Sabato 27 ottobre 2012 - Pacini Editore

COmuNiCaziONi ORali
plastic disease of other organs. In the past, Ong et al. suggested that
the development of motile cilia in tubular cells could represent a
reversion to a more primitive or less differentiated state consequent
to different tubular injuries. The presence of motile cilia have not
been described in human nephrogenesis, but, in the last years, is
has been shown that two types of epithelial cells, multi-cilia cells
and principal cells, are present in the epithelia of the zebrafish
distal pronephric duct. In mammals, pronephros is a nonfunctional
transitory structure that is replaced by the mesonephros and then by
the metanephros. In the early life of fish and amphibians, however,
the pronephros is a functional filtration organ that is likely to give
rise to metanephron, so to be used as a model for kidney development.
While motile cilia on the apical side of the multi-cilia cells
coordinate the movement of the fluid along the lumen of the pronephric
duct, principal cells, which account for the majority of the
cells in the kidney, reabsorb ions and other molecules according to
fluid balance requirements. In our cases proximal tubules showed
injury due to acute AMBR as well as iatrogenic toxic damage, with
loss of brush border, detachment from basal membrane and isometric
vacuolization. These data support the hypothesis of a correlation
between ciliated metaplasia and morpho-functional alteration of
tubular cells which recover a primitive phenotype as an adaptive
response to improve fluid excretion.
references
Liu Y, Pathak N, Kramer-Zucker A, et al. Notch signaling controls the
differentiation of transporting epithelia and multiciliated cells in the
zebrafish pronephros. Development 2007;134:1111-22.
Lungarella G, de Santi MM, Tosi P. Ultrastructural study of the ciliated
cells from renal tubular epithelium in acute progressive glomerulonephritis.
Ultrastruct Pathol 1984;6:1-7.
Kramer-Zucker AG, Olale F, Haycraft CJ, et al. Cilia-driven fluid flow in
the zebrafish pronephros, brain and Kupffer’s vesicle is required for
normal organogenesis. Development 2005;132:1907-21.
Ma M, Jiang YJ. Jagged 2a-notch signaling mediates cell fate choice in
the zebrafish pronephric duct. Plos Genet 2007;3:e18.
Nadasdy T, Laszik Z, Blick KE, et al. Human acute tubular necrosis: a
lectin and immunohistochemical study. Hum Pathol 1995;26:230-9.
Ong AC, Wagner B. Detection of proximal tubular motile cilia in a
patient with renal sarcoidosis associated with hypercalcemia. Am J
Kidney Dis 2005;45:1096-9.
Racusen LC, Solez K, Colvin RB, et al. The Banff 97 working classification
of renal allograft pathology. Kidney Int 1999;55:713-23.
Rubio CA, Nesi G, Zampi GC, et al. Gastric ciliated metaplasia. A study
of 3406 gastrectomy specimen from dwellers of the Atlantic and the
Pacific basins. J Clin Pathol 2005;58:605-10.
Solez K, Colvin RB, Racusen LC, et al. Banff 07 classification of renal
allograft pathology: update and future directions. Am J Transplant
2008;8:753-60.
TCTP (translationally controlled tumor protein)
is present in normal renal cortex and renal cancer
M.F. Ambrosio, B.J. Rocca, M.G. Mastrogiulio, A. Barone,
V. Mourmouras, F. Scaramuzzino, N. Palummo, L. Barbagli,
S.A. Tripodi
Department of human Pathology and Oncology, Anatomic Pathology Section,
University of Siena, Italy
Background. The translationally controlled tumor protein (TCTP) is
a protein of 23 kDa, ubiquitously expressed in eukaryotes. Its name
originates from the observation that TCTP transcripts accumulate
in resting cells and are rapidly translated into the protein when the
cells require it. Since the discovery of TCTP by Yenofsky, it became
clear that this protein is involved in multiple biological processes:
cell growth, apoptosis, cell cycle progression, cell division and
proliferation. It also functions as a histamine releasing factor and a
calcium-binding protein. It has been assessed that TCPT is expressed
in all human tissues except kidney, as reported by “Swiss Prot”, the
most important database on protein expressions. We decided to use
renal tissue as negative control for evaluation of TCTP expression by
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immunohistochemistry (IHC). Unexpectedly, a positivity of renal tubular
epithelium was detected. Thus we carried out a study on TCTP
expression in normal and neoplastic renal tissue.
Material and methods. we performed Western blotting and IHC
on normal and neoplastic renal tissue. Specifically we used 32
samples of clear cell carcinoma, 21 of papillary carcinoma, 9
of chromophobe carcinoma and 2 cases of Bellini’s carcinoma.
Cortical and medullary zone without any lesions were evaluated
as normal renal tissue.
Results. Western blot analysis: a single band of molecular weight
of approximately 23,000 Da was detected in all neoplastic specimens
and in cortical tissue, not in normal medullary tissue.
Immunohistochemistry: strong TCTP expression was observed in
the cytoplasm of the cells of the proximal and distal tubules. Thin
loop of Henle segment cells, glomerulus parietal cells, podocytes
and collecting duct cells did not show TCTP positivity. TCTP
was expressed in all neoplastic specimens, however with different
patterns of immunostaining: a membrane positivity in clear
cell carcinoma, a cytoplasmic positivity in papillary and chromophobe
carcinoma and a cytoplasmic staining with membrane
reinforce in Bellini’s carcinoma.
Conclusion. In our study we demonstrated, for the first time, the
presence of TCTP in proximal and distal tubules while not in
renal medulla. TCTP was also present in the vascular structures
and in the urothelium of renal pelvis. Interestingly, immunohistochemical
distribution of TCTP follows that of calcium reabsorption,
being stronger in the cortical structures. It may be postulated
that in normal kidney TCTP acts as calcium-binding protein. The
expression of TCTP in renal carcinomas may suggest a potential
role in carcinogenesis but further studies are necessary to confirm
our findings and to correlate TCTP expression with clinical
and prognostic determinants in the different tumor histotypes.
Considering that a series of pharmaceutical compounds are able
to diminish TCTP expression through down regulation of TCTP
expression at protein level, larger studies may also help to determine
whether TCTP may act as a target for drugs, contributing
to find new alternatives in the treatment of renal carcinoma for
which adjuvant effective drugs do not exist.
references
Susini L, Besse S, Duflaut D, et al. TCTP protects from apoptotic cell
death by antagonizing bax function. Cell Death Differ 2008;15:1211-
20.
Tessari P, Puricelli L, Iori E, et al. Altered chaperone and protein turnover
regulators expression in cultured skin fibroblasts from type 1
diabetes mellitus with nephropathy. J Proteome Res 2007; 6:976-86.
Sanchez JC, Schaller D, Ravier F, et al. Translationally controlled tumor
protein: a protein identified in several nontumoral cells including
erythrocytes. Electrophoresi 1997;18:150-5.
Yarm FR. Plk phosphorylation regulates the microtubule-stabilizing protein
TCTP. Mol Cell Biol 2002;22:6209-21.
Tuynder M, Fiucci G, Prieur S, et al. Translationally controlled tumor
protein is a target of tumor reversion. Proc Natl Acad Sci USA
2004;101:15364-9.
Koide Y, Kiyota T, Tonganunt M, et al. Embryonic lethality of fortilinnull
mutant mice by BMP-pathway overactivation. Biochim Biophys
Acta 2009;1790:326-38.
Systemic reactive (AA) amyloidosis complicating
hyperimmunoglobulinemia D with periodic fever
syndrome: a case report
R. Passantino1 , G. Li Cavoli2 , L. Bono2 , A. Ferrantelli2 , C. Giammaresi2
, C. Tortorici2 , U. Rotolo2 1 Unità Operativa di Anatomia Patologica/Ospedale ARNAS Civico Di
Cristina Benfratelli, Palermo, Italia; 2 Unità Operativa di Nefrologia e
Dialisi/ Ospedale ARNAS Civico Di Cristina Benfratelli, Palermo, Italia
Introduction. Systemic reactive (AA) Amyloidosis is the most
serious potential complication of the inherited autoinflammatory
syndromes and frequently results in end-stage renal failure. The