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Titlebook: IgA Nephropathy; Anthony R. Clarkson Book 1987 Martinus Nijhoff Publishing, Boston 1987 biology.biopsy.children.classification.cognition.d

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21#
發(fā)表于 2025-3-25 04:13:22 | 只看該作者
Clinical and Laboratory Features of IgA Nephropathy,sufficiently severe to mask a renal presentation. From the nephrologic point of view, the features are diverse. Patients with biopsy-proved IgA nephropathy have been presented to medical attention with nephrotic syndrome, acute nephritis, acute renal failure, malignant hypertension, and chronic rena
22#
發(fā)表于 2025-3-25 09:17:36 | 只看該作者
23#
發(fā)表于 2025-3-25 11:46:22 | 只看該作者
,Henoch-Sch?nlein Purpura and IgA Nephropathy: To Separate or Unify?,itic rash especially on the legs and buttocks, flitting arthropathy, gastrointestinal problems, and glomerulonephritis. The introduction of immunofluorescence studies of renal biopsies brought confirmation of the immunologic nature of the pathologic lesions and the remarkable similarity between the
24#
發(fā)表于 2025-3-25 16:17:34 | 只看該作者
25#
發(fā)表于 2025-3-25 23:04:37 | 只看該作者
26#
發(fā)表于 2025-3-26 00:26:49 | 只看該作者
IgA Nephropathy: Clinicopathologic Correlations,oglobulin [1, 2]. As pointed out by Berger in his first description, clinical presentation and symptoms as well as glomerular aspects by light microscopy vary from patient to patient. Some present with recurrent macroscopic hematuria while in the others the disease is discovered by “chance” finding
27#
發(fā)表于 2025-3-26 07:18:56 | 只看該作者
28#
發(fā)表于 2025-3-26 10:33:14 | 只看該作者
29#
發(fā)表于 2025-3-26 12:59:07 | 只看該作者
The Biology of IgA Mucosal Immunity,sally derived IgA immune complex-mediated disease process. Of course, to obtain conclusive evidence for immune complex pathogenesis, it is necessary to demonstrate that the same antigen and antibody present in the serum are also present in glomerular mesangial deposits. Although this proof does not
30#
發(fā)表于 2025-3-26 17:52:56 | 只看該作者
Lymphocyte Function in IgA Nephropathy,ence suggests that the mesangial IgA deposits are likely to be either IgA polymers or IgA-dominant immune complexes [3, 4]. These IgA seem to circulate in the blood because of a frequent recurrence of this disease after renal allotransplantation [5, 6] and a rapid disappearance of IgA deposits in a
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