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Department of Pediatrics, University of Nebraska Medical Center, Omaha, Nebraska 68198-2169
Puberty accelerates
microvascular complications of diabetes mellitus, including
nephropathy. Animal studies confirm a different renal hypertrophic
response to diabetes before and after puberty, probably due to
differences in the production of transforming growth factor-
(TGF-). Many of the complex physiological changes during puberty
could affect potentially pathogenic mechanisms of diabetic kidney
disease. Increased blood pressure, activation of the growth
hormone-insulin-like growth factor I axis, and production of sex
steroids could all play a role in pubertal susceptibility to diabetic
renal hypertrophy and nephropathy. These factors may influence the
effects of hyperglycemia and several systems that ultimately control
TGF- production, including the renin-angiotensin system, cellular
redox systems, the polyol pathway, and protein kinase C. These
phenomena may also explain gender differences in kidney function and
incidence of end-stage renal disease. Normal changes during puberty,
when coupled with diabetes and superimposed on a genetically
susceptible milieu, are capable of accelerating diabetic hypertrophy
and microvascular lesions. A better understanding of these processes
may lead to new treatments to prevent renal failure in diabetes mellitus.
gender; transforming growth factor-; protein kinase C; oxidative
stress
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