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Attenuating effect of castration or oestrogen administration on glomerular injury in adriamycin‐induced nephropathy of rats
Author(s) -
OHTSUKA Noriaki,
SAKEMI Takanobu,
TOMIYOSHI Yoshiyuki,
MORITO Fumitake
Publication year - 1996
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.1996.tb00065.x
Subject(s) - medicine , castration , endocrinology , glomerulosclerosis , proteinuria , testosterone (patch) , nephropathy , hormone , diabetes mellitus , kidney
Summary: To clarify the role of sex‐related factors in the development of focal segmental glomerulosclerosis (FSGS) we investigated the effect of castration or oestrogen administration in adriamycin (ADR)‐induced nephropathy of Sprague‐Dawley rats. At 6 weeks of age, group 1 (control group) and group 3 were shamoperated and group 2 was castrated. Adriamycin 2 mg/kg was administered intravenously to all rats at 8 weeks of age twice at a 20‐day interval. Group 3 was administered 0.2 mg oestrogen subcutaneously once a month. Bodyweight (BW) and urinary protein were measured every 4 weeks (mm 15 to 23 weeks of age. Blood pressure and serum constituents were measured at 15 and 23 weeks of age. Each group was studied morphologically at 23 weeks of age. Adriamycin induced massive proteinuria in group 1, whereas castration or oestrogen significantly attenuated proteinuria, accompanied by a significant reduction of urinary sex‐related low molecular weight (LMW) protein. the glomerulosclerosis index was significantly higher in the control group than in the castrated group or oestrogen‐treated group. Attenuation in glomerular injury was more associated with reduction of urinary sex‐related LMW protein than the reduction of serum testosterone. These observations suggest that sex‐related factors, such as a sex‐related LMW protein, influenced by castration or oestrogen administration may play a contributory role in the development of glomerulosclerosis in ADR‐induced nephropathy.