Genetic and molecular markers of proteinuria and glomerulosclerosis IJpelaar, D.H.T.

The studies described in this thesis were performed at the Department of Pathology (Head: Prof. Fleuren), Leiden University Medical Center, Leiden, The Netherlands.

In a minority of patients a recognized etiologic association is found (secondary FSGS). They include genetic mutations in podocyte-associated molecules such as a-actinin-4,

Differentiation between chronic rejection and chronic cyclosporine A toxicity Expression of ECM molecules and regulatory cytokines may help in improving diagnostic

QTL with suggestive and significant linkage to the glomerular damage score, the percentage of glomeruli with microaneurysms, the area percentage expressing aSMA,

Moreover, our data suggest that susceptibility to the development of proteinuria in Lewis/Maastricht rats is governed by genes expressed in the kidney, by bone marrow-derived

In conclusion, our data show, for the first time, that development of albuminuria in male and female MWF rats is preceded by glomerular hypertrophy and accompanied by

12 , the tip lesion variant of FSGS transformed to FSGS NOS in many subsequent biopsies, in both the native and the transplant kidneys; however, some patients with FSGS NOS in

Complete absence of Narp immunostaining on a paraffin section of glomeruli of Lew/Moll kidneys at 7 days after induction of anti-Thy-1 nephritis (A,C).. The staining was