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Maria Pia Rastaldi

Publications and source records attributed to Maria Pia Rastaldi.

26 records · Page 2Linked to original sources
PubMedDate not supplied

Histopathological atlas of renal diseases: ANCA-associated vasculitis (Second part).

In the first part of Histopathological Atlas of Renal Diseases we described the typical morphological features of Anca-associated vasculitis. The histological features in Wegener's granulomatosis, Micropolyarteritis and its renal-limited variant, are characterized by "pauci immune" necrotizing extracapillary glomerulonephritis. The cellular composition of glomerular crescent and the mechanisms underlying crescent formation are still incompletely understood. The recent availability of monoclonal antibodies directed against epithelial cells and leucocytes allowed a more precise identification of the crescent cells. In this chapter we will describe the prevalent presence of monocytes in the crescents, the possible mechanisms of recruitment of these cells and the morphological consequences of this glomerular infiltration for the chronic progression of lesions.

Antibodies, Antineutrophil Cytoplasmic↗
PubMedDate not supplied

Histopathological atlas of renal diseases: light chain deposition disease.

Monoclonal diseases of B-cell lineage, often referred to as plasma cell dyscrasias, are characterized by abnormal and uncontrolled proliferation of a single clone of B cells at different maturation stages, with a more or less marked differentiation to immunoglobulin (Ig)-secreting plasma cells. Thus B-cell proliferation is usually associated with the production and secretion in blood of a monoclonal Ig or a fragment thereof. An ominous consequence of secretion of monoclonal Ig products is their deposition in tissue. These proteinaceous deposits can take the form of casts (in myeloma cast nephropathy), cristals (in myeloma-associated Fanconi's syndrome), fibrils (in light-chain [LC] amyloidosis), or granular precipitates (in monoclonal Ig deposition disease [LCDD]).

B-Lymphocytes↗
PubMedDate not supplied

Henoch-Schonlein nephritis.

Henoch-Schonlein purpura is a clinical syndrome characterized by the association of skin, joint, and gastrointestinal symptoms. Henoch-Schonlein purpura is characterized by wide-spread vasculitis. Although the clinical symptoms of this disease are characteristic, the diagnosis is not always easy to establish because other forms of systemic vasculitis - mainly the microscopic form of periarteritis nodosa - may mimic the disease. In addition, in contrast to systemic lupus erythematosus, there are no biological tests that can identify Henoch-Schonlein purpura with certainty. Immunofluorescence microscopic techniques have made an important contribution to both the diagnosis and the study of the pathogenesis of the disease, particularly since they have demonstrated the presence of IgA deposits in the glomeruli and in the vessel walls. These findings not only confirmed the immunologic nature of the pathologic lesions but also drew attention to the remarkable similarity between Henoch-Schonlein purpura nephritis and IgA nephropathy.

Humans↗
PubMedDate not supplied

Histopathological atlas of renal diseases: diabetic nephropathy.

Renal involvement in type 2 diabetes is a well known clinical occurrence. According to data from the literature, besides diabetic glomerulosclerosis, type 2 diabetic nephropathy may occur as a non specific chronic damage mostly related to vascular changes, or as a glomerular disease superimposed on or even unrelated to diabetic glomerulosclerosis. The most common picture remains in any case diabetic glomerulosclerosis (diabetic GS), that is characterized by variable degrees of mesangial sclerosis.

Diabetic Nephropathies↗
PubMedDate not supplied

Renal amyloidosis (part I).

The term amyloidosis refers to the deposition of an amorphous substance defined by the presence of a fibrillar structure by electron microscopy and a characteristic beta-pleated sheet structure by x-ray diffraction. The existence of this group of diseases has been recognized for centuries, but major advances in the elucidation of the nature of the deposits have been achieved in the past few years. It is now recognized that the beta-sheet configuration responsible for the general appearance of amyloid deposits is common to a large array of proteins with a different origin. This tertiary structure is responsible for the characteristic tinctorial and optical properties evident by Congo red staining. The material that accumulates in the extracellular compartment progressively destroys the involved organ. The accumulation of amyloid deposits may complicate the course of a wide variety of diseases. Classifications of amyloid disorders reflect some of the current concepts concerning the protein composition of amyloid fibrils in different diseases.

Amyloid↗
PubMedDate not supplied

Renal amyloidosis (Part II).

As reported in the previous chapter (Part I) the term amyloidosis refers to the deposition of an amorphous substance defined by the presence of fibrillary structure by electron microscopy and a characteristic betapleated sheet structure by X-ray diffraction. Renal biopsy is fundamental in diagnostic terms because morphological demonstration is necessary and the tissue most frequently involved by amyloidosis is the kidney. In the previous chapter we presented the different histochemical and immunohistochemical techniques that are necessary to differentiate the two main types of amyloidosis defined as AL and AA. Here we show the variability of deposition of amyloid in glomerular, vascular and interstitial compartments.

Amyloidosis↗
PubMedDate not supplied

Epithelial-mesenchymal transition and its implications for the development of renal tubulointerstitial fibrosis.

Despite a lot of research efforts, the origin of renal fibroblasts is still matter of debate. Epithelial-mesenchymal transition (EMT) of tubular epithelial cells could be at least one of the mechanisms by which renal fibroblasts are generated. Every kind of renal injury is potentially able to induce renal tubular cells to go through the various steps of EMT and generate fibroblasts, as it has been demonstrated by experimental models, in vitro experiments, and renal biopsy studies. It means that, if EMT is a common process of progression of renal failure, further studies and a better understanding of this process can lead us to envisage specific treatments to counteract the progression of renal disease.

Basement Membrane↗