fibrin and Kidney-Failure--Chronic

Peritoneal dialysis is a renal substitutive therapy used in an increasing number of patients with end-stage renal failure as it allows greater freedom to perform daily activities. Peritoneal dialysis catheter obstruction is a significant non-infectious complication of peritoneal dialysis. We describe three cases of peritoneal dialysis catheter obstruction with complete fibrin casts, its surgical management and a review of the literature in management techniques and have proposed an algorithm to guide clinical practise when a complete intraluminal peritoneal dialysis catheter obstruction is suspected.

Topics: Aged; Catheter Obstruction; Catheters, Indwelling; Fibrin; Humans; Kidney Failure, Chronic; Male; Middle Aged; Peritoneal Dialysis; Therapeutic Irrigation; Treatment Outcome; Vascular Surgical Procedures

Topics: beta-Thromboglobulin; Biocompatible Materials; Blood Coagulation; Blood Platelets; Cell Adhesion; Fibrin; Humans; Infections; Kidney Failure, Chronic; Leukocytes; Leukopenia; Lymphocyte Activation; Membranes, Artificial; Platelet Activation; Platelet Adhesiveness; Platelet Factor 4; Polymethyl Methacrylate; Renal Dialysis; Respiratory Burst; Thrombin; Thromboxane A2

Topics: Adrenal Glands; Aldosterone; Anemia; Biopsy, Needle; Cholinesterases; Erythropoietin; Fibrin; Graft Rejection; Humans; Hyperparathyroidism; Hypertension; Juxtaglomerular Apparatus; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Polycythemia; Proteinuria; Radioisotope Renography; Renin; Transplantation, Homologous; Ultrasonography

Topics: Abruptio Placentae; Adrenal Glands; Aminocaproates; Animals; Basement Membrane; Biopsy; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Platelets; Brain; Female; Fibrin; Fibrinogen; Fibrinolysis; Fluorescent Antibody Technique; Hemorrhage; Hemorrhagic Disorders; Heparin; Humans; Hypertension, Malignant; Kidney Cortex Necrosis; Kidney Failure, Chronic; Kidney Glomerulus; Liver; Maternal Mortality; Microscopy, Electron; Myocardium; Placental Extracts; Pre-Eclampsia; Pregnancy; Rabbits; Shwartzman Phenomenon; Thromboplastin; Thrombosis

The aim of this study was to determine the clinical and histologic outcomes related to transplanting kidneys from deceased donors with glomerular fibrin thrombi (GFT). We included all cases transplanted between October 2003 and October 2014 that had either a preimplantation biopsy or an immediate postreperfusion biopsy showing GFT. The study cohort included 61 recipients (9.9%) with GFT and 557 in the control group without GFT. Delayed graft function occurred in 49% of the GFT group and 39% in the control group (p = 0.14). Serum creatinine at 1, 4, and 12 months and estimated GFR at 12 months were similar in the two groups. Estimated 1-year graft survival was 93.2% in the GFT group and 95.1% in the control group (p = 0.22 by log-rank). Fifty-two of the 61 patients in the GFT group (85%) had a 1-month protocol biopsy, and only two biopsies (4%) showed residual focal glomerular thrombi. At the 1-year protocol biopsy, the prevalence of moderate to severe interstitial fibrosis and tubular atrophy was 24% in the GFT group and 30% in the control group (p = 0.42). We concluded that GFT resolves rapidly after transplantation and that transplanting selected kidneys from deceased donors with GFT is a safe practice.

Topics: Adult; Cadaver; Female; Fibrin; Follow-Up Studies; Glomerular Filtration Rate; Graft Rejection; Graft Survival; Humans; Kidney Failure, Chronic; Kidney Function Tests; Kidney Glomerulus; Kidney Transplantation; Male; Middle Aged; Prognosis; Retrospective Studies; Risk Factors; Thrombosis; Tissue Donors

Patients with end-stage renal disease (ESRD) suffer from high mortality rates of cardiovascular diseases, conditions closely linked to the magnitude of their chronic low-grade inflammation. As heparins have been suggested to possess anti-inflammatory properties, we set out to investigate the impact of long-term treatment with intraperitoneal heparin on local and systemic inflammation in peritoneal dialysis (PD) patients.. In a double-blinded cross-over study, 21 PD patients with ESRD were randomised to inject either 4,500 anti-Xa IU tinzaparin or placebo (isotonic saline) into their morning dialysis bags every day for two periods of 3 months separated by a 1-month wash-out period. Blood and dialysate samples were analysed for inflammatory markers at the start and end of each treatment period. In dialysate, the appearance rates of the inflammatory markers were calculated to adjust for ultrafiltration variations.. Eleven patients completed the trial. Treatment with intraperitoneal tinzaparin was accompanied with a median 25.8% reduction of the plasma C-reactive protein concentration (p = 0.032), a 7.3% reduction of the plasma fibrinogen concentration (p = 0.042) and a 54.5% reduction of the dialysate interleukin 6 appearance rate (p = 0.007) compared with placebo.. Long-term treatment with intraperitoneal tinzaparin of ESRD patients on PD reduces local and systemic concentrations of inflammatory markers.

