fibrin and Hemolytic-Uremic-Syndrome

The hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. These features reflect the underlying histopathologic lesion: fibrin-rich thrombi that predominate in the renal microvasculature. HUS most commonly affects children younger than 5 years and is associated with Shiga toxin-producing enteric bacteria, the most important of which is Escherichia coli O157:H7. In this setting, HUS is epidemic and also might affect adults, particularly elderly people. Sporadic cases of HUS more commonly occur in adults and are associated with a wide variety of inciting agents and conditions. Although the disease manifestations might be similar and endothelial activation or injury likely represents a common etiologic event, differing responses to therapy suggest different pathogenic mechanisms. As more is understood about the underlying pathogenesis of the diseases that we now lump together as HUS, more efficacious and rational treatment and prevention strategies are likely to follow.

Topics: Complement Factor H; Escherichia coli O157; Fibrin; Hemolytic-Uremic Syndrome; Humans; Shiga Toxin

Topics: Acute Disease; Adolescent; Adult; Child; Child, Preschool; Chronic Disease; Female; Fibrin; Fibrinogen; Glomerulonephritis; Hemolytic-Uremic Syndrome; Humans; Immune Complex Diseases; Immunoglobulin A; Immunoglobulin G; Kidney Diseases; Lupus Erythematosus, Systemic; Male; Middle Aged; Nephritis; Nephrosis; Nephrotic Syndrome; Purpura; Streptococcal Infections

Topics: Acute Kidney Injury; Animals; Blood Coagulation; Child; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Glomerulonephritis; Graft Rejection; Hemolytic-Uremic Syndrome; Heparin; Humans; Kidney Diseases; Kidney Glomerulus; Kidney Transplantation; Mice; Phagocytosis; Pre-Eclampsia; Pregnancy; Rabbits; Transplantation, Homologous

Topics: Abruptio Placentae; Animals; Blood Platelets; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinolysis; Heat Exhaustion; Hemolytic-Uremic Syndrome; Heparin; Humans; Polymers; Pregnancy; Shock

The treatment of five children with the haemolytic-uraemic syndrome using streptokinase is described to illustrate the difficulties and limitations of thrombolytic therapy in this disease. This experience is germane to the design of multicentre clinical trials.A multivariate analysis relating clinical outcome to the data obtained at the time of admission was also carried out for 31 children with the disease treated in four centres. The results suggest that this technique may help to identify those patients likely to have a fatal outcome. An expanded form of this type of analysis should be incorporated in future clinical trials.

Topics: Blood Cell Count; Blood Coagulation; Blood Platelets; Child; Child, Preschool; Clinical Trials as Topic; Fibrin; Glomerular Filtration Rate; Hemolytic-Uremic Syndrome; Heparin; Humans; Infant; Kidney; Peritoneal Dialysis; Prognosis; Statistics as Topic; Streptokinase

Topics: Animals; Blood Platelets; Fibrin; Hemolytic-Uremic Syndrome; Humans; Kidney Glomerulus; Mice; Shiga Toxin 2

Essentials An international collaboration provides a consensus for clinical definitions. This concerns thrombotic microangiopathies and thrombotic thrombocytopenic purpura (TTP). The consensus defines diagnosis, disease monitoring and response to treatment. Requirements for ADAMTS-13 are given.. Background Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS) are two important acute conditions to diagnose. Thrombotic microangiopathy (TMA) is a broad pathophysiologic process that leads to microangiopathic hemolytic anemia and thrombocytopenia, and involves capillary and small-vessel platelet aggregates. The most common cause is disseminated intravascular coagulation, which may be differentiated by abnormal coagulation. Clinically, a number of conditions present with microangiopathic hemolytic anemia and thrombocytopenia, including cancer, infection, transplantation, drug use, autoimmune disease, and pre-eclampsia and hemolysis, elevated liver enzymes and low platelet count syndrome in pregnancy. Despite overlapping clinical presentations, TTP and HUS have distinct pathophysiologies and treatment pathways. Objectives To present a consensus document from an International Working Group on TTP and associated thrombotic microangiopathies (TMAs). Methods The International Working Group has proposed definitions and terminology based on published information and consensus-based recommendations. Conclusion The consensus aims to aid clinical decisions, but also future studies and trials, utilizing standardized definitions. It presents a classification of the causes of TMA, and criteria for clinical response, remission and relapse of congenital and immune-mediated TTP.

