96. Jahrestagung der Deutschen Gesellschaft für Pathologie e. V ...
96. Jahrestagung der Deutschen Gesellschaft für Pathologie e. V ...
96. Jahrestagung der Deutschen Gesellschaft für Pathologie e. V ...
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Results. The papillary RCC type II were all positive for membranous<br />
N-Cadherin staining, whereas type I did not show any membranous<br />
positivity for N-Cadherin. The E-Cadherin staining showed a stronger<br />
membranous as well as cytoplasmic expression in type II than in type I<br />
RCC. A relevant expression of KSP- and P-Cadherin could not be demonstrated.<br />
Conclusions. Our data show that all papillary RCC type II are characterized<br />
by a membranous N-Cadherin expression. In contrast the papillary<br />
RCC type I do not express N-Cadherin membranous at all. Thus<br />
N-Cadherin represents the first immunhistochemical marker for a clear<br />
differentiation between papillary RCC type I and type II.<br />
SA-P-092<br />
Myoglobin expression in renal cell carcinoma is regulated by<br />
hypoxia<br />
C .L . Behnes1 , J . Bedke2 , A . Strauss3 , F . Bremmer1 , H .-J . Radzun1 1 2 University of Göttingen, Institute of Pathology, University of Tübingen,<br />
Institute of Urology, 3University of Göttingen, Institute of Urology<br />
Aims. Myoglobin (Mb) is a member of the hemoprotein superfamily, including<br />
in addition hemoglobin, neuroglobin and cytoglobin. The functions<br />
of the cytoplasmic localized Mb are the prevention of hypoxia and<br />
radical scavenging, well known from the myocytes of skletal and myocardic<br />
muscles. In case of hypoxia Mb acts as an oxygen reservoir by<br />
binding O2 and improving the diffusion of oxygen into the cell. It could<br />
be shown that some cancers do express Mb preventing hypoxia. In this<br />
study we investigated whether Mb also plays a role in renal cell carcinoma<br />
(RCC) and a potential influence of hypoxia on the expression.<br />
Methods. Four different RCC cell lines were cultivated un<strong>der</strong> hypoxic<br />
conditions and the expression of Mb was evaluated by real-time PCR.<br />
For the correlatin between microvessel density and Mb expression tissue<br />
microarrys (TMAs) with 42 different RCCs were immunhistochemically<br />
stained with a myoglobin- as well as CD31-antibody.<br />
Results. We could show that RCC do express Mb. Immunhistochemical<br />
examinations of RCC tissues show a reverse relationship between Mbexpression<br />
and capillary density. Especially in clear cell RCC a significant<br />
relationship between decrease in capillary density and increased<br />
expression of Mb could be shown. Furthermore, the expression of Mb<br />
in all analyzed RCC cell lines increased un<strong>der</strong> hypoxia up to 60-fold.<br />
Conclusions. Mb especially known as a marker for myogenic differentiation<br />
is expressed in RCC and RCC cell lines un<strong>der</strong> hypoxia. A significant<br />
reverse correlation between capillary density and Mb expression<br />
exist in clear cell RCC. Thus, Mb might be a marker for hypovascularized<br />
tumor entities/tumor areas.<br />
SA-P-093<br />
Impact of early ultrastructural damage after ABO-incompatible<br />
and ABO-compatible kidney transplantation<br />
V . Broecker1 , A . Pfaffenbach1 , C . Bockmeyer1 , M . Dämmrich1 , S . Immenschuh2<br />
, A . Schwarz3 , H . Kreipe1 , F . Heinemann4 , J .U . Becker1 1 2 Hannover Medical School, Institute for Pathology, Hannover, Hannover<br />
Medical School, Institute for Transfusion Medicine, Hannover, 3Hannover Medical School, Department of Nephrology, Hannover, 4Essen University,<br />
Institute for Transfusion Medicine, Essen<br />
Aims. Following ABO-incompatible kidney transplantation (iABO),<br />
c4d in peritubular capillaries (ptc) is frequently positive without further<br />
indicators of humoral rejection. Using electron microscopy (EM), we<br />
investigated the presence and prognostic relevance of early endothelial<br />
damage to glomerular and ptc in transplant kidneys with c4d positivity<br />
un<strong>der</strong> different circumstances.<br />
Methods. In 20 iABO patients (57 biopsies), 16 ABO-compatible (cABO)<br />