Topics: Adult; Aged; C-Reactive Protein; Cross-Over Studies; Double-Blind Method; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Heparin, Low-Molecular-Weight; Humans; Inflammation; Injections, Intraperitoneal; Kidney Failure, Chronic; Male; Middle Aged; Tinzaparin

To examine whole blood coagulation in uremic patients presenting for surgery with the thromboelastogram and the Sonoclot analyzer.. Prospective, observational study.. Operating rooms of a university-affiliated hospital.. 30 ASA physical status II and III patients with chronic renal failure, and 30 age-matched and gender-matched patients with normal renal function, presenting for elective surgery.. Blood sampling for thromboelastograph and Sonoclot analysis immediately after anesthetic induction, prior to surgical incision.. Thromboelastographic indices of coagulation, reflecting coagulation factor function (R time), fibrinogen-platelet interaction (K time and alpha angle), and qualitative platelet function (maximum amplitude) were hypercoagulable in the uremic group compared with the control group (p < 0.05). Fibrinolysis (%) was decreased in the uremic group (p < 0.05). Fibrin formation (initial slope) and platelet function (time to peak) of the Sonoclot trace also were hypercoagulable in the uremic group (p < 0.05).. The high incidence of arteriovenous graft and fistulae thromboses in uremic patients belies in vitro laboratory evidence of platelet dysfunction. We have demonstrated perioperative hypercoagulability in uremic patients with viscoelastic measures of whole blood coagulation. These data suggest that traditional concern for coagulopathy and platelet dysfunction in uremic patients may require re-assessment in light of this "pro-thrombotic" state.

Topics: Adult; Blood Coagulation Disorders; Blood Viscosity; Elective Surgical Procedures; Female; Fibrin; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prospective Studies; Thrombelastography; Uremia

The role of Indobufen in preventing the formation of microthrombi on hemodialysis membranes has been investigated in 18 patients in a placebo controlled randomized double-blind cross-over study. All patients had been on regular maintenance hemodialysis for at least 3 months. Indobufen was given as 100 mg b.d. and 200 mg b.d. each for a 7 day period with a 7 day wash-out period between the treatments. Both Indobufen regimens prevented the fall in platelet count, reduced the increase in plasma BTg levels during dialysis, increased the post dialysis plasma heparin levels (p less than 0.05) and inhibited pre-dialysis platelet aggregation with collagen (p less than 0.05), when compared with placebo treatment. Scanning electron microscopy demonstrated minimal fibrin and reduced platelet deposition following Indobufen treatment. There was no difference in the effect of 100 mg b.d. and 200 mg b.d. Indobufen doses. The drug was well tolerated, despite the relatively high levels measured, only one patient withdrew because of side effects. This study indicates that Indobufen when added to a routine hemodialysis treatment schedule, can significantly reduce platelet activation and the thrombus formation on the hemodialysis membranes.

Topics: Blood Platelets; Clinical Trials as Topic; Double-Blind Method; Female; Fibrin; Humans; Isoindoles; Kidney Failure, Chronic; Male; Membranes, Artificial; Phenylbutyrates; Platelet Adhesiveness; Random Allocation; Renal Dialysis; Thrombosis

End-stage renal disease (ESRD) is a condition accompanied by increased inflammation, oxidative stress, risk of cardiovascular complications, and coagulopathies. The structure of fibrinogen and characteristics of fibrin from plasma samples of ESRD patients on peritoneal dialysis (PD) was investigated. Fibrinogen from ESRD patients had a higher degree of carbonylation than fibrinogen from healthy individuals. The Aα chain was the most susceptible to oxidation, followed by the Bβ chain, whereas the γ-chain was the most resistant to oxidation. Spectrofluorimetric analysis suggested a higher extent of modification of amino acid side chains in fibrinogen from ESRD patients. The tertiary structure of fibrinogen was more affected than its secondary structure. The kinetics (time and rate) of fibrinogen coagulation did not differ between the tested groups. Fibrin prepared from the isolated fibrinogen had a similar structure in both groups. Our results confirm that oxidation and structural alterations of fibrinogen occur in ESRD patients on PD, although these modifications produce no direct effect on the fibrin formation. Taking into account that some patients suffer from bleeding, whereas others develop thrombotic complications, further research on this subject is required to identify other components and processes that contribute to the outcome.