Topics: ADAMTS13 Protein; Adult; Blood Platelets; Child; Complement System Proteins; Consensus; Diagnosis, Differential; Erythrocytes; Female; Fibrin; Hematology; Hemolysis; Hemolytic-Uremic Syndrome; Humans; Inflammation; Platelet Aggregation; Platelet Count; Pregnancy; Purpura, Thrombotic Thrombocytopenic; Recurrence; Remission Induction; Societies, Medical; Terminology as Topic; Thrombotic Microangiopathies; Treatment Outcome; von Willebrand Factor

Glomerular fibrin thrombi may be an early indication of antibody-mediated rejection in renal allograft biopsies. However, fibrin thrombi have a broad differential; thus, we sought to evaluate the etiology and implications of glomerular fibrin thrombi in allograft biopsies of blood group and cytotoxic crossmatch compatible renal allografts. Biopsies were identified from the pathology files of Oregon Health & Science University. Detailed histopathologic findings were retrospectively correlated with clinical data, treatment, and outcome. Sixteen early posttransplant biopsies had glomerular fibrin thrombi, including three surveillance biopsies. Six of 16 biopsies had no other histopathologic findings; 5/16 had glomerulitis and peritubular capillaritis; 4/16 had concomitant cellular vascular rejection; one had parenchymal infarction. C4d staining was positive in 4/16 cases. Most patients were treated with IVIg and plasmapheresis, others with rapamycin, thymoglobulin, or rituximab. At an average follow-up of 62 months, 8 patients with functioning grafts had a mean serum creatinine of 1.4 mg/dL (122 μmol/L). Antibody-mediated rejection is an important consideration in blood group compatible allograft biopsies with glomerular fibrin thrombi, even with C4d-negative biopsies. However, multidisciplinary evaluation is necessary, given other etiologies, including drug toxicity, hemolytic-uremia syndrome, and large vessel thrombosis. Despite aggressive treatment, both short and long-term graft survival may be compromised.

Topics: ABO Blood-Group System; Biopsy; Blood Grouping and Crossmatching; Complement C4b; Fibrin; Graft Rejection; Hemolytic-Uremic Syndrome; Humans; Immunosuppression Therapy; Inflammation; Kidney; Kidney Diseases; Kidney Glomerulus; Kidney Transplantation; Peptide Fragments; Thrombosis; Thrombotic Microangiopathies; Time Factors; Transplantation, Homologous; Treatment Outcome

We investigated a patient with atypical hemolytic uremic syndrome without diarrhea to determine the presence of antibodies and the specificity of the related antigens. The patient experienced repeated episodes of hemolytic uremic syndrome. She is dialysis dependent. von Willebrand factor (vWF), vWF multimers, platelet aggregation, ADAMTS-13 activity and platelet immunoblots were determined. During acute episodes vWF increased threefold, with unusually large vWF multimers on two occasions. Platelet aggregation was normal but the plasma caused spontaneous aggregation of normal platelets. Reactivity was removed after absorption with protein A. Protein blotting against platelet and microvascular endothelial cells showed strong and persistent reactivity against antigens of 200 and 55 kDa. Two-dimensional immunoblots of the whole platelet proteome and incubation with plasma identified strong immunoreactivity with two target spots in the 55-kDa area. Mass spectroscopy confirmed the target as beta-fibrin, molecular weight 50.73 kDa, isoelectric point 7.95, with MASCOT scores of 859 and 750, Two years after presentation another band was detected at 66 kDa and identified as the alpha subunit of fibrin. This patient's plasma contained a platelet-aggregating factor that was removed by immunoglobulin absorption. She developed antibodies against the alpha and beta subunits of fibrin/fibrinogen.

Topics: ADAM Proteins; ADAMTS13 Protein; Adolescent; Antigen-Antibody Reactions; Autoantibodies; Blood Platelets; Female; Fibrin; Fibrinogen; Hemolytic-Uremic Syndrome; Humans; Immunoglobulin G; Platelet Aggregation; Recurrence; Renal Insufficiency; von Willebrand Factor

Severe deficiency of ADAMTS13 activity was recently found in patients with thrombotic thrombocytopenic purpura (TTP). The great advance associated with these basic and clinical studies on ADAMTS13 is the possible elucidation of the pathogenesis of TMA (thrombotic microangiopathy). However, the exact pathogenetic mechanism in TMA without severe deficiency of ADAMTS13 activity remains unknown due to heterogeneity of the disease. In this study, there were 7 patients with TTP, 7 with HUS, 3 with drug-induced HUS, 1 with VOD, and 1 with IVL out of 19 TMA patients with a moderate deficiency (6-70%) of ADAMTS13 activity. Five of the 7 TTP patients had a poor outcome. Plasma thrombomodulin and t-PA-PAI-1 complex levels in TMA patients with a moderate deficiency of ADAMTS13 activity were significantly higher than those in patients with a severe deficiency of ADAMTS13 activity. These data suggest that the etiology in these patients may be systemic vascular endothelial cell damage.

Topics: ADAM Proteins; ADAMTS13 Protein; Adolescent; Adult; Aged; Biomarkers; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Lipoproteins; Male; Metalloendopeptidases; Middle Aged; Peptide Fragments; Protein Precursors; Prothrombin; Purpura, Thrombotic Thrombocytopenic; Thromboplastin

Ten thousand & thirty seven autopsies performed from the year 1982 to 1992 were studied retrospectively, to find out the number of deaths due to bleeding diathesis. Eighty-seven (0.87%) patients died due to bleeding diathesis, out of which haemolytic uraemic syndrome (HUS) was seen in 9 cases (10.34%), disseminated intravascular coagulation (DIC) in 67 cases (77.01%) & 11 cases were grouped as miscellaneous. Martius scarlet blue stain was carried out to demonstrate fibrin & depending on the number of thrombi in the glomerulus & blood vessels, the lesions were graded as mild, moderate or severe. Kidney was the most common organ involved in all groups of bleeding diathesis. In DIC kidney & lung involvement was almost equal.

Topics: Autopsy; Disseminated Intravascular Coagulation; Female; Fibrin; Hemolytic-Uremic Syndrome; Hemorrhagic Disorders; Humans; Kidney; Lung; Male; Necrosis; Retrospective Studies; Staining and Labeling; Thrombosis

Diarrhoea-associated haemolytic uraemic syndrome (D+ HUS) is usually caused by verotoxin producing Eschericia coli. We hypothesized that verotoxin binding to glomerular endothelial cells causes localised endothelial cell activation and thus activation of coagulation and reduction of fibrinolytic potential. We also proposed that treatment with fresh frozen plasma or dialysis would not affect these changes. Markers of activation of coagulation and fibrinolysis were measured in 30 children with acute D+ HUS serially, in healthy children and in children on dialysis. In acute D+ HUS, levels of thrombin-antithrombin III complex and prothrombin fragment 1+2 were significantly increased (p <0.001). The source of thrombin generation was unclear. Factor XIIa levels were increased in patients and controls with renal failure. Factor VIIa levels were not significantly raised in children with acute D+ HUS. D-dimers were increased, but fibrinolytic potential as measured by fibrin plate was reduced. Levels of plasminogen activator inhibitor antigen and activity and tissue plasminogen activator antigen were increased. Neither peritoneal dialysis nor administration of blood products, the most common treatments, altered parameters of coagulation or fibrinolysis.

Topics: Antithrombin III; Blood Coagulation; Blood Transfusion; Child; Diarrhea; Factor VIIa; Factor XIIa; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Hemolytic-Uremic Syndrome; Humans; Peptide Fragments; Peritoneal Dialysis; Plasma Exchange; Plasminogen Activator Inhibitor 1; Prothrombin; Renal Dialysis; Thrombin; Tissue Plasminogen Activator

We report here, a patient of systemic lupus erythematosus (SLE) with severe fibrinoid necrosis in the afferent arteriole of the glomerulus, in whom antiphospholipid antibody might have contributed to the pathogenesis. A 24-year-old female who was suffering from severe anemia with fragmented red blood cells, acute renal failure and thrombocytopenia, was admitted to our hospital. Further examinations revealed findings compatible with active lupus nephritis. Moreover, she was found to be positive for antiphospholipid antibody, and anticardiolipin antibody, as well as for lupus anticoagulant and syphilis test. Intensive treatment by methylprednisolone pulse therapy, hemodialysis, and double filtration plasmapheresis were performed. However, 13 days after admission she died suddenly because of intracranial hemorrhage. Pathological investigation of renal tissue revealed severe fibrinoid necrosis of the arterioles mainly in the glomerular afferent arteriole associated with diffuse proliferative lupus nephritis. In this case, hemolytic uremic syndrome (HUS) was associated with SLE. Antiphospholipid antibody was considered to be not only an accelerator in the arterial lesions of HUS, but also an initiator of HUS itself.

