000			03199nam a22003615i 4500
001			76612
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005			20230207040231.0
007			cr nn 008mamaa
008			100301s2006 sz | s |||| 0|eng d
020			_a9783764374280
024	7		_a10.1007/3-7643-7428-4 _2doi
050		4	_aRC903 _b.C66 2006 EB
082	0	4	_a616.079
245	0	0	_aComplement and Kidney Disease _cedited by Peter F. Zipfel
260			_aBasel _bBirkhäuser Basel _c2006
300			_a1 recurso en línea (XVI, 236 p.) _b32 ilustraciones, 4 in color
336			_aTexto (visual) _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
490	1		_aProgress in Inflammation Research
505	0		_aThe complement system in renal diseases -- Complement in renal transplantation -- C1q and the glomerulonephritides: therapeutic approaches for the treatment of complement-mediated kidney diseases -- Complement deficient mice as model systems for kidney diseases -- Non-Shiga toxin-associated hemolytic uremic syndrome -- Role of complement and Factor H in hemolytic uremic syndrome -- Genetic testing in atypical HUS and the role of membrane cofactor protein (MCP; CD46) and Factor I -- Towards a new classification of hemolytic uremic syndrome -- Therapeutic strategies for atypical and recurrent hemolytic uremic syndromes (HUS) -- Complement defects in children which result in kidney diseases: diagnosis and therapy -- The role of complement in membranoproliferative glomerulonephritis -- The experience of a patient advocacy group
520	3		_aIt is evident that a defective or deregulated complement system results in kidney diseases. An important role of complement effector and regulatory proteins in pathological settings of the kidney has been demonstrated. A large panel of distinct human kidney diseases is caused by defective complement control. Genetic analyses have identified mutations in complement regulators that are associated with these diseases. Mutations have been identified in the fluid phase alternative pathway regulator Factor H and the membrane regulator Membrane Cofactor Protein MCP (CD46). The functional characterization of the mutant proteins allows to define the pathophysiological events on a molecular level. These new concepts and data on disease mechanisms allowed establishing new diagnostic and promising therapeutic approaches for several human kidney diseases. Molecular biology, clinics and therapy are discussed in this volume
942			_2lcc _cLE
988			_aEBOOK, EBSPRINGERrevisando
650		7	_aRiñones _xEnfermedades _9168885 _0comprobar BNE19901053650 _2embne
700	1		_aZipfel, Peter F. _eeditor literario _985763 _0Local
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://link.springer.com/book/10.1007/3-7643-7428-4 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
901			_ai9783764374280
907			_a.b12822309 _b10-10-17 _c01-10-14
998			_am _a_alco _a_vill _b19-09-17 _cm _dz _ek _feng _gsz _h0
945			_aRC903 .C66 2006 EB _g1 _ieBOOK _j0 _lmae _o- _pEUR0.00 _q- _r- _sb _t15 _u0 _v0 _w0 _x0 _y.i11551513 _z06-04-17
999			_c76612 _d76612 _x1