Topics: Adult; Aged; Aged, 80 and over; Blood Coagulation; Female; Fibrin; Fibrinogen; Humans; Kidney Failure, Chronic; Male; Middle Aged; Oxidation-Reduction; Oxidative Stress; Peritoneal Dialysis; Protein Carbonylation; Protein Structure, Secondary; Protein Structure, Tertiary; Young Adult

Topics: Aged, 80 and over; Anti-Bacterial Agents; Catheter-Related Infections; Catheterization, Central Venous; Catheters, Indwelling; Central Venous Catheters; Device Removal; Echocardiography, Transesophageal; Endocarditis, Bacterial; Enterococcus faecalis; Female; Fibrin; Gram-Positive Bacterial Infections; Humans; Kidney Failure, Chronic; Predictive Value of Tests; Renal Dialysis; Thrombosis; Treatment Outcome

Topics: Catheters, Indwelling; Equipment Failure; Female; Fibrin; Humans; Kidney Failure, Chronic; Laparoscopy; Peritoneal Dialysis, Continuous Ambulatory; Young Adult

Haemodialysis patients are at an increased risk of cardiovascular (CV) morbidity and mortality. Both end-stage renal disease (ESRD) and thromboembolic coronary events have been shown to be associated with the formation of dense fibrin clots resistant to fibrinolysis. The aim of the present study was to investigate the effect of long-term haemodialysis on clot structure/function and analyse an influence of markers of inflammation, oxidative stress and lipoprotein(a). We sought also to investigate if clot features might be related to CV events and mortality in haemodialysis patients. Subjects and methods. In 33 patients (19 males, 14 females), aged 27 to 89 years, on long-term haemodialysis and 33 age- and sex-matched apparently healthy controls, we investigated fibrin clot properties and susceptibility to lysis using recombinant tissue plasminogen activator by using permeation and turbidity assays.. Haemodialysis patients produced fibrin clots that had less porous structure (P < 0.0001) were less susceptible to fibrinolysis (P < 0.0001), began fibrin protofibril formation more quickly (P < 0.0001) and showed increased overall fibre thickness (P < 0.0001) compared with controls. Clot permeability and lysis time correlated with F2-isoprostanes (P < 0.01), Lp(a) (P < 0.0001) and fibrinogen (P < 0.01). None of the clot variables showed associations with the duration of haemodialysis treatment or the cause of ESRD. During a 36-month follow-up, 10 CV deaths were recorded. Mortality was associated with reduced clot permeability (P < 0.0001), prolonged lysis time (P < 0.0001), faster fibrin protofibril formation (P = 0.0004), thicker fibres (P < 0.0001) and increased fibrin clot mass (P < 0.0001).. Unfavourably altered clot properties can be detected in haemodialysis patients and may be associated with increased CV mortality.

Topics: Adult; Aged; Aged, 80 and over; Blood Coagulation; Cardiovascular Diseases; Case-Control Studies; Cohort Studies; Coronary Thrombosis; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolytic Agents; Humans; Kidney Failure, Chronic; Long-Term Care; Male; Middle Aged; Nephelometry and Turbidimetry; Permeability; Probability; Reference Values; Renal Dialysis; Risk Assessment; Statistics, Nonparametric; Survival Analysis

Fibrin clots with reduced permeability, increased clot stiffness and reduced fibrinolysis susceptibility may predispose to cardiovascular disease (CVD). Little is known, however, about the structure of fibrin clots in patients with end-stage renal disease (ESRD). These patients suffer from a high risk of CVD in addition to their chronic low-grade inflammation. Using permeability, compaction and turbidity studies in 22 ESRD patients and 24 healthy controls, fibrin clots made from patient plasma were found to be less permeable (p < 0.001), less compactable (p < 0.001), and less susceptible to fibrinolysis (p < 0.001) than clots from controls. The maximum rate of turbidity increase was also higher for the patients than controls (p < 0.001), and scanning electron microscopy revealed higher clot density of fibrin fibers in clots from patients than clots from controls (p < 0.001). Patients had higher plasma concentrations of fibrinogen, C-reactive protein and interleukin 6 than controls. These plasma markers of inflammation correlated significantly with most of the fibrin structure characteristics observed in the patients. In contrast, plasma markers of azothemia showed no such correlations. The results suggest that in ESRD patients fibrin clots are significantly different from healthy controls, and that the fibrin structure characteristics in the patients are associated primarily with the inflammatory plasma milieu rather than with level of azothemia.

Topics: Azotemia; Biomarkers; Blood Coagulation; Case-Control Studies; Female; Fibrin; Fibrinolysis; Humans; Inflammation; Kidney Failure, Chronic; Male; Microscopy, Electron, Scanning; Middle Aged; Nephelometry and Turbidimetry; Permeability

Scleroderma renal crisis (SRC) can lead to end-stage renal disease (ESRD) and subsequent need for dialysis and/or renal transplantation. We review all reported cases of renal transplantations in scleroderma patients from PubMed search, present UNOS data on transplant outcomes, and identify predictors for allograft SRC. Of the five cases with recurrent SRC, all developed ESRD within a year of onset of native kidney SRC, whereas none of those who developed ESRD more than 1-2 years after the onset of SRC developed recurrence. Anemia preceded allograft SRC in two cases, pericardial effusion in one, and skin tightening in two others. UNOS data (October 1987-July 2004) documented 260 transplants performed for the renal diagnosis of scleroderma, with a 5-year graft survival rate of 56.7%. The risk for allograft SRC recurrence appears to correlate with early native renal function loss following the onset of SRC. Recurrent SRC in the allograft may be heralded by multiple clinical markers known to be predictive of severe scleroderma, including progression of diffuse skin thickening, new-onset anemia and cardiac complications.

Topics: Anemia; Arterioles; Autoimmune Diseases; Disease Progression; Edema; Female; Fibrin; Graft Rejection; Graft Survival; Humans; Kidney; Kidney Diseases; Kidney Failure, Chronic; Kidney Glomerulus; Kidney Transplantation; Kidney Tubules; Leukocytes, Mononuclear; Lymphocytes; Middle Aged; Pericardial Effusion; PubMed; Recurrence; Renal Dialysis; Risk Factors; Scleroderma, Systemic; Skin; Thrombosis; Time Factors; Transplantation, Homologous

The risk for endstage renal failure in patients with proliferative lupus nephritis (PLN) depends largely on the severity and reversibility of the inflammatory process as determined by light microscopy (LM). As the intrarenal formation of immune complexes is thought to initiate this inflammation, we studied whether renal immunofluorescence microscopy (IFM) provides clinical or prognostic information in addition to LM findings. Clinical data at the time of renal biopsy and during a mean follow-up of 46 months were extracted from the records of 69 SLE patients with proliferative LN (WHO class III/IV). Biopsy specimens were analyzed by LM for AI and CI, while IFM was performed on cryostat sections with the use of antisera against IgG, IgM, IgA, C3, C1q and fibrin. IFM findings were recorded in terms of the localization (glomerular, tubular or vascular) and intensity of fluorescence (score from zero to three). IFM findings were then related to clinical and LM findings and its prognostic value studied by survival analysis. Glomerular immune deposits were present in 99% of patients, tubular deposits in 38% and vascular deposits in 17%. A 'full-house' pattern (all three Ig classes) was found in 67% of biopsies and C3 and C1q deposits in 93% and 74% respectively. Median scores for AI and CI were 6 (1-18) and 3 (0-10); aside from a negative correlation between IgA deposits and CI, we found no other correlation between the amount or type of immune deposits and AI or CI. IgM deposits were associated with high serum levels of anti-dsDNA, while IgG deposits correlated with high ESR and serum creatinin levels. IFM scores were not related to steroid dose at the time of biopsy and neither type of glomerular, tubular or overall renal immune deposits had prognostic value for renal survival. Renal immunofluorescence does not reflect light microscopy findings in patients with PLN and does not contribute prognostic information in patients with PLN. Lupus (2000) 9, 504-510.

Topics: Adolescent; Adult; Complement C1q; Complement C3; Female; Fibrin; Fluorescent Antibody Technique; Humans; Immunoglobulin A; Immunoglobulin M; Inflammation; Kidney; Kidney Failure, Chronic; Kidney Glomerulus; Lupus Nephritis; Male; Microscopy, Fluorescence; Middle Aged; Predictive Value of Tests; Risk Factors; Survival Analysis

