Diabetic kidney disease: impact of puberty.
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-beta (TGF-beta). 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-beta 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.
Lane
Pascale H
PH
Department of Pediatrics, University of Nebraska Medical Center, Omaha 68198-2169, USA. phlane@unmc.edu
D000293:Adolescent; D003928:Diabetic Nephropathies / Q000503:physiopathology*; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006801:Humans; D007668:Kidney / Q000502:physiology; D008297:Male; D011627:Puberty / Q000502:physiology*
D012739:Gonadal Steroid Hormones