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FASCICOLI E ARTICOLI   I PIÙ LETTI   eTOC

ULTIMO FASCICOLOPANMINERVA MEDICA

Rivista di Medicina Interna

Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,6

Periodicità: Trimestrale

ISSN 0031-0808

Online ISSN 1827-1898

 

Panminerva Medica 2003 Marzo;45(1):23-41

 REVIEW ARTICLES

Kidney involvement and disease in patients with diabetes

Chiarelli F., Trotta D., Verrotti A., Mohn A.

Department of Paediatrics University of Chieti, Chieti, Italy

Diabetic neph­rop­athy is the ­leading ­cause of end-­stage ­renal dis­ease in ­western or west­er­nised coun­tries and the ­largest con­trib­utor to the ­total ­cost of dia­betes ­care ­around the ­world. In addi­tion to the devel­op­ment of dia­betic neph­rop­athy and end-­stage ­renal ­failure, dia­betic ­patients ­with evi­dence of albu­mi­nuria ­have a ­much ­higher ­risk of devel­oping myo­car­dial infarc­tions, cereb­ro­vas­cular acci­dents, ­severe pro­gres­sive reti­nop­athy, and periph­eral and auto­nomic neu­rop­athy. A cumu­la­tive inci­dence of dia­betic neph­rop­athy has ­been doc­u­mented ­after dura­tion of dia­betes of at ­least 25 ­years in ­both ­type 1 and ­type 2 dia­betic ­patients, ­although ­more ­recent ­studies ­have dem­on­strated a sub­stan­tial reduc­tion of its inci­dence. Before the ­onset of ­overt pro­tei­nuria, ­there are sev­eral ­renal func­tional ­changes, ­including ­renal hyper­fil­tra­tion, hyper­per­fu­sion, and ­increasing cap­il­lary perme­ability to mac­ro­mol­e­cules. Basement-mem­brane thick­ening and mesan­gial expan­sion ­have ­long ­been rec­og­nized as path­o­log­ical hall­mark of dia­betic neph­rop­athy. It has ­been pos­tu­lated ­that dia­betic neph­rop­athy ­occurs as a ­result of the inter­play of meta­bolic and hae­mod­y­namic fac­tors in the ­renal micro­cir­cu­la­tion. Hyperglycaemia ­plays a piv­otal ­role in the path­o­gen­esis of dia­betic ­renal dis­ease, but ­genetic fac­tors are ­also of cru­cial impor­tance. The accu­mu­la­tion of ­advanced gly­cos­i­la­tion end prod­ucts (AGEPs), the acti­va­tion of iso­forms of pro­tein ­kinase C (PKC) and the accel­er­a­tion of the ­aldose reduc­tase ­pathway may ­explain how hyper­gly­caemia dam­ages ves­sels. Growth fac­tors (i.e. TGF-β, IGF-1, ­VEGF) may ­also ­play an impor­tant ­role in the path­o­gen­esis. There is a ­familial clus­tering of dia­betic ­kidney dis­ease: a ­number of ­gene ­loci ­have ­been inves­ti­gated to try to ­explain the ­genetic sus­cep­ti­bility to ­this com­pli­ca­tion. The two ­main treat­ment strat­e­gies for pre­ven­tion of dia­betic neph­rop­athy are ­improved gly­caemic con­trol and ­blood pres­sure low­ering, par­tic­u­larly ­using ­drugs ­such angio­tensin-con­verting ­enzyme inhib­i­tors and angio­tensin II ­receptor antag­o­nists. Many poten­tial treat­ment modal­ities in pre­venting and ­treating dia­betic neph­rop­athy are pres­ently ­being eval­u­ated; ­some of ­them ­will pos­sibly be avail­able in the ­near ­future in ­order to try to ­modify the nat­ural ­course of ­kidney involve­ment and dis­ease in ­patients ­with dia­betes.

lingua: Inglese


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