Projects / Programmes
Immune and nonimmune mechanisms in renal and systemic diseases
Code |
Science |
Field |
Subfield |
3.01.00 |
Medical sciences |
Microbiology and immunology |
|
Code |
Science |
Field |
B520 |
Biomedical sciences |
General pathology, pathological anatomy |
B500 |
Biomedical sciences |
Immunology, serology, transplantation |
Pathology, immunopathology, systemic diseases, renal diseases, ANCA, transplantation, athero-arteriosclerosis, cell adhesion molecules, renal peritubular capillaries, progression of kidney diseases
Researchers (16)
Organisations (1)
Abstract
A systematic semiquantitative analysis of histopathologic changes in all segments of intrarenal and extrarenal vessels in surgically removed kidney transplants of patients with acute and chronic rejection was carried out for the first time. Our hypothesis that the rejection involves the whole vasculature of the transplant was confirmed. However, the differences in the involvement between the segments were evident. Our original findings of rejection phlebitis and involvement of vasa vasorum and vasa recta were proven. The differences between affection of the segments could only partly be explained by the differences in the expression of cell adhesion molecules. Our studies confirmed that, similarly as in the heart grafts, accelerated atherosclerotic and arteriosclerotic changes also occur in the kidney grafts. Their development is obviously mediated not only by immune but also by nonimmune factors. We found similar changes in renal peritubular capillaries which have been insufficiently studied so far. Our electron microscopic study revealed that glomerular as well as peritubular capillaries are simultaneously affected by a peculiar form of capillarosclerosis in chronic rejection and diabetic glomerulosclerosis. Furtheremore, our studies proved that humoral immune mechanisms are very probably involved in the development of vascular rejection in transplanted kidney and heart. The important role of kidney tranplant biopsy in the diagnosis of frequently recurring focal glomerulosclerosis, and less frequently recurring IgA glomerulonephritis, as well as most probably multifactorial involvement of the graft in a patient with Alport’s syndrome was proven.
Our original finding of capillarosclerosis, limited to the renal interstitium in Balkan endemic nephropathy, may contribute to the understanding of the pathogenesis of the disease. Brenner''s
hyperperfusion theory was confirmed by our studies demonstrating that intrauterine growth retardation affects the course and prognosis of IgA glomerulonephritis and idiopathic nephrotic syndrome with minimal changes. In systemic lupus erythematosus, the association of skeletal muscle immune deposits with histological changes, autoantibodies in the serum and clinical involvement confirmed their key pathogenetic role. Antineutrophil cytoplasmic antibodies in two patients with atheroembolic disease were described for the first time and were supposed to aggravate the vasculopathy and deterioration of renal function.