Topics: Adult; Arterioles; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Kidney Glomerulus; Lupus Erythematosus, Systemic; Necrosis

Diarrhea-associated hemolytic uremic syndrome (D+ HUS) is the most common cause of acute renal failure in children. The authors report their experience with D+ HUS with 114 patients assessed in Calgary from 1980 to 1992. Epidemiologic, clinical, and pathologic aspects are discussed.

Topics: Adolescent; Alberta; Child; Child, Preschool; Colitis, Ulcerative; Diarrhea; Feces; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Incidence; Infant; Male; Thrombosis

We report three cases of haemolytic-uraemic syndrome following bone marrow transplantation in young males. None of them was treated with cyclosporin A. All died in renal failure. Renal histology showed the typical appearances of haemolytic-uraemic syndrome. Immunoperoxidase examination of renal biopsies showed IgM and complement in blood vessels and glomeruli of all three cases. Cytomegalovirus infection was present in two cases and probable in the third. Two cases had been infected with herpes zoster. All had episodes of graft-versus-host disease. Possible pathogenetic mechanisms are discussed.

Topics: Adolescent; Basement Membrane; Biopsy, Needle; Bone Marrow Transplantation; Child; Complement System Proteins; Cyclosporins; Fibrin; Hemolytic-Uremic Syndrome; Humans; Immunoenzyme Techniques; Immunoglobulins; Kidney; Leukemia, Lymphoid; Lymphoma, Non-Hodgkin; Male; Microscopy, Electron

Four patients who took the antitumor agent mitomycin manifested microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. At autopsy, kidneys from all four patients had a microangiopathy typical of the hemolytic-uremic syndrome (HUS), with thromboses in glomerular capillaries and arterioles, fibrin deposition in mesangium, and prominent cellular intimal proliferation of the interlobular arteries. Development of the HUS was an important factor contributing to death in all four patients. From a review of the literature and our initial results of a randomized chemotherapy protocol for metastatic adenocarcinoma of the colorectum, it appears that mitomycin was the most likely cause for the development of the HUS in these patients. As more patients are being treated with mitomycin, particular care must be taken to monitor them for development of a drug-induced HUS.

Topics: Arteries; Autopsy; Capillaries; Fibrin; Glomerular Mesangium; Hemolytic-Uremic Syndrome; Humans; Kidney; Kidney Glomerulus; Male; Mitomycins; Staining and Labeling

The localization of intrarenal cross-linked fibrin was examined by the effect of monochloroacetic acid treatment on the kidney sections. In acute glomerulonephritis or in mild diffuse or focal proliferative type of nephritis, cross-linked fibrin was observed mainly within glomerular capillary walls. Extension of cross-linked fibrin deposit over the mesangium or sclerotic area was seen in moderate to severe proliferative type of nephritis or in membranoproliferative glomerulonephritis. In hemolytic uremic syndrome or disseminated intravascular coagulation syndrome, cross-linked fibrin was detected within glomeruli and vessels.

Topics: Acetates; Child; Disseminated Intravascular Coagulation; Factor XIII; Fibrin; Glomerulonephritis; Hemolytic-Uremic Syndrome; Histocytochemistry; Humans; IgA Vasculitis; Immunoglobulin G; Kidney; Kidney Diseases; Nephrotic Syndrome; Tissue Distribution

The term "Endotheliotropic Hemolytic Nephroangiopathy" (EHN) comprises various clinically or pathomorphologically defined disease states with severe renal lesions (e.g. hemolytic uremic syndrome, malignant nephrosclerosis, post partum renal insufficiency) which, to date, have been considered as different entities. We attempted to assign accompanying glomerular changes based upon light and electron microscopy to the above mentioned clinical pictures and their various stages. The accordingly classified glomerular lesions (G1--G3 and Ga) are of critical importance in pathohistological differential diagnosis. Since it is assumed that fibrin is a causing event in the pathogenesis of the vascular lesions, quantitative evaluation of glomerular fibrin deposits was done. The results, when viewed with respect to time, lead to the conclusion that the microthrombotic component represents a secondary phenomenon. Thus, the primary and hence pathogenetically most important finding is a severe damage to the endothelium of the terminal renal vasculature. This endothelial damage although being expressed with variable intensity has to be regarded as the common denominator inherent to all types of glomerular lesions in EHN.