To prospectively evaluate the efficacy of a low-dose, 3-hour recombinant tissue plasminogen activator (rt-PA) infusion for the treatment of hemodialysis catheter (HDC)-associated fibrin sheaths.. Seventeen patients with end-stage renal disease (female, n = 11; male, n = 6), who were undergoing catheter-directed hemodialysis, were evaluated for 28 episodes of HDC dysfunction. This patient group ranged in age from 25 to 92 years (mean, 57 years). Radiographic contrast and/or clinical evaluation were consistent with the presence of a fibrin sheath on either the arterial and/or venous port in all cases. Patients subsequently underwent a thrombolytic infusion consisting of 2.5 mg rt-PA in 50 mL normal saline at a rate of 17 mL/h (3-hour infusion) per port. All infusions were performed in the interventional radiology recovery room, on an outpatient basis. Patients were followed-up prospectively for technical success, complications, catheter patency, and long-term outcome.. The immediate technical success rate, defined as return of manual aspiration and infusion capabilities to both ports, was 100%. No potential patients required exclusion from thrombolytic therapy secondary to contraindications, and no procedure-related complications occurred. The arithmetic mean and median catheter patency at the end of the study was 41 and 25 days, respectively (range, 1-116 days). A Kaplan-Meier survival analysis yielded a 30-, 60-, and 90-day probability of patency of 0.67, 0.61, and 0.51, respectively. At the end of the study period, all 17 patients remained on catheter-directed hemodialysis and 13 (76%) were utilizing the same catheter present at the time of entrance into the study.. Thrombolytic therapy utilizing a 2.5-mg rt-PA infusion through each port during a 3-hour period would appear to be a safe, efficient method for treating HDC-associated fibrin sheaths. Three-month patency rates are comparable to those reported for other methods of restoring function to HDC catheters, including new catheter placement, catheter exchange over a guide wire, thrombolytic infusions with urokinase, and percutaneous fibrin sheath stripping.

Topics: Adult; Aged; Aged, 80 and over; Catheterization, Central Venous; Catheters, Indwelling; Equipment Failure; Female; Fibrin; Fibrinolytic Agents; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prospective Studies; Radiography, Interventional; Renal Dialysis; Survival Analysis; Tissue Plasminogen Activator; Treatment Outcome; Vascular Patency

Persistent fibrin deposition has been observed in kidneys undergoing chronic rejection, and has been suggested to contribute to the obliteration of the vasculature in these grafts. The mechanisms leading to it are not clear. Fibrinolysis, the process to remove fibrin in tissues, is initiated by tissue type plasminogen activator (tPA) and suppressed by type 1 plasminogen activator inhibitor (PAI-1). To investigate their roles in chronic rejection and fibrin deposition, we serially examined the expression of tPA and PAI-1 in an unmodified chronic rejection model, using a Fisher 344 to Lewis rat renal transplant, at 0, 2, 4, 6, 10, 12, 16 and 20 weeks post-transplantation (N = 4 rats/time point in each group). We also analyzed fibrin deposition and the development of chronic changes in the grafts. Our results show that tPA was up-regulated only in the acute phase of rejection (P < 0.05), whereas PAI-1 was induced and persistently expressed during the progressive phase of chronic rejection, together with persistent fibrin deposition in the grafts. Immunohistochemistry showed PAI-1 was mainly localized to the damaged/proliferative vascular intima. The results suggest that persistent induction of PAI-1 may be responsible for the continuance of fibrin deposition, which is associated with irreversible damage and chronic graft loss.

Topics: Animals; Creatinine; Fibrin; Gene Expression; Graft Survival; Immunohistochemistry; Kidney Failure, Chronic; Kidney Transplantation; Male; Plasminogen Activator Inhibitor 1; Plasminogen Activators; Rats; Rats, Inbred F344; Rats, Inbred Lew; RNA, Messenger; Survival Analysis; Tissue Plasminogen Activator; Transplantation, Homologous

We describe a 50-year-old man with a severe acquired haemorrhagic syndrome. He had slightly prolonged clotting times using bovine thrombin, human thrombin and reptilase. His plasma contained a polyclonal IgG which interfered with the generation of fibrin monomers without inhibiting the aggregation of preformed monomers. The inhibitor delayed thrombin-induced fibrinopeptide A release. The IgG bound to insolubilized synthetic fibrinopeptide A (one binding site per molecule) and, with higher affinity, to fibrinogen (two binding sites per molecule). It did not bind to insolubilized fibrin monomers. The IgG did not impair the catalytic activity of thrombin toward a small synthetic substrate but inhibited the binding of thrombin to fibrinogen without binding to thrombin. The binding of the anti-fibrinopeptide A autoantibody to fibrinogen might have impaired thrombin-induced fibrinogen to fibrin conversion in vivo. This may have favoured the reported haemorrhagic syndrome which was associated with severe chronic renal insufficiency.

Topics: Autoantibodies; Binding Sites; Blood Coagulation Disorders; Fibrin; Fibrinogen; Fibrinopeptide A; Hemorrhage; Humans; Immunoglobulin G; Kidney Failure, Chronic; Male; Middle Aged; Thrombin

Catheter obstruction due to fibrin deposits during CAPD can cause poor outflow of peritoneal fluid and recurrent peritonitis. In order to treat this complication, 75,000 IU of diluted Urokinase (UK) were infused into catheters obstructed by fibrin in 10 CAPD patients (4 of which had peritonitis), without adverse reactions. After 60 minutes, a 2 liter exchange of peritoneal fluid was performed. In all the cases a normal outflow was restored. Hemostasis parameters (PT, PTT, TT, Fibrinogen, FDP, Fibrin monomers, BT, AT III) and blood cells count (RBC, HGB, HCT, WBC, PTL), were assayed before and two hours after the UK infusion, and did not show any significant variation, except for a decrease of white blood cells, which remained, however, within the normal range. No peritonitis episode occurred in the follow-up period. UK fibrinolytic therapy is safe and effective in treating fibrin obstruction of CAPD catheters without catheter removal and prevents recurrent peritonitis.

