↗
PubMed1996

Prescription of calcium concentration and PTH control.

The use of calcium-containing oral phosphate binders, introduced in an effort to avoid aluminum-containing compounds, had led to more frequent episodes of hypercalcemia. This prompted the introduction of continuous ambulatory peritoneal dialysis (CAPD) solutions with diminished calcium content. The problems raised by such solutions included stimulation of parathyroid hormone (PTH) secretion and long-term maintenance of calcium balance. Some of these issues can today be answered on the basis of controlled prospective trials. Variability of the rate of intestinal calcium uptake of bone turnover, of baseline parathyroid activity, and other factors make it necessary to individualize the indication for the use of CAPD solutions with low calcium content.

Calcium↗
PubMed1995

Low dialysate calcium in continuous ambulatory peritoneal dialysis: a randomized controlled multicenter trial. The Peritoneal Dialysis Multicenter Study Group.

Hypercalcemia is a common complication in continuous ambulatory peritoneal dialysis (CAPD) patients treated with calcium-containing phosphate binders and using the standard dialysate calcium concentration of 3.5 mEq/L (SCa). Lowering the dialysate calcium was proposed to overcome this problem. The current randomized controlled multicenter study was designed to investigate efficiency and safety of a low calcium dialysate (2.00 mEq/L; LCa) compared with SCa (3.5 mEq/L) in CAPD patients. After an 8-week run-in period, 103 stable CAPD patients, 68 men, 35 women, aged 54.5 years (range, 20 to 77)) were randomly allotted to treatment with either LCa or SCa. All patients received calcium carbonate as oral phosphate binder to achieve serum phosphate levels < 6.2 mg/dL. If persistent hypercalcemia arose, CaCO3 was replaced by Al(OH)3 until normocalcemia was achieved. All patients received 0.25 microgram calcitriol/d. Parameters monitored included total and ionized serum calcium, serum phosphate, phosphate binder intake, incidence of hypercalcemia, serum aluminium, intact parathyroid hormone (1,84PTH), osteocalcin, alkaline phosphatase, bone mineral density and hand skeletal x-ray. Primary end points were (a) number of hypercalcemic episodes, (b) tolerated doses of calcium-containing phosphate binders, and (c) 1,84PTH. After 6 months of therapy, total and ionized calcium were lower in LCa patients (total Ca:9.6 v 10.08 mEq/L, P = 0.005; iCa: 4.76 v 5.15 mg/dL; P = 0.013). In the LCa group, significantly fewer episodes of hypercalcemia were recorded (total S-calcium > 10.8 mg/dL: LCa 24 v SCa 86 episodes; P < 0.005). Use of LCa permitted the administration of more CaCO3 (mean daily tablet number: LCa, 5.9 v SCa, 4.2; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1995

In vitro effects of low-calcium peritoneal dialysis solutions on peritoneal macrophage functions.

The use of low-calcium peritoneal dialysis solutions (PDS) for continuous ambulatory peritoneal dialysis is becoming widely accepted to reduce the risk of serum hypercalcemia in patients taking calcium salts as phosphate binders. We compared the in vitro effects of low-calcium PDS (1,000 mumol calcium/L), calcium-free buffer, and buffers with increasing calcium concentrations (500 to 5,000 mumol calcium/L) on peritoneal macrophage (PMO) functions. Peritoneal macrophages isolated from 10 continuous ambulatory peritoneal dialysis patients were incubated in the different solutions and tested for phagocytic and killing capacity, superoxide generation (cytochrome-C reduction and lucigenin-enhanced chemiluminescence), and the rate of myeloperoxidase-dependent oxidative metabolism (luminol-enhanced chemiluminescence). All functions of the PMO incubated in calcium-free buffer were significantly suppressed compared with the PMO incubated in calcium buffers. No dose-dependent increase of a single PMO function could be found after incubating the PMO in calcium buffer with increasing concentrations. Incubation of PMO in otherwise identical PDS containing 1,000, 1,450, or 1,750 mumol calcium/L did not result in significantly different PMO functions. Acidic PDS (pH 5.3 to 5.5) suppressed all measured PMO functions as compared with their neutralized counterparts (pH 7.4), irrespective of the calcium concentration. Results of our in vitro study show that low-calcium PDS does not suppress PMO functions any more than standard-calcium PDS (1,750 mumol calcium/L) does.

Acridines↗
PubMed1994

In vitro effects of amino-acid-based versus glucose-based continuous ambulatory peritoneal dialysis fluids on peritoneal macrophage function.

We studied the in vitro effects of peritoneal dialysis fluids (PDF) containing 1 and 1.5% amino acids (AA) as compared to approximately equiosmolar glucose (GLU)-based PDF (1.5 and 4.25%) and control buffer, respectively, on peritoneal macrophage (PMO) function. The media were tested at original pH (5.3-5.5) and after pH adjustment to 7.4. PMO were isolated from the effluents of 10 on continuous ambulatory peritoneal dialysis (CAPD) patients and tested for luminol- and lucigenin-enhanced chemiluminescence (CL), superoxide generation measured by cytochrome c reduction, killing capacity and phagocytosis after incubation (30 min, 37 degrees C) in the PDF used. All AA-based PDF exhibited a statistically significant depressive effect on integral CL response, O2- production and bacterial killing of PMO at pH 7.4 in comparison with pH-adjusted GLU-based PDF of similar osmolality and buffer. Exposure of PMO to acidic AA-based media did not result in a significantly different suppression of the oxidative metabolism and the killing capacity as compared to fresh GLU-based fluids. Phagocytosis of PMO did not show significant differences after incubation in the solutions studied. Thus, the AA-based PDF employed compromise the oxidative metabolism and the killing capacity of PMO at pH 7.4 in vitro significantly more than GLU-based fluids. Since pH-identical and almost equiosmolar PDF were compared, the specific composition of the AA-based fluids, especially the high content of lactate and several essential AA, could be responsible for this detrimental impact.

Amino Acids↗
PubMed1994

Bicarbonate-based dialysis solution preserves granulocyte functions.

OBJECTIVE: Intraperitoneal phagocytes play an important role in local defense in preventing continuous ambulatory peritoneal dialysis (CAPD) peritonitis. This study therefore investigates the effect of the conventional lactate-based dialysis solution-pH 5.2 (LBDS-pH 5.2) and a bicarbonate-based dialysis solution (BBDS) on various cell functions. DESIGN: We studied C5a-induced actin polymerization (AP) as a measure of the cytoskeletal alteration, phagocytosis of zymosan particles, and chemotaxis in neutrophils incubated in either LBDS-pH 5.2, LBDS-pH 7.4, or BBDS-pH 7.4, comparing the data with cells treated with phosphate-buffered saline-pH 7.4 (PBS-pH 7.4) as a control. SUBJECTS: Polymorphonuclear neutrophils (PMNs) were isolated from the blood of healthy donors and incubated with dialysis solution prior to the experiment. RESULTS: C5a-induced AP was dramatically inhibited in PMNs incubated in LBDS-pH 5.2, paralleled by a complete inhibition of phagocytosis and C5a-induced chemotaxis. In comparison, BBDS improved AP to values above the control and also nearly normalized phagocytosis. Chemotaxis markedly improved in cells treated with the low glucose-containing BBDS (Bic 20), containing high glucose concentrations (Bic 30). CONCLUSION: In comparison with conventional lactate-based dialysis solution-pH 5.2, bicarbonate-based dialysis solution at low osmolality better preserves neutrophil functions that involve the cytoskeleton.

Actins↗
PubMed1994

In-vitro biocompatibility of alternative CAPD fluids; comparison of bicarbonate-buffered and glucose-polymer-based solutions.