Topics: Acute Kidney Injury; Adult; Aged; Biopsy; Child; Child, Preschool; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Infant; Kidney Glomerulus; Male; Microscopy, Electron; Middle Aged; Nephrosclerosis; Pregnancy; Puerperal Disorders

Topics: Child; Chromatography, Gel; Electrophoresis, Polyacrylamide Gel; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Glomerulonephritis; Hemolytic-Uremic Syndrome; Humans; Kidney Diseases; Kidney Glomerulus; Lupus Erythematosus, Systemic; Nephrotic Syndrome

Serum concentrations of Clq, C4, C3, and Factor B but not properdin were significantly decreased in patients with HUS compared to values in normal control subjects (p value less than 0.01). Sera from 13 HUS patients obtained early after the onset of the disease showed breakdown products of Factor B (Ba, Bb) by immunoelectrophoresis; 12 of these sera showed C3 breakdown products (C3c, C3d). Sera from seven patients studied 1 month to 3 years later no longer demonstrated any breakdown products of Factor B or C3. These data suggest that the complemented system is activate in HUS. The concept that immunological mechanisms play a major role in this disease is additionally supported by the occurrence of IgM, C3, and fibrin in glomeruli and renal vessels.

Topics: Adolescent; Adult; Capillaries; Child; Child, Preschool; Complement C3; Complement C4; Complement System Proteins; Fibrin; Glycoproteins; Hemolytic-Uremic Syndrome; Humans; Immunoglobulin M; Infant; Kidney Glomerulus; Properdin

The clinical and renal biopsy findings from two patients in whom renal functional abnormalities developed in the late postpartum period are described. Both biopsies showed fibrin deposition in the renal vasculature, in one case marked and in the other mild. The patient with the more severely damaged kidney subsequently died, and the other is alive but with evidence of slowly progressing renal damage. The clinicopathological spectrum and pathogenesis of late postpartum renal failure are discussed.

Topics: Acute Kidney Injury; Animals; Biopsy; Blood Coagulation; Disseminated Intravascular Coagulation; Ergot Alkaloids; Female; Fibrin; Fluorescent Antibody Technique; Hemolytic-Uremic Syndrome; Humans; Hypertension; Ischemia; Kidney; Kidney Glomerulus; Pregnancy; Puerperal Disorders

Topics: Adolescent; Adult; Blood Platelets; Blood Transfusion; Diagnosis, Differential; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Hematuria; Hemolytic-Uremic Syndrome; Hemorrhagic Disorders; Heparin; Humans; Male; Melena; Middle Aged; Neurologic Manifestations; Prednisolone; Pregnancy; Pregnancy Complications, Hematologic; Thrombocytopenia

On healthy individuals fibrin(ogen) split products cannot be demonstrated in the blood. Catabolic products of fibrin and fibrinogen appear in the blood in case of general fibrinolysis, consumption coagulopathy with secondary fibrinolysis as well as local fibrin films with secondary fibrinolysis. The regular routine determination of fibrin(ogen) split products in serum or urine may indicate starting complications of many diseases. The appearance of these split products in case of renal affections indicates acute and active processes on the kidneys themselves; fibrin films appear in case of acute and chronic glomerulonephritis, casting-off crises on renal transplants, EPH gestosis, renal phlebothrombosis, hemolytic-uremic syndrom and occasionally urinary tract infections. The demonstration of fibrin(ogen) split products in serum or urine allows the following conclusions: a) acute and active process on the kidneys themselves; b) HMWS in urine indicate a fibrin film in the kidneys; c) an immediate beginning of an anticoagulation therapy; d) good possibilities to judge the therapeutic effect and by this the further progress of disease.

