Dissociation between kallikrein and aldosterone in Cushing's disease with periodic hormonogenesis.
It has been suggested that the renal kallikrein-kinin system is dependent on mineralocorticoid activity. This hypothesis was studied in a patient with cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion. The 24-h urinary excretions of sodium, potassium, cortisol, active and inactive kallikrein, aldosterone, and prostaglandin E2 (PGE2) were studied during normal and excessive cortisol secretion and after bilateral adrenalectomy. Kallikrein, PGE2 and potassium rose during cortisol overproduction while aldosterone and sodium decreased. Kallikrein, PGE2 and potassium were positively related to cortisol excretion, whereas urinary aldosterone and sodium showed a negative relationship to cortisol. Kallikrein was inversely related to aldosterone. Excretion of inactive kallikrein followed closely the changes of active kallikrein. During cortisol excess, as in our patient, the mineralocorticoid activity of cortisol will exceed that of aldosterone. This suggests that the alterations in kallikrein, aldosterone and PGE2 during cortisol excess in the present study were due to the mineralocorticoid potency of the steroid.
D000315:Adrenalectomy; D000450:Aldosterone / Q000652:urine*; D003480:Cushing Syndrome / Q000503:physiopathology / Q000652:urine*; D015232:Dinoprostone; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism / Q000652:urine; D007610:Kallikreins / Q000652:urine*; D008875:Middle Aged; D011188:Potassium / Q000652:urine; D011458:Prostaglandins E / Q000652:urine; D012964:Sodium / Q000652:urine
D011458:Prostaglandins E; D000450:Aldosterone; D012964:Sodium; D007610:Kallikreins; D015232:Dinoprostone; D011188:Potassium; D006854:Hydrocortisone