title: Gender and the progression of chronic renal diseases: does apoptosis make the difference?
abstract: Several studies in patients with chronic kidney diseases have shown that men have a more rapid disease progression than women. Also, with ageing, men exhibit greater decrements in renal function and increased glomerular sclerosis than women. Data from meta-analysis studies indicate that women with several non-diabetic renal diseases such as membranous nephropathy, IgA nephropathy and polycystic kidney disease present a slower progression, but in diabetic renal disease this is not yet established. Thus, men appear to be at greater risk for renal injury than are women, but the underlying mechanisms are unknown. Sex hormones may mediate the effects of gender on chronic renal disease, through the interaction with the renin-angiotensin system, the modulation of nitric oxide synthesis and the downregulation of collagen degradation. New observations indicate that androgens may contribute to continuous loss of kidney cells though the stimulation of apoptotic pathways. Apoptosis is an unique type of programmed cell death which is activated in several chronic kidney diseases. Studies in vitro indicate that androgens prime a Fas/FasL dependent apoptotic pathway in kidney tubule cells. This apoptotic cell death pathway is receptor-linked and interacts with the mitochondrial pathway, which may be activated by other mechanisms, such as toxins and ischemia. Therefore, the mechanisms to cell death which are primed by androgens may interact with others occurring in several conditions leading to the loss of renal cells. These findings are consistent with a role for androgens to promote chronic renal injury in men.
authors.affiliation: Nephrology Division, Department of Internal Medicine, University of Genoa, Genoa, Italy.
authors.forename: M T
authors.initials: MT
authors.lastname: Gandolfo
authors.forename: D
authors.initials: D
authors.lastname: Verzola
authors.forename: F
authors.initials: F
authors.lastname: Salvatore
authors.forename: G
authors.initials: G
authors.lastname: Gianiorio
authors.forename: V
authors.initials: V
authors.lastname: Procopio
authors.forename: A
authors.initials: A
authors.lastname: Romagnoli
authors.forename: M
authors.initials: M
authors.lastname: Giannoni
authors.forename: G
authors.initials: G
authors.lastname: Garibotto
mesh_terms: D000818:Animals; D017209:Apoptosis; D002908:Chronic Disease; D048909:Diabetes Complications / Q000453:epidemiology; D018450:Disease Progression; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006439:Hemodynamics; D006801:Humans; D007668:Kidney / Q000166:cytology / Q000502:physiology; D007674:Kidney Diseases / Q000453:epidemiology / Q000473:pathology*; D008297:Male; D012737:Sex Factors; D013739:Testosterone / Q000502:physiology
chemical_list: D012739:Gonadal Steroid Hormones; D013739:Testosterone