Evidence is accumulating that conventional dialysis fluids for CAPD are incompatible with peritoneal host defence. We therefore investigated the effect of alternative CAPD fluids on mononuclear leukocyte (PBMC) viability and cytokine production in vitro. Fluids tested were bicarbonate-buffered solutions containing 1.5% or 4.25% glucose, 7.5% glucose polymer dialysis fluid (GPDF), and conventional 1.5% glucose fluid (G1.5%). PBMC were stimulated (2 h, 37 degrees C) in the different test fluids with a clinical isolate of Staphylococcus epidermidis or Escherichia coli lipopolysaccharide. The cytokines TNF alpha and IL-6 in PBMC supernatants were measured by specific enzyme immunoassays. Induction of cytokine messenger RNA was evaluated by reverse transcription-polymerase chain reaction. Conventional G1.5% (pH 5.5) inhibited cytokine release from activated PBMC by > 95%, whereas cell responses in low-glucose bicarbonate fluid were not significantly reduced. In contrast, high-glucose bicarbonate fluid exerted > 80% inhibition despite its neutral pH. GPDF was inhibitory at its initial low pH, whereas cytokine release was restored following pH neutralization. Cytokine mRNA expression was suppressed by conventional G1.5% fluid and by high-glucose bicarbonate fluid. These data indicate that pH neutralization leads to a substantial improvement of dialysis fluid biocompatibility; however, hyperosmolality and/or high glucose content inhibit cell responsiveness even at normal pH. Replacement of glucose by glucose polymer might prove beneficial provided that the initial low pH is neutralized.

Actins↗
PubMed1993

Short-term clinical study with bicarbonate-containing peritoneal dialysis solution.

OBJECTIVE: The evaluation of the efficacy, adequacy, clinical tolerance, and safety of a new bicarbonate continuous ambulatory peritoneal dialysis (CAPD) solution. DESIGN AND PATIENTS: A 6-week cross-over clinical study in 6 stable CAPD patients was performed. After a control period (2 weeks) with a standard CAPD solution (lactate, 35 mmol/L), a two-chamber bag containing 34 mmol/L of bicarbonate was used for 4 weeks. A breakable valve divided the two chambers, one containing bicarbonate and the other calcium. The two solutions were mixed just before use, thus avoiding the calcium and magnesium carbonate precipitation. RESULTS: No differences between control and study periods were found for blood urea nitrogen, creatinine, total proteins, albumin, total and ionized calcium, phosphate, sodium, potassium, chlorine, and hemoglobin. Blood bicarbonate significantly increased from 21.25 +/- 2.02 to 23.36 +/- 1.15 (p < 0.05) during the study. The peritoneal equilibration tests for urea nitrogen, creatinine, proteins, sodium, potassium, and glucose were slightly reduced during bicarbonate dialysate, but this effect was compensated for by a slight increase of ultrafiltration, thus keeping peritoneal clearances constant. Residual renal function did not change during the study. No side effects occurred during the bicarbonate period. CONCLUSION: A CAPD bicarbonate solution is effective in uremic acidosis correction, does not affect dialysis adequacy, is safe, and well tolerated.

Adult↗
PubMed1993

Transperitoneal calcium mass transfer using dialysate with a low calcium concentration (1.0 mM).

Lower dialysate calcium concentrations were recently proposed to overcome the risk of hypercalcemia in continuous ambulatory peritoneal dialysis (CAPD) patients on calcium-containing phosphate binders and/or vitamin D metabolites using the standard dialysate calcium concentration (SCa) of 1.75 mM. To assess transperitoneal calcium mass transfer (CaMT) in CAPD patients using a dialysate with a low calcium concentration (LCa, 1.00 mM), 18 stable patients were randomly allocated to receive either LCa or SCa. CaMT was assessed over 4 hours using 2L dialysate bags with three different dialysate glucose concentrations (1.5%, 2.3%, 4.25%). Total serum calcium (tCa), ionized calcium (iCa), and the exact dialysate volume were measured before and after the 4-hour dwell. A sample of the drained dialysate was obtained to measure the dialysate calcium concentration. The tCa and iCa levels were not significantly different in both groups prior to and did not change throughout the test. CaMT (median/range) was -0.64 mmol/exchange (-0.35(-)-1.29 mmol/exchange) using LCa with 1.5% glucose compared to 0.23 mmol (-0.18-0.87 mmol) with SCa (p < 0.0001). CaMT was negatively correlated to iCa and ultrafiltration volume [4.25%: LCa-1.22 (-0.84(-)-1.9); SCa -0.43 (-1.35-0.13); p < 0.001]. In summary, LCa results in a loss of calcium into the dialysate even at low ultrafiltration volumes and serum iCa levels. This might facilitate the prevention and therapy of renal osteodystrophy with calcium-containing phosphate binders and calcitriol. However, patients using LCa must be carefully monitored for calcium homeostasis and bone turnover.

Aged↗