Topics: Catheters, Indwelling; Female; Fibrin; Hemostasis; Humans; Infusions, Parenteral; Kidney Failure, Chronic; Male; Peritoneal Dialysis, Continuous Ambulatory; Peritonitis; Recurrence; Urokinase-Type Plasminogen Activator

A low molecular heparin fragment (Fragmin, mol. wt. 4-6000 d), given as a single injection (dose 5000 anti-Xa U), was used as an anticoagulant during hemodialysis in 11 patients. In comparison, our routine heparinization procedure was used; conventional heparin was given as a bolus injection at the start and then as continuous infusion during dialysis to prolong the whole blood activated clotting time (WBACT) 125-175%. Fibrin formation, followed by visual inspection and the measuring of fibrinopeptide A and fibrin monomer concentrations were equally suppressed by the two regimens. WBACT was less prolonged with Fragmin. Anti-Xa activity above 0.39 U/ml was maintained throughout the dialyses with Fragmin. In conclusion a single dose of Fragmin gives sufficient anticoagulation for hemodialysis lasting up to 4 hours.

Topics: Adult; Aged; Female; Fibrin; Fibrinopeptide A; Heparin; Humans; Kidney Failure, Chronic; Male; Middle Aged; Molecular Weight; Renal Dialysis

Low molecular weight (LMW)-heparin was used as the sole anticoagulant during hemodialysis and hemofiltration in a pilot study on 32 patients. A LMW-heparin dose corresponding to 50% of the patients usual unfractionated, standard (UF)-heparin dose was found to produce comparable plasma heparin levels (anti-FXa-activity). No thrombosis of the extracorporal system and no bleeding complications occurred at this LMW-heparin dose. In contrast to UF-heparin, LMW-heparin produced only slight increases in PTT and thrombin time in all patients. Lipoprotein lipase was stimulated only marginally by LMW-heparin, with a correspondingly reduced release of free fatty acids. Both heparin species caused similar elevations in factor VIII and fibrin monomers, thus excluding a difference in coagulation activation. On the basis of these results, long-term studies have been started at four nephrology centers. To date, 26 patients have been treated with LMW-heparin for 6 months. A LMW-heparin dose was used that produced plasma anti-FXa-activity of 0.5 to 0.9 U/ml (initial dose: 30 to 40; dose/hr: 8 to 15 anti-FXa-units/kg body wt). PTT and thrombin time were only increased by 5 sec on average. Surprisingly, the elevated pre-dialysis levels of factor VIII and fibrin monomers decreased during this 6-month period. Bleeding complications did not occur and thrombotic complications were not observed when the anti-FXa levels were above 0.5 U/ml. LMW-heparin, therefore, appears to be a good alternative to UF-heparin for dialysis patients and may present less risk of bleeding because of its reduced effect on PTT, thrombin time, and thrombocytes.

Topics: Blood; Factor VIII; Fatty Acids, Nonesterified; Female; Fibrin; Heparin; Humans; Kidney Failure, Chronic; Lipase; Male; Partial Thromboplastin Time; Renal Dialysis; Thrombin Time; Ultrafiltration

After reduction and splitting of disulfide linkages the fibrinmonomer and fibrin of 45 patients with histologically confirmed liver cirrhosis and 38 patients with chronic renal failure (serum creatinine greater than 5 mg%) were analysed by SDS-PAA electrophoresis. Furthermore the activity of factor XIII was measured immunologically. The results indicated no polymerization of alpha-chains of fibrin while gamma-dimers were formed regularly in 71% of patients with liver cirrhosis and in 45% of patients with chronic renal failure. In liver cirrhosis and in 45% of patients with chronic renal failure. In liver cirrhosis the lack of alpha-polymerization correlated to the severity of the disease and to the decrease of factor XIII activity (no alpha-polymers formed when below 80% of normal). In renal failure this correlation was not demonstrable since in all cases the activity of factor XIII was within the normal range. After the addition of C14-labelled urea to normal plasma during clotting an incorporation of this tracer could be demonstrated by scintiscanner diamins like urea, forming in the course of renal failure, probably serve as the "wrong substrate" for the transaminidase factor XIII.

