Projects / Programmes source: ARIS

Immune and nonimmune mechanisms in renal and systemic diseases

Research activity

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
Evaluation (rules)
source: COBISS
Researchers (16)
no. Code Name and surname Research area Role Period No. of publicationsNo. of publications
1.  17952  Tomo Brezovar    Researcher  1997 - 1999 
2.  02273  PhD Dušan Ferluga  Microbiology and immunology  Head  1997 - 1999  531 
3.  02127  PhD Nina Gale  Oncology  Researcher  1997 - 1999  406 
4.  17945  Branka Grmek    Researcher  1997 - 1999 
5.  07190  PhD Anastazija Hvala  Microbiology and immunology  Researcher  1997 - 1999  172 
6.  17946  Metka Janc    Researcher  1997 - 1999 
7.  17948  Alenka Jurančič    Researcher  1997 - 1999 
8.  11204  PhD Vesna Jurčić  Microbiology and immunology  Researcher  1997 - 1999  150 
9.  02051  Tatjana Kobenter  Microbiology and immunology  Researcher  1998 - 1999  20 
10.  15472  PhD Boštjan Luzar  Oncology  Researcher  1997 - 1999  459 
11.  17965  Breda Nagode    Researcher  1997 - 1999  14 
12.  02748  Tatjana Perković  Microbiology and immunology  Researcher  1997 - 1999  58 
13.  17947  Nataša Štok-Pfajfar    Researcher  1998 - 1999 
14.  07182  PhD Alenka Vizjak  Microbiology and immunology  Researcher  1997 - 1999  377 
15.  15471  Aleksandar Vodovnik  Microbiology and immunology  Researcher  1997 - 1999  30 
16.  12955  PhD Nina Zidar  Microbiology and immunology  Researcher  1997 - 1999  391 
Organisations (1)
no. Code Research organisation City Registration number No. of publicationsNo. of publications
1.  0381  University of Ljubljana, Faculty of Medicine  Ljubljana  1627066  48,724 
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.
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