Topics: Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Fibrinolysis; Glomerulonephritis; Graft vs Host Reaction; Hemolytic-Uremic Syndrome; Humans; Immunoelectrophoresis; Infant; Kidney Diseases; Kidney Transplantation; Molecular Weight; Pre-Eclampsia; Pregnancy; Prognosis; Thrombosis; Transplantation, Homologous; Urinary Tract Infections

Four patients had clinical manifestations of the hemolytic-uremic syndrome. No evidence of active intravascular coagulation was found during the acute phase of the illness, using a sensitive assay to measure soluble circulating fibrin in the plasma of these patients, three of whom developed the clinical syndrome while hospitalized for gastro-enteritis. These findings, coupled with the findings of others, suggest that either the episode of intravascular coagulation precedes the development of the clinical manifestations, or that platelet thrombosis is occurring in the absence of activation of plasma clotting factors. In any case, heparin anticoagulant therapy does not seem indicated.

Topics: Anuria; Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Blood Pressure; Blood Urea Nitrogen; Carbon Radioisotopes; Child; Child, Preschool; Creatinine; Disseminated Intravascular Coagulation; Factor V; Factor VIII; Female; Fibrin; Fibrinogen; Hematuria; Hemoglobins; Hemolytic-Uremic Syndrome; Heparin; Humans; Infant; Male; Proteinuria; Prothrombin Time; Thromboplastin; Thrombosis

Topics: Adult; Blood Coagulation Tests; Blood Platelets; Child, Preschool; Chromium Radioisotopes; Creatinine; Factor V; Factor VIII; Factor XIII; Female; Fibrin; Fibrinogen; Fibrinolysis; Haptoglobins; Hematocrit; Hemolytic-Uremic Syndrome; Humans; Infant; Male; Middle Aged; Plasminogen; Prothrombin; Purpura, Thrombotic Thrombocytopenic; Thrombin

Topics: Aspirin; Blood Coagulation; Complement System Proteins; Diabetic Nephropathies; Dipyridamole; Fibrin; Fibrinogen; Glomerulonephritis; Hemolytic-Uremic Syndrome; Heparin; Humans; Iodine Radioisotopes; Kidney; Kidney Diseases; Kidney Glomerulus; Kidney Transplantation; Plasminogen; Proteinuria; Thrombosis; Transplantation, Homologous; Uremia; Warfarin

Topics: Blood Coagulation Tests; Child; Child, Preschool; Disseminated Intravascular Coagulation; Factor V; Factor VIII; Fibrin; Fibrinogen; Hemolytic-Uremic Syndrome; Humans; Infant; Prothrombin Time; Sepsis

Topics: Acute Kidney Injury; Adult; Arteries; Capillaries; Cell Division; Epithelial Cells; Epithelium; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Infarction; Kidney Glomerulus; Postpartum Hemorrhage; Pregnancy; Puerperal Disorders

Topics: Fibrin; Glomerulonephritis; Hemolytic-Uremic Syndrome; Kidney Diseases; Nephrosis; Purpura; Urinary Tract Infections

Topics: Arteries; Australia; Autopsy; Brain; Child, Preschool; Fibrin; Hemolytic-Uremic Syndrome; Heparin; Humans; Infant; Infant, Newborn; Kidney; Kidney Glomerulus; Prognosis; Seasons

Topics: Acute Kidney Injury; Basement Membrane; Blood Coagulation Disorders; Diabetic Nephropathies; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Fibrinolysis; Glomerulonephritis; Hemagglutination Tests; Hemolytic-Uremic Syndrome; Humans; Ischemia; Kidney; Kidney Diseases; Male; Middle Aged; Pre-Eclampsia; Pregnancy; Thrombosis; Urokinase-Type Plasminogen Activator

Topics: Anemia, Hemolytic; Child, Preschool; Fibrin; Hemolytic-Uremic Syndrome; Heparin; Humans; Male; Plasminogen; Streptokinase; Uremia

Topics: Anemia, Hemolytic; Child, Preschool; Complement System Proteins; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Infant; Kidney; Kidney Function Tests; Male; Prognosis; Uremia

Topics: Anemia, Hemolytic; Blood Coagulation; Blood Coagulation Factors; Blood Platelets; Fibrin; Fibrinogen; Hemolytic-Uremic Syndrome; Heparin; Humans; Uremia