Topics: Factor XIII; Fibrin; Fibrinogen; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Protein Conformation

We have estimated the degree of fibrin deposition as well as changes in dialyzer efficiency of Gambro Optima 13.5 mu dialyzers, re-used up to six times in six regular dialysis patients. After each dialysis the dialyzer was rinsed and left filled with formaldehyde. The patients were given I-125-fibrinogen before the study. The radioactivity from the dialyzer was continuously measured during each dialysis and rinsing procedure. Urea and creatinine clearances were determined 30 min after start of each dialysis. After the last re-use the dialyzer membranes were removed and divided into sections and the radioactivity of each section was measured. Twice as much fibrin deposition was found near the blood inlet of the dialyzer as near the outlet. A higher fibrin deposition was found after each re-use than after the initial dialysis. The clearances of urea and creatinine were scarcely influenced by the re-use. The half-life of fibrinogen in the patients was in the same range as in normal subjects.

Topics: Adult; Aged; Disposable Equipment; Female; Fibrin; Fibrinogen; Half-Life; Humans; Kidney Failure, Chronic; Kidneys, Artificial; Male; Middle Aged

To determine whether sulphinpyrazone reduces thrombus formation within artificial kidneys, dialyzer 125I-fibrinogen and platelet and fibrinogen levels during dialysis were compared during a non-treatment control period and while patients were receiving sulphinpyrazone. Mean fibrin deposition within the dialyzers, measured as gram X 10(-3) of clottable fibrinogen, was significantly less during sulphinpyrazone treatment (2.5) than during the control period (5.3). Arterial blood platelet counts and plasma fibrinogen levels during dialysis were higher on treatment despite similar predialysis values during control and treatment periods. The results indicate that sulphinpyrazone reduces fibrin formation within artificial kidneys and, since the reduction in deposition of fibrin alone is insufficient to explain the higher plasma fibrinogen levels during treatment with sulphinpyrazone, suggests that this therapy reduces fibrinogen consumption within the patient during hemodialysis.

Topics: Blood Platelets; Fibrin; Fibrinogen; Humans; Kidney Failure, Chronic; Kidneys, Artificial; Sulfinpyrazone; Thrombocytopenia

In order to determine the role of intrarenal vascular coagulation (IVC) in chronic glomerulonephritis, coagulant parameters in renal blood (RVB), urine FDP's and renal histology were examined in 70 patients with chronic glomerulonephritis (CGN). RVB was obtained by Seldinger's technique. A correlation was obtained between an increase of fibrinogen, FDP and soluble fibrin monomer complexes (SFMC) in RVB and the degree of intraglomerular fibrin deposition shown on immunofluorescence. An increase of FDP's, SFMC and a slight decrease of fibrinolytic activity in RVB were observed in patients with CGN with decreased renal function or with the nephrotic syndrome. Daily excretion of FDP in the urine and the extent of intraglomerular fibrin deposition were greater in nephrotics than in non-nephrotics. We conclude that measurement of coagulation parameters in RVB is a reliable and sensitive method of assessing IVC, and that IVC plays an important role in aggravation of chronic glomerulonephritis, particularly when the nephrotic syndrome is present.

Topics: Chronic Disease; Fibrin; Fibrin Fibrinogen Degradation Products; Glomerulonephritis; Histocytochemistry; Humans; Kidney Failure, Chronic; Kidney Glomerulus; Nephrotic Syndrome; Renal Veins

The influence of hemofiltration on the number of platelets and on coagulation factors was investigated in patients with chronic renal insufficiency. These investigations were done on 12 patients during 22 treatments with hemofiltration. Blood samples were taken before hemofiltration, 10, 30 and 120 minutes after the beginning of the treatment and at the end of hemofiltration. In comparison to the original values we found a loss of platelets, a small decrease in the concentration of fibrinogen and a small increase in the fibrin monomer complex, plasminogen, antithrombin III, alpha1-antitrypsin and in alpha2-macroglobulin. The thrombin time, the partial thromboplastin time and Quick's test showed that the blood of these patients contained sufficient hepatin. Use of fibrin plates (Astrup) showed no signs of fibrinolytic activity. Compared to the results, which were obtained some years ago during hemodialysis, we found a smaller extent of alterations of blood coagulation factors and number of platelets.

