Glomerular vasculopathy after unrelated cord blood transplantation
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Thrombotic microangiopathy
Mesangium
Microangiopathy
Cord blood
We describe here a case of Purtscher-like retinopathy (PLR) linked with Hematopoietic Stem Cell Transplant (HSCT) associated thrombotic microangiopathy (TA-TMA). TA-TMA causes endothelial damage and results in micro-thrombi in capillaries and arterioles. PLR is associated with micro-thrombi that occlude the retinal arteries and cause retinal injury. This report describes the clinical course for PLR which has similar features to and can mimic hypertensive retinopathy.
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Membranous glomerulonephritis was diagnosed in five dogs with patent Dirofilaria immitis infections. Electron-dense deposits were present on the epithelial side of the glomerular basement membrane. An immunofluorescent study demonstrated immunoglobulins in the capillary wall and mesangium of the glomeruli. The glomerular lesions were considered to represent an immune complex form of glomerulonephritis induced by the D. immitis infection.
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Glomerular mesangium
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Immunoglobulin A nephropathy (IgAN) is considered as mesangiopathy since it initiates in the mesangium; however, other glomerular components are involved and the glomerular capillary wall offers the first contact to circulating macromolecular IgA1. Acute and active forms of IgAN are associated with endocapillary hypercellularity and vascular damage of various degrees, in severe cases with microangiopathy (MA) without or with thrombosis [thrombotic microangiopathy (TMA)]. Vascular damage activates complement and coagulation cascades. A defective complement regulation has recently been detected in active and progressive cases of IgAN. C4d deposits in renal biopsies have been found to be an early risk factor. These observations have raised interest in manifestation of MA and TMA in progressive cases of IgAN. MA-TMA lesions have been found in various percentages (2-53%) of patients with IgAN according to patients' selection and pathology definition of TMA. The association with hypertension (HTN) was so strong that it led to the hypothesis that MA/TMA in IgAN was a mere consequence of severe HTN. Old and new clinical and experimental data indicate that in IgAN the interaction of the glomerular capillary wall with immune reactants and complement uncontrolled activation leading to C4b deposits favours the development of MA-TMA, which plays a role in progression and renal function decline. The central role of complement activation is relevant also for the new therapeutic interventions offered by the pharma.
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Müftüoǧlu, Asuman U., Erbengi, Türkân, Harmanci, M., Karayel, T., Gürsoy, E., and Tahsinoǧlu, M.: Acute glomerulonephritis. Immunofluorescent and electron-microscopic observations in sporadic cases. Am J Clin Pathol 63: 300–309, 1975. The authors studied by immunofluorescent and electron microscopy renal biopsy specimens from 29 patients with various glomerular diseases. Poststreptococcal glomerulonephritis was characterized by the presence of complement (β1C) in the mesangium and/or on the basement membrane in all cases. Immunoglobulin G (IgG) was also present in less than half of the cases in the same distribution. Electron microscopy, carried out in six cases, revealed no uniform ultrastructural change: minimal subepithelial deposits were observed in three cases, intra-membranous deposits were seen in two cases, and the basement membrane was normal in one case. Glomerular abnormalities during the courses of some systemic diseases were similar. Mild renal involvement was characterized by only β1C deposition. This finding raises the question whether a mechanism other than or in addition to that involving immune complexes is operative in the pathogenesis of acute glomerulonephritis. There is circumstantial experimental evidence that an alternate pathway of complement activation and deposition may be operative in acute glomerulonephritis.
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Malignant hypertension (MHT) concerns 7 to 15% of IgA nephropathy (IgAN) patients. In some studies, a significant association of MHT with microangiopathy in IgAN has been reported. Herein, we describe the prevalence and characteristics of MHT in primitive IgAN patients with thrombotic microangiopathy (TMA).
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THE AIM: to show a rare combination and possible pathogenetic relationship of thrombotic microangiopathy and acute lymphoblastic leukemia in a child. PATIENTS AND METHODS. The analysis of the history and clinical laboratory data of the patient. RESULTS. 9 months after the debut of thrombotic microangiopathy with damage to the central nervous system, acute lymphoblastic leukemia was diagnosed in the form of transient attacks of cerebral circulation and kidneys with the development of the nephrotic syndrome. The literature data show that in rare cases secondary thrombotic microangiopathy precedes the unfolded picture of hematologic disease, pathogenetic therapy of leukemia leads to remission of thrombotic microangiopathy. The article discusses the possible relationship between the two states in a child. CONCLUSION. Although the relationship of thrombotic microangiopathy and acute leukemia in the present case is not obvious, the authors believe that it is necessary to remember about the possibility of developing secondary microangiopathy on the background of oncohematological diseases, and in doubtful cases to conduct a study of the bone marrow in patients.
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Thrombotic microangiopathy is a set of clinico-pathological syndrome that not uncommon.But still now,we don't understand the mechanism clearly and lack efficacious therapy about this disease,and the prognosis is always poor.In recent years,numerous progresses have been made both in mechanism and treatment,this article will review these progresses in thrombotic microangiopathy.
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Thrombotic microangiopathy (TMA) is characterized by a clinical presentation composed by thrombocytopenia, microangiopathic hemolytic anemia and organ damage. It may be manifested through several presentations, including acute kidney injury, which is a common feature due to the apparent propensity of the glomerular circulation to endothelial damage and occlusion. Regarding systemic lupus erythematosus, thrombotic microangiopathy is reported in 8%-15% of the biopsies performed in patients with this autoimmune disease. The pathogenic mechanisms related to this specific situation are still unknown and the treatment to be performed is the one specific to lupus.
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Microangiopathic hemolytic anemia
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We describe two children with poststreptococcal glomerulonephritis associated with prolonged oligoanuria (12, 13 days). Kidney biopsies at 10 and 6 days, respectively, revealed acute glomerulonephritis with prominent mesangiolysis. Both patients recovered uneventfully. It is proposed that damage to the mesangium accounts for the clinical course.
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