Gotta admit, Doc, this is not your ordinary AP question -- but we take all comers! It's been so long since I studied this area of physiology that I can't even remember if I've forgotten it.

According to
Harrison's Principles of Internal Medicine, 14th Ed. (1998), p. 2052 (the section on primary adrenocortical deficiency, but should apply here as well):
quote:
The hyponatremia is due both to loss of sodium into the urine (due to aldosterone deficiency) and to movement into the intracellular compartment. This extravascular sodium loss depletes extracellular fluid volume and accentuates hypotension. Elevated plasma vasopressin and angiotensin II levels may contribute to the hyponatremia by impairing fee water clearance.
Note that vasopressin is also known as ADH (antidiuretic hormone) or AVP (arginine vasopressin).
As usual, in trying to disentangle the roles of multiple homeostatic feedback mechanisms operating simultaneously, the trick is to sort out cause from effect.
I'm not sure I agree with your statement that "mineralocorticoid activity is not affected in secondary aldosteronism". Aldosterone is by far the most important mineralocorticoid, so whether aldosterone deficiency is primary (adrenal pathology) or secondary (renal pathology), you still have Na+ loss, causing decreased extracellular volume causing hypovolemia causing increased ADH secretion.
Take a look at the diagram
here as well (a page on
hypoaldost. that seems to be erroneously titled
hyperaldost., from a
tutorial on regulation of sodium and ECF, from Medical College of Georgia).
If this doesn't help, I doubt I can be of further assistance. You'll have to consult an expert. Good luck!