Topics: alpha 1-Antitrypsin; alpha-Macroglobulins; Antithrombins; Blood Cell Count; Blood Coagulation Factors; Blood Platelets; Fibrin; Fibrinogen; Humans; Kidney Failure, Chronic; Plasminogen; Renal Dialysis; Ultrafiltration

Topics: Acute Kidney Injury; Anemia; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Fibrin; Hemostasis; Humans; Kidney Diseases; Kidney Failure, Chronic; Peritoneal Dialysis; Polycythemia; Renal Dialysis

Topics: Binding Sites; Cell Movement; Fibrin; Histamine Release; Humans; Kidney Failure, Chronic; Kinetics; Leukocytes; Platelet Aggregation; Renal Dialysis

Topics: Antigens; Electrophoresis, Polyacrylamide Gel; Factor XIII; Female; Fibrin; Fibrinogen; Heparin; Humans; Hypertension, Malignant; Immunodiffusion; Kidney Failure, Chronic; Kidneys, Artificial; Male; Middle Aged; Platelet Adhesiveness; Renal Dialysis; Time Factors

Topics: Adult; Fibrin; Humans; Kidney Failure, Chronic; Kidneys, Artificial; Male; Methods; Muscle Cramp; Renal Dialysis; Ultrafiltration

Topics: Azathioprine; Biopsy; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Female; Fibrin; Granulomatosis with Polyangiitis; Heparin; Humans; Immunosuppressive Agents; Kidney; Kidney Failure, Chronic; Kidney Glomerulus; Prednisone; Pregnancy

Topics: Anuria; Disseminated Intravascular Coagulation; Escherichia coli Infections; Fibrin; Humans; Kidney Failure, Chronic; Sepsis

Topics: Fibrin; Humans; Kidney; Kidney Failure, Chronic; Multiple Myeloma

Topics: Adolescent; Adult; Arteries; Azaserine; Azathioprine; Basement Membrane; Creatine; Cryptococcosis; Dactinomycin; Epithelial Cells; Female; Fibrin; Fluorescent Antibody Technique; Follow-Up Studies; Graft Rejection; Hematuria; Humans; Immunoglobulin G; Immunoglobulin M; Immunosuppressive Agents; Kidney Failure, Chronic; Kidney Glomerulus; Kidney Papillary Necrosis; Kidney Transplantation; Male; Mercaptopurine; Pneumonia; Prednisone; Proteinuria; Thrombosis; Transplantation Immunology; Transplantation, Homologous

Topics: Adult; Age Factors; Antibodies; Antigen-Antibody Reactions; Autopsy; Basement Membrane; Biopsy; Complement System Proteins; Female; Fibrin; Glomerular Filtration Rate; Glomerulonephritis; Humans; Immunoelectrophoresis; Immunoglobulin G; Kidney Failure, Chronic; Kidney Glomerulus; Kidney Transplantation; Male; Middle Aged; Neutrophils; Streptococcal Infections; Transplantation, Homologous

Topics: Acute Disease; Acute Kidney Injury; Adult; Aged; Amylases; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Female; Fibrin; Humans; Kidney; Kidney Failure, Chronic; Kidney Glomerulus; Male; Middle Aged; Pancreas; Pancreatitis

Topics: Acute Kidney Injury; Cholelithiasis; Cholestasis; Diabetic Nephropathies; Factor XIII; Fibrin; Fibrinogen; Glomerulonephritis; Humans; Kidney Failure, Chronic; Nephrotic Syndrome; Pyelonephritis; Renal Dialysis; Tuberculosis, Renal; Uremia; Wound Healing

In chronic renal failure and after acute renal failure, fibrinogen levels are raised and there is diminished fibrinolysis as the result of renal damage. A similar situation is found in nephrosis, possibly due to fibrinolytic inhibitors. Increased levels of cryofibrinogen were found in one quarter of cases of acute nephritis, nephrosis, and acute and chronic renal failure. In addition, after acute renal failure low platelet counts, prolonged thrombin times, and high levels of fibrin degradation products, yet with diminished fibrinolysis, indicate that intravascular coagulation has occurred. A positive result for fibrin degradation products was found in 17 of 20 cases of acute renal failure but in none of 10 cases of chronic uraemia. Intravascular coagulation is a process in which fibrin is deposited in the glomerular filters and may account for anuria, and, in the renal vasculature, where it may cause ischaemic tubular necrosis.

Topics: Acute Kidney Injury; Blood Coagulation Disorders; Blood Coagulation Tests; Fibrin; Fibrinogen; Fibrinolysis; Hemagglutination Inhibition Tests; Humans; Immunoelectrophoresis; Kidney Diseases; Kidney Failure, Chronic; Nephritis; Nephrotic Syndrome; Plasminogen; Uremia

Topics: Blood Chemical Analysis; Blood Pressure Determination; Blood Proteins; Dialysis; Fibrin; Hematocrit; Heparin; Kidney Failure, Chronic; Nitrogen; Peritoneal Dialysis; Potassium; Pyelonephritis; Renal Dialysis; Sulfates; Urea; Urine