patients (26 biopsies with c4d-positivity of ptc) and 14 transplant patients<br />
(14 biopsies) without c4d and signs of humoral rejection (controls)<br />
were included. 10 different EM parameters were semiquantitatively evaluated:<br />
loss of foot processes (FF), lamina rara interna widening (LRI),<br />
swelling of glomerular and ptc endothelial cells (GES and ptcES), inflammatory<br />
cell adhesion to glomerular and ptc endothelial cells (GIS<br />
and ptcIS), glomerular basement membrane double contours (DK), glomerular<br />
and ptc basement membrane lamellation (LG and Lptc), loss of<br />
glomerular endothelial fenestration (FE). Status of donor specific antibodies<br />
(DSA) was available for 35/50 patients. Kidney function (GFR) at<br />
biopsy and follow up (51.8±31.74 months) was available for all patients.<br />
Results. 3/10 EM parameters were significantly less severe in iABO versus<br />
cABO (FF, FE, ptcES); 1/10 significantly more severe in cABO versus<br />
controls (FE). No differences were seen between iABO and controls.<br />
GFR at biopsy and follow up was significantly lower in cABO versus<br />
iABO, although the decline (GFR/time) was not different. GFR at biopsy<br />
and follow up correlated with 2/10 EM parameters in iABO (LRI, FE),<br />
2/10 in cABO (GIS, FF). None of the EM parameters correlated with<br />
GFR decline. Patients with positive DSA (6/35) had significantly lower<br />
GFR at biopsy and follow up, although, GFR decline was not different<br />
between DSA positive and negative patients. The presence of DSA correlated<br />
with 6/10 EM parameters (FF, LRI, GES, ptcES, DK, FE).<br />
Conclusions. Long term outcome in iABO patients is favourable despite<br />
c4d positivity of ptc. In this context the value of EM in the detection of<br />
early endothelial damage, although more pronounced in cABO patients<br />
with signs of humoral rejection, is limited and lacks prognostic relevance.<br />
In contrast, the presence of DSA correlates with ultrastructural<br />
signs of endothelial alteration and is associated with impaired kidney<br />
function.<br />
SA-P-094<br />
Large scale in vivo isolation of glomerular podocytes by cationic<br />
colloidal silica-coated ferromagnetic nanoparticles<br />
A . Blutke1 , R . Wanke1 1Ludwig-Maximilians-University Munich, Institute of Veterinary Pathology<br />
at the Centre for Clinical Veterinary Medicine, München<br />
Aims. Podocyte homeostasis plays a crucial role for maintenance of the<br />
physiological glomerular function and podocyte injury is regarded as a<br />
major determinant of development and progression of various renal diseases.<br />
Since cultured podocytes cannot completely reflect the complex<br />
properties of podocytes in the glomerular environment in vivo, analyses<br />
of the molecular processes occurring during podocyte development<br />
and injury require appropriate methods for preparation of fresh podocyte<br />
isolates.<br />
Methods. A novel, fast, antibody-free and most cost-efficient method<br />
for reproducible large scale isolation of fresh podocytes from mouse<br />
kidney glomeruli is described. Briefly, cationic silica-coated colloidal<br />
ferromagnetic nanoparticles were utilized to bind to negatively charged<br />
cell surfaces of podocytes in preparations of isolated glomeruli. After<br />
enzymatic and mechanical dissociation of the glomerular cells, nanoparticle-coated<br />
podocytes were isolated in a magnetic field.<br />
Results. Podocytes isolated with this method displayed characteristic<br />
phenotypical and ultrastructural features. Protein and mRNA expression<br />
abundances of marker-molecules of podocytes, endothelial or mesangial<br />
glomerular cells indicated a significant enrichment of podocytes<br />
in the generated isolates.<br />
Conclusions. The described method offers a great potential for different<br />
downstream transcript- and protein profiling analysis technologies,<br />
which might contribute to an improved un<strong>der</strong>standing of podocyte<br />
biology and of the molecular mechanisms involved in podocyte injury<br />
in vivo.<br />
Der Pathologe · Supplement 1 · 2012 |<br />
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