Vol.6, No 1, 1999 pp. 31 - 47
UC UC 616.379 
DIABETIC NEPHROPATHY: FRESH PERSPECTIVES
Eli A. Friedman
Renal Disease Division, Department of Medicine, State University o f New York, Health Science Center at Brooklyn, Brooklyn, New York, USA
Summary. Diabetes is the disorder most often linked with development of end-stage renal disease (ESRD) in the USA, Europe, South America, Japan, India, and Africa. Kidney disease is as likely to develop in long-duration non-insulin dependent diabetes (type 2) as in insulin-dependent diabetes mellitus (type 1). Nephropathy in diabetes — if suboptimally managed — follows a predictable course starting with microalbuminuria through proteinuria, azotemia and culminating in ESRD. The rate of renal functional decline in diabetic nephropathy is slowed by normalization of hypertensive blood pressure, establishment of euglycemia, and a reduced dietary protein intake. When compared with other causes of ESRD, the diabetic patient sustains greater mortality and morbidity due to concomitant (co-morbid) systemic disorders especially coronary artery and cerebrovascular disease. A functioning kidney transplant provides the uremic diabetic patient better survival with superior rehabilita-tion than does either CAPD or maintenance hemodialysis. There are no reports, however, of prospective con-trolled studies of dialysis versus kidney transplantation in diabetic patients whose therapy was assigned randomly. For the minority (<10%) of diabetic ESRD patients who have, performance of a combined pancreas and kidney transplant may cure diabetes and permit full rehabilitation. No matter which ESRD therapy has been elected, optimal rehabilitation in diabetic ESRD patients requires that effort be devoted to recognition and management of co-morbid conditions.
Survival in treating ESRD in diabetes by dialytic therapy and renal transplantation is continuously improving. This inexorable progress in therapy reflects multiple small advances in understanding of the pathogenesis of extrarenal micro- and macrovasculopathy in an inexorable disease, coupled with safer immunosuppression. In this context, trials of pimagidine and aldose reductase inhibitors are now being conducted. Recognizing the perturbed biochemical reactions underlying the pathogenesis of diabetic vasculopathy — especially the adverse impact of accumulated advanced glycosylated end-products (AGEs) — raises the possibility of blocking end-organ damage without necessarily correcting hyperglycemia.
Key words: Diabetes, epidemiology, dialysis, transplantation
DIJABETESNA NEFROPATIJA: PERSPEKTIVE

Kratak sadržaj: U SAD, Evropi, Južnoj Americi, Japanu, Indiji i Africi dijabetes je najčešći uzrok terminalne hronične bubrežne insuficijencije (THBI). Bubrežno oboljenje se javlja posle više godina trajanja insulin-nezavisnog dijabetesa (tip 2), kao i insulin-zavisnog dijabetesa (tip 1). Nefropatija u dijabetesu ? ako nije adekvatno lečena ? razvija se određenim tokom tako što počinje sa mikroalbuminurijom preko proteinurije, azotemije i završava se sa THBI. Stepen propadanja bubrežne funkcije usporava se kontrolom krvnog pritiska, glikemije i smanjenim unosom proteina. U poređenju sa drugim bolesnicima u THBI, dijabetesni bolesnik ima veći morbiditet i mortalitet, zbog istovremeno prisutnih (ko-morbidnih) sistemskih poremećaja, posebno koronarnog i cerebrovaskularnog oboljenja. Funkcionalni kalem bubrega omogućuje dijabetesnom uremičnom bolesniku bolje preživljavanje sa boljom rehabilitacijom, nego što to omogućuje CAPD ili trajna hemodijaliza. Međutim, nema prospektivnih kontrolisanih studija odnosa dijalize i transplantacije bubrega sa raspodelom bolesnika u grupe slučajnim izborom. Za manji broj (<10%) dijabetesnih bolesnika u THBI kombinovani kalem bubrega i pankreasa može da izleči dijabetes i omogući potpunu rehabilitaciju. No, bez obzira na izbor načina lečenja THBI, optimalna rehabilitacija zahteva napor da se prepoznaju i leče ko-morbidni poremećaji.
Preživljavanje dijabetesnih bolesnika sa THBI na dijalizi i sa presađenim bubregom se neprekidno popravlja. Neumitni napredak u lečenju odražava brojne manje pomake u razumevanju patogeneze mikro- i makrovaskularnih poremećaja, povezano sa sigurnijom imunosupresijom. Prepoznavanjem poremećenih biohemijskih procesa koji se nalaze u osnovi patogeneze dijabetske vaskulopatije, posebno nepovoljan uticaj nagomilanih krajnjih produkata glikozilacije, otvara se mogućnost za prevenciju oštećenja pojednih organa bez neophodne korekcije hiperglikemije.
Ključne reči: Dijabetes, epidemiologija, dijaliza, transplantacija