Preservation of normal adrenal androgen secretion in end stage renal disease.
A common endocrine defect in uremia is gonadal dysfunction with decreased testosterone production. Since gonadal and adrenal tissues share androgen biosynthetic pathways, we studied the stimulated adrenal androgen response in uremic patients. In contrast to the delayed or subnormal gonadal response to hCG reported by others, the adrenal response of androgens, as well as cortisol and aldosterone, to cosyntropin stimulation was unimpaired. In summary, the secretory reserve capacity of the adrenal gland for androgen, glucocorticoids and mineralocorticoids in uremia was studied with cosyntropin stimulation and found to be wall preserved.
D000311:Adrenal Glands / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone; D000328:Adult; D000450:Aldosterone / Q000378:metabolism; D000728:Androgens / Q000378:metabolism*; D000735:Androstenedione / Q000378:metabolism; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000378:metabolism; D019314:Dehydroepiandrosterone Sulfate; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D013997:Time Factors
D000728:Androgens; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D000450:Aldosterone; D019314:Dehydroepiandrosterone